Phototherapy Coding and Documentation in the Time of Biologics

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Phototherapy Coding and Documentation in the Time of Biologics

In this era of biologics for psoriasis with ever-increasing effectiveness and safety as well as patients who have less and less time to visit the physician's office, it would seem that the days of in-office UV treatments would be numbered. However, rumors of the demise of phototherapy may be greatly exaggerated. Phototherapy is still one of the safest and most cost-effective treatments for psoriasis and other dermatoses.1 Its use often is a prerequisite for biologic therapy, and it may be the only therapeutic option for certain subsets of patients, such as children, pregnant women, and immunosuppressed patients. Moreover, narrowband UVB technology has breathed new life into phototherapy, with better efficacy and less long-term risk. Although the utilization of psoralen plus UVA (PUVA) light therapy has indeed decreased over the last 2 decades, the use of UVB therapies continues to increase dramatically.2

Phototherapy Codes

There are 4 chief Current Procedural Terminology (CPT) codes for reporting phototherapy services: (1) 96900: actinotherapy (UV light treatment); (2) 96910: photochemotherapy, tar, and UVB (Goeckerman treatment) or petrolatum and UVB; (3) 96912: photochemotherapy and PUVA; and (4) 96913: photochemotherapy (Goeckerman and/or PUVA) for severe photoresponsive dermatoses requiring at least 4 to 8 hours of care under direct supervision of the physician.3

There is lack of specificity of the CPT code descriptions for phototherapy. Moreover, insurer guidance for documentation for phototherapy is vague to nonexistent, and of course whenever the use of any medical service increases, insurer scrutiny is sure to follow. Therefore, it is not surprising that dermatology practices have reported that private insurers as well as Medicare are auditing medical records for phototherapy treatments.4 In fact, recently we have seen a Midwest private insurer demand payment from dermatologists for hundreds of 96910 phototherapy services, which the insurer asserted should have been coded as 96900 because topical therapies were not applied by the dermatology staff. The insurer did not just evaluate medical records but also contacted patients directly and asked how services had been provided. Clearly, more detailed guidance for dermatologists and insurers on documentation and performance standards for each phototherapy service is needed.

Existing coding guidance for phototherapy indicates that actinotherapy (96900) defines the basic service of treating a patient with a UV light unit.5 Actinotherapy does not involve application of topical medications while the patient is in the office.

In contrast, photochemotherapy (96910) implies addition of a chemo agent to phototherapy. Despite the somewhat nonspecific nature of the code descriptor, it is apparent that application of photoenhancing agents such as tar, petrolatum, or distillates of petrolatum meet the requirements of 96910. The Coder's Desk Reference for Procedures 2017 describes 96910 as "the physician uses photosensitizing chemicals and light rays to treat skin ailments."6 Application of light-enhancing topical products should occur within the office by either staff or the patient. In fact, examination of practice expense data from the Centers for Medicare & Medicaid Services indicated that the 96910 code includes payment for clinical staff time to apply topical products as well as the cost of the topical agent(s).7 

The PUVA code 96912 is defined by the use of photosensitizing psoralen medication, which can be administered topically or orally, followed by UVA treatment. In my experience, PUVA has similar performance standards with in-office application of psoralen, if applicable. If application of topical photoenhancing products occurs outside the office, the requirements of photochemotherapy are not met, and 96900 should be reported. 

The 96913 code defines prolonged phototherapy service with intensive topical therapy requirements and multiple phototherapy sessions per day.3 This code is rarely reported (average of fewer than 100 times in the Medicare population per year), and most insurers do not reimburse this service. 

Protecting Yourself From an Audit

In my experience, review of private insurer audits of phototherapy services has yielded important lessons. First, having a written standard operating procedure in place regarding the performance of phototherapy services and how application of topicals will be handled has been helpful in audit defense. The other key to beating audits for phototherapy services is to have detailed documentation or a flowchart in the medical record regarding the topical agent and the light administration. The medical record should include what topical agent was applied, if any; whether the topical agent was applied in the office; where the topical product was applied; and who applied the topical product. Sometimes topical product application by a physician or staff is not feasible because of patient preference or the site of application. If the patient applied the topical, document that assistance was offered and refused, along with what type of UV light was used and the dosage. Inclusion of these elements in the medical record provides a clear picture of the delivery of the phototherapy service and will aid in responding to medical record audit.

 

 

Final Thoughts

Phototherapy is a critical treatment modality that continues to be utilized frequently in the expanding armamentarium of treatments for dermatoses. Phototherapy is performed almost exclusively by dermatologists and allows dermatologists to offer a unique level of care and value in the treatment of skin disease. Careful documentation, a written standard operating procedure, and adherence to proper performance standards will allow dermatologists to be compensated fairly for this important treatment modality and pass audits that are likely to occur.

References
  1. Lapolla W, Yentzer BA, Bagel J, et al. A review of phototherapy protocols for psoriasis treatment. J Am Acad Dermatol. 2011;64:936-949.  
  2. Simpson GL, Yelverton CB, Rittenberg S, et al. Do utilization management controls for phototherapy increase the prescription of biologics? J Dermatolog Treat. 2006;17:359-361.
  3. Current Procedural Terminology 2017, Professional Edition. Chicago IL: American Medical Association; 2016.
  4. American Academy of Dermatology Association. Insurers review billing for photochemotherapy (CPT 96910). Derm Coding Consult. Spring 2009;13:4.  
  5. American Academy of Dermatology Association. Coding Q&A's. Derm Coding Consult. Spring 2007;11:5, 7, 8.  
  6. Coders' Desk Reference for Procedures 2017. Chicago, IL: Optum360; 2017.  
  7. Relative Value Scale Update Committee Database. Chicago, IL: American Medical Association; 2016.
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In this era of biologics for psoriasis with ever-increasing effectiveness and safety as well as patients who have less and less time to visit the physician's office, it would seem that the days of in-office UV treatments would be numbered. However, rumors of the demise of phototherapy may be greatly exaggerated. Phototherapy is still one of the safest and most cost-effective treatments for psoriasis and other dermatoses.1 Its use often is a prerequisite for biologic therapy, and it may be the only therapeutic option for certain subsets of patients, such as children, pregnant women, and immunosuppressed patients. Moreover, narrowband UVB technology has breathed new life into phototherapy, with better efficacy and less long-term risk. Although the utilization of psoralen plus UVA (PUVA) light therapy has indeed decreased over the last 2 decades, the use of UVB therapies continues to increase dramatically.2

Phototherapy Codes

There are 4 chief Current Procedural Terminology (CPT) codes for reporting phototherapy services: (1) 96900: actinotherapy (UV light treatment); (2) 96910: photochemotherapy, tar, and UVB (Goeckerman treatment) or petrolatum and UVB; (3) 96912: photochemotherapy and PUVA; and (4) 96913: photochemotherapy (Goeckerman and/or PUVA) for severe photoresponsive dermatoses requiring at least 4 to 8 hours of care under direct supervision of the physician.3

There is lack of specificity of the CPT code descriptions for phototherapy. Moreover, insurer guidance for documentation for phototherapy is vague to nonexistent, and of course whenever the use of any medical service increases, insurer scrutiny is sure to follow. Therefore, it is not surprising that dermatology practices have reported that private insurers as well as Medicare are auditing medical records for phototherapy treatments.4 In fact, recently we have seen a Midwest private insurer demand payment from dermatologists for hundreds of 96910 phototherapy services, which the insurer asserted should have been coded as 96900 because topical therapies were not applied by the dermatology staff. The insurer did not just evaluate medical records but also contacted patients directly and asked how services had been provided. Clearly, more detailed guidance for dermatologists and insurers on documentation and performance standards for each phototherapy service is needed.

Existing coding guidance for phototherapy indicates that actinotherapy (96900) defines the basic service of treating a patient with a UV light unit.5 Actinotherapy does not involve application of topical medications while the patient is in the office.

In contrast, photochemotherapy (96910) implies addition of a chemo agent to phototherapy. Despite the somewhat nonspecific nature of the code descriptor, it is apparent that application of photoenhancing agents such as tar, petrolatum, or distillates of petrolatum meet the requirements of 96910. The Coder's Desk Reference for Procedures 2017 describes 96910 as "the physician uses photosensitizing chemicals and light rays to treat skin ailments."6 Application of light-enhancing topical products should occur within the office by either staff or the patient. In fact, examination of practice expense data from the Centers for Medicare & Medicaid Services indicated that the 96910 code includes payment for clinical staff time to apply topical products as well as the cost of the topical agent(s).7 

The PUVA code 96912 is defined by the use of photosensitizing psoralen medication, which can be administered topically or orally, followed by UVA treatment. In my experience, PUVA has similar performance standards with in-office application of psoralen, if applicable. If application of topical photoenhancing products occurs outside the office, the requirements of photochemotherapy are not met, and 96900 should be reported. 

The 96913 code defines prolonged phototherapy service with intensive topical therapy requirements and multiple phototherapy sessions per day.3 This code is rarely reported (average of fewer than 100 times in the Medicare population per year), and most insurers do not reimburse this service. 

Protecting Yourself From an Audit

In my experience, review of private insurer audits of phototherapy services has yielded important lessons. First, having a written standard operating procedure in place regarding the performance of phototherapy services and how application of topicals will be handled has been helpful in audit defense. The other key to beating audits for phototherapy services is to have detailed documentation or a flowchart in the medical record regarding the topical agent and the light administration. The medical record should include what topical agent was applied, if any; whether the topical agent was applied in the office; where the topical product was applied; and who applied the topical product. Sometimes topical product application by a physician or staff is not feasible because of patient preference or the site of application. If the patient applied the topical, document that assistance was offered and refused, along with what type of UV light was used and the dosage. Inclusion of these elements in the medical record provides a clear picture of the delivery of the phototherapy service and will aid in responding to medical record audit.

 

 

Final Thoughts

Phototherapy is a critical treatment modality that continues to be utilized frequently in the expanding armamentarium of treatments for dermatoses. Phototherapy is performed almost exclusively by dermatologists and allows dermatologists to offer a unique level of care and value in the treatment of skin disease. Careful documentation, a written standard operating procedure, and adherence to proper performance standards will allow dermatologists to be compensated fairly for this important treatment modality and pass audits that are likely to occur.

In this era of biologics for psoriasis with ever-increasing effectiveness and safety as well as patients who have less and less time to visit the physician's office, it would seem that the days of in-office UV treatments would be numbered. However, rumors of the demise of phototherapy may be greatly exaggerated. Phototherapy is still one of the safest and most cost-effective treatments for psoriasis and other dermatoses.1 Its use often is a prerequisite for biologic therapy, and it may be the only therapeutic option for certain subsets of patients, such as children, pregnant women, and immunosuppressed patients. Moreover, narrowband UVB technology has breathed new life into phototherapy, with better efficacy and less long-term risk. Although the utilization of psoralen plus UVA (PUVA) light therapy has indeed decreased over the last 2 decades, the use of UVB therapies continues to increase dramatically.2

Phototherapy Codes

There are 4 chief Current Procedural Terminology (CPT) codes for reporting phototherapy services: (1) 96900: actinotherapy (UV light treatment); (2) 96910: photochemotherapy, tar, and UVB (Goeckerman treatment) or petrolatum and UVB; (3) 96912: photochemotherapy and PUVA; and (4) 96913: photochemotherapy (Goeckerman and/or PUVA) for severe photoresponsive dermatoses requiring at least 4 to 8 hours of care under direct supervision of the physician.3

There is lack of specificity of the CPT code descriptions for phototherapy. Moreover, insurer guidance for documentation for phototherapy is vague to nonexistent, and of course whenever the use of any medical service increases, insurer scrutiny is sure to follow. Therefore, it is not surprising that dermatology practices have reported that private insurers as well as Medicare are auditing medical records for phototherapy treatments.4 In fact, recently we have seen a Midwest private insurer demand payment from dermatologists for hundreds of 96910 phototherapy services, which the insurer asserted should have been coded as 96900 because topical therapies were not applied by the dermatology staff. The insurer did not just evaluate medical records but also contacted patients directly and asked how services had been provided. Clearly, more detailed guidance for dermatologists and insurers on documentation and performance standards for each phototherapy service is needed.

Existing coding guidance for phototherapy indicates that actinotherapy (96900) defines the basic service of treating a patient with a UV light unit.5 Actinotherapy does not involve application of topical medications while the patient is in the office.

In contrast, photochemotherapy (96910) implies addition of a chemo agent to phototherapy. Despite the somewhat nonspecific nature of the code descriptor, it is apparent that application of photoenhancing agents such as tar, petrolatum, or distillates of petrolatum meet the requirements of 96910. The Coder's Desk Reference for Procedures 2017 describes 96910 as "the physician uses photosensitizing chemicals and light rays to treat skin ailments."6 Application of light-enhancing topical products should occur within the office by either staff or the patient. In fact, examination of practice expense data from the Centers for Medicare & Medicaid Services indicated that the 96910 code includes payment for clinical staff time to apply topical products as well as the cost of the topical agent(s).7 

The PUVA code 96912 is defined by the use of photosensitizing psoralen medication, which can be administered topically or orally, followed by UVA treatment. In my experience, PUVA has similar performance standards with in-office application of psoralen, if applicable. If application of topical photoenhancing products occurs outside the office, the requirements of photochemotherapy are not met, and 96900 should be reported. 

The 96913 code defines prolonged phototherapy service with intensive topical therapy requirements and multiple phototherapy sessions per day.3 This code is rarely reported (average of fewer than 100 times in the Medicare population per year), and most insurers do not reimburse this service. 

Protecting Yourself From an Audit

In my experience, review of private insurer audits of phototherapy services has yielded important lessons. First, having a written standard operating procedure in place regarding the performance of phototherapy services and how application of topicals will be handled has been helpful in audit defense. The other key to beating audits for phototherapy services is to have detailed documentation or a flowchart in the medical record regarding the topical agent and the light administration. The medical record should include what topical agent was applied, if any; whether the topical agent was applied in the office; where the topical product was applied; and who applied the topical product. Sometimes topical product application by a physician or staff is not feasible because of patient preference or the site of application. If the patient applied the topical, document that assistance was offered and refused, along with what type of UV light was used and the dosage. Inclusion of these elements in the medical record provides a clear picture of the delivery of the phototherapy service and will aid in responding to medical record audit.

 

 

Final Thoughts

Phototherapy is a critical treatment modality that continues to be utilized frequently in the expanding armamentarium of treatments for dermatoses. Phototherapy is performed almost exclusively by dermatologists and allows dermatologists to offer a unique level of care and value in the treatment of skin disease. Careful documentation, a written standard operating procedure, and adherence to proper performance standards will allow dermatologists to be compensated fairly for this important treatment modality and pass audits that are likely to occur.

References
  1. Lapolla W, Yentzer BA, Bagel J, et al. A review of phototherapy protocols for psoriasis treatment. J Am Acad Dermatol. 2011;64:936-949.  
  2. Simpson GL, Yelverton CB, Rittenberg S, et al. Do utilization management controls for phototherapy increase the prescription of biologics? J Dermatolog Treat. 2006;17:359-361.
  3. Current Procedural Terminology 2017, Professional Edition. Chicago IL: American Medical Association; 2016.
  4. American Academy of Dermatology Association. Insurers review billing for photochemotherapy (CPT 96910). Derm Coding Consult. Spring 2009;13:4.  
  5. American Academy of Dermatology Association. Coding Q&A's. Derm Coding Consult. Spring 2007;11:5, 7, 8.  
  6. Coders' Desk Reference for Procedures 2017. Chicago, IL: Optum360; 2017.  
  7. Relative Value Scale Update Committee Database. Chicago, IL: American Medical Association; 2016.
References
  1. Lapolla W, Yentzer BA, Bagel J, et al. A review of phototherapy protocols for psoriasis treatment. J Am Acad Dermatol. 2011;64:936-949.  
  2. Simpson GL, Yelverton CB, Rittenberg S, et al. Do utilization management controls for phototherapy increase the prescription of biologics? J Dermatolog Treat. 2006;17:359-361.
  3. Current Procedural Terminology 2017, Professional Edition. Chicago IL: American Medical Association; 2016.
  4. American Academy of Dermatology Association. Insurers review billing for photochemotherapy (CPT 96910). Derm Coding Consult. Spring 2009;13:4.  
  5. American Academy of Dermatology Association. Coding Q&A's. Derm Coding Consult. Spring 2007;11:5, 7, 8.  
  6. Coders' Desk Reference for Procedures 2017. Chicago, IL: Optum360; 2017.  
  7. Relative Value Scale Update Committee Database. Chicago, IL: American Medical Association; 2016.
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How to raise HPV vaccine rates: Work together

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Despite widespread availability of the human papillomavirus vaccine over the last 11 years, vaccination rates continue to lag behind national targets and are far behind other vaccines routinely administered in adolescence, such as the meningococcal and tetanus vaccines.

Better collaboration among pediatricians and obstetrician-gynecologists to promote the HPV vaccine may be one answer to turning the tide, said David W. Kimberlin, MD, codirector of the division of pediatric infectious diseases at the University of Alabama at Birmingham and president of the Pediatric Infectious Diseases Society.

Courtesy Steve Wood/University of Alabama, Birmingham
Dr. David Kimberlin coauthored a paper on the importance of collaboration between ob.gyns. and pediatricians to raise HPV vaccination rates.
“Prevention of HPV-related cancers is in the pediatric period, but the disease being prevented [occurs] in women and men who are well into adulthood,” Dr. Kimberlin said in an interview. “We have to work together to raise awareness so that lives can be saved. Every patient encounter is an opportunity to do so, thereby the coordination between ob.gyn. and pediatrics that we are advocating is all the more important.”

As of 2015, just 63% of eligible U.S. girls completed the first dose of the HPV vaccination, 52% completed two doses, and 42% finished the three-dose series, according to a recent “Call to Action” paper in the American Journal of Obstetrics and Gynecology (doi: 10.1016/j.ajog.2017.02.026). Although the HPV vaccine has been recommended for boys since 2011, just half of eligible boys completed the first dose, 39% completed two doses, and 28% finished the full series. By contrast, 86% of adolescents received the tetanus, diphtheria, and acellular pertussis vaccine, and 81% received the first dose of the meningococcal vaccine. The federal government’s Office of Disease Prevention and Health Promotion aims for an 80% HPV vaccination completion rate for girls and boys aged 13-15 years by 2020.

[polldaddy:{"method":"iframe","type":"survey","src":"//newspolls2017.polldaddy.com/s/how-to-raise-hpv-vaccine-rates?iframe=1"}]The CDC now recommends that 11- to 12-year-olds get two doses of the HPV vaccine, rather than three, with the second dose given 6-12 months after the first (MMWR. 2016;65:1405-8).

The common ways in which the HPV vaccine is introduced to parents likely contributes to the low vaccination rates, said Beth Auslander, PhD, a clinical psychologist and associate professor in the department of pediatrics at the University of Texas Medical Branch in Galveston. Some pediatricians may tell parents about school-mandated vaccines first and then as a side note, mention the HPV vaccine.

“The way it’s presented at times is being separate from the other vaccines,” Dr. Auslander said. “Sometimes it sounds optional.”

Parents often are uncertain about the safety and efficacy of the HPV vaccine, she added, and some wrongly assume the vaccine will lead to sexual activity among their children.

Dr. Jennie Yoost
Both ob.gyns. and pediatricians could do a better job of giving stronger recommendations about the HPV vaccine, said Jennie Yoost, MD, a Huntington, W.Va.–based pediatric and adolescent gynecologist and a member of the American Congress of Obstetricians and Gynecologists’ (ACOG) Immunization Expert Work Group. She is also an assistant professor of ob.gyn. at Marshall University in Huntington, W.Va.* 

“Sometimes it can take a little longer to talk about,” Dr. Yoost said in an interview. “A lot of times, parents will bring up questions or concerns about the HPV vaccine. If physicians aren’t comfortable talking about those topics, they may not give the best recommendation. Pediatricians are not dealing with cervical cancer, so they may have a harder time recommending a vaccine based on outcomes they don’t deal with.”

Ob.gyns. are in a unique position to reach out to their pediatric counterparts and discuss strategies for catching more patients eligible for the HPV vaccine, said Sarah Dilley, MD, a gynecologic oncology fellow at the University of Alabama at Birmingham and the lead author of the recent Call to Action paper.

“We offer a unique perspective in that we are treating the conditions that the HPV vaccine is preventing, so we have more of a sense of urgency and an understanding of why that is so important,” Dr. Dilley said in an interview. “Obviously, pediatricians understand this as well, but it’s not something they see every day in their practice. We, as ob.gyns., have the opportunity to talk to our pediatric colleagues about the importance and really how devastating these conditions can be and how important it is to prevent them.”

In the recent paper, Dr. Dilley and her colleagues recommend that ob.gyns. speak to pediatricians and primary care physicians in their community to promote the vaccine and encourage them to view the Centers for Disease Control and Prevention’s You Are the Key presentation. The CDC resources include tips for how to discuss the burden of HPV-related diseases and effective communication with parents, an update on state vaccination rates, and the latest HPV vaccination recommendations.

Dr. Dilley encourages ob.gyns. and pediatricians to find different opportunities and venues to discuss the HPV vaccine. Ask about the pediatrician’s current approach to the vaccine, the doctor’s communication with parents, and how such practices could be improved, she said.

“People like to hear from their colleagues,” Dr. Dilley said. “Hearing from ob.gyns. [about] their experiences could be really helpful, whether it’s doing lunch and learns, formal education, grand rounds, or even more informal talks at the hospital.”

Ob.gyns. and pediatricians also need to better coordinate their messaging so that there is more consistent emphasis during each patient encounter about the need of the HPV vaccination, Dr. Kimberlin said. There needs to be a renewed focus on the vaccine as a cancer vaccination, he said.

“The nuances of HPV and the way that HPV is acquired, namely sexually transmitted, has taken too much of a front row consideration in the conversations that parents sometimes want to have with their child’s health care providers,” Dr. Kimberlin said. “We have to stress this is a cancer vaccine. This is a vaccine that prevents the deaths of thousands of women and men. We simply need to get that message out more forcefully.”

In addition, there’s a need for joint action to debunk myths about the vaccine and work toward eliminating the stigma surrounding it, Dr. Dilley said.

“I talk to a lot parents about the HPV vaccine and there’s so much misinformation online,” she said. “But a lot of patients do look at websites of their ob.gyn. or their pediatrician, [and] if they see something reputable coming from one of those sites, they might listen. We have a lot of patients who are mothers or grandmothers of kids; that’s also an opportunity for us to say, ‘Hey while we’re screening you for cervical cancer, let’s talk about the HPV vaccine.’ That’s a really good opportunity to help our [pediatric] colleagues out.”

 

 

5 steps to increase HPV vaccination

Melissa Kottke, MD, director of the Jane Fonda Center for Adolescent Reproductive Health at Emory University offered her practice steps for increased HPV vaccination rates.

1. Be clear about your recommendation. For example, “I recommend the HPV vaccine. It can help prevent cancer.”

Dr. Melissa Kottke
2. Do not delay. From an immune response and potential HPV exposure standpoint, receiving the vaccine at a younger age is better than receiving it at an older age.

3. Educate the entire clinical team (front desk staff, nursing, medical assistants, etc.) about the HPV vaccine so there is consistent messaging and delivery.

4. Establish streamlined systems. The vaccine recommendation, order, and follow-up should be streamlined and automated, if possible. Systems should also ensure documentation of vaccine receipt.

5. Make time for conversations with patients who are mothers and grandmothers. Recommend the HPV vaccine for males and females aged 9-26 years old. Encourage parents/grandparents to follow-up with the child’s doctor or offer to provide the vaccine in your office.

*This story was updated 8/22/2017.
 

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Despite widespread availability of the human papillomavirus vaccine over the last 11 years, vaccination rates continue to lag behind national targets and are far behind other vaccines routinely administered in adolescence, such as the meningococcal and tetanus vaccines.

Better collaboration among pediatricians and obstetrician-gynecologists to promote the HPV vaccine may be one answer to turning the tide, said David W. Kimberlin, MD, codirector of the division of pediatric infectious diseases at the University of Alabama at Birmingham and president of the Pediatric Infectious Diseases Society.

Courtesy Steve Wood/University of Alabama, Birmingham
Dr. David Kimberlin coauthored a paper on the importance of collaboration between ob.gyns. and pediatricians to raise HPV vaccination rates.
“Prevention of HPV-related cancers is in the pediatric period, but the disease being prevented [occurs] in women and men who are well into adulthood,” Dr. Kimberlin said in an interview. “We have to work together to raise awareness so that lives can be saved. Every patient encounter is an opportunity to do so, thereby the coordination between ob.gyn. and pediatrics that we are advocating is all the more important.”

As of 2015, just 63% of eligible U.S. girls completed the first dose of the HPV vaccination, 52% completed two doses, and 42% finished the three-dose series, according to a recent “Call to Action” paper in the American Journal of Obstetrics and Gynecology (doi: 10.1016/j.ajog.2017.02.026). Although the HPV vaccine has been recommended for boys since 2011, just half of eligible boys completed the first dose, 39% completed two doses, and 28% finished the full series. By contrast, 86% of adolescents received the tetanus, diphtheria, and acellular pertussis vaccine, and 81% received the first dose of the meningococcal vaccine. The federal government’s Office of Disease Prevention and Health Promotion aims for an 80% HPV vaccination completion rate for girls and boys aged 13-15 years by 2020.

[polldaddy:{"method":"iframe","type":"survey","src":"//newspolls2017.polldaddy.com/s/how-to-raise-hpv-vaccine-rates?iframe=1"}]The CDC now recommends that 11- to 12-year-olds get two doses of the HPV vaccine, rather than three, with the second dose given 6-12 months after the first (MMWR. 2016;65:1405-8).

The common ways in which the HPV vaccine is introduced to parents likely contributes to the low vaccination rates, said Beth Auslander, PhD, a clinical psychologist and associate professor in the department of pediatrics at the University of Texas Medical Branch in Galveston. Some pediatricians may tell parents about school-mandated vaccines first and then as a side note, mention the HPV vaccine.

“The way it’s presented at times is being separate from the other vaccines,” Dr. Auslander said. “Sometimes it sounds optional.”

Parents often are uncertain about the safety and efficacy of the HPV vaccine, she added, and some wrongly assume the vaccine will lead to sexual activity among their children.

Dr. Jennie Yoost
Both ob.gyns. and pediatricians could do a better job of giving stronger recommendations about the HPV vaccine, said Jennie Yoost, MD, a Huntington, W.Va.–based pediatric and adolescent gynecologist and a member of the American Congress of Obstetricians and Gynecologists’ (ACOG) Immunization Expert Work Group. She is also an assistant professor of ob.gyn. at Marshall University in Huntington, W.Va.* 

“Sometimes it can take a little longer to talk about,” Dr. Yoost said in an interview. “A lot of times, parents will bring up questions or concerns about the HPV vaccine. If physicians aren’t comfortable talking about those topics, they may not give the best recommendation. Pediatricians are not dealing with cervical cancer, so they may have a harder time recommending a vaccine based on outcomes they don’t deal with.”

Ob.gyns. are in a unique position to reach out to their pediatric counterparts and discuss strategies for catching more patients eligible for the HPV vaccine, said Sarah Dilley, MD, a gynecologic oncology fellow at the University of Alabama at Birmingham and the lead author of the recent Call to Action paper.

“We offer a unique perspective in that we are treating the conditions that the HPV vaccine is preventing, so we have more of a sense of urgency and an understanding of why that is so important,” Dr. Dilley said in an interview. “Obviously, pediatricians understand this as well, but it’s not something they see every day in their practice. We, as ob.gyns., have the opportunity to talk to our pediatric colleagues about the importance and really how devastating these conditions can be and how important it is to prevent them.”

In the recent paper, Dr. Dilley and her colleagues recommend that ob.gyns. speak to pediatricians and primary care physicians in their community to promote the vaccine and encourage them to view the Centers for Disease Control and Prevention’s You Are the Key presentation. The CDC resources include tips for how to discuss the burden of HPV-related diseases and effective communication with parents, an update on state vaccination rates, and the latest HPV vaccination recommendations.

Dr. Dilley encourages ob.gyns. and pediatricians to find different opportunities and venues to discuss the HPV vaccine. Ask about the pediatrician’s current approach to the vaccine, the doctor’s communication with parents, and how such practices could be improved, she said.

“People like to hear from their colleagues,” Dr. Dilley said. “Hearing from ob.gyns. [about] their experiences could be really helpful, whether it’s doing lunch and learns, formal education, grand rounds, or even more informal talks at the hospital.”

Ob.gyns. and pediatricians also need to better coordinate their messaging so that there is more consistent emphasis during each patient encounter about the need of the HPV vaccination, Dr. Kimberlin said. There needs to be a renewed focus on the vaccine as a cancer vaccination, he said.

“The nuances of HPV and the way that HPV is acquired, namely sexually transmitted, has taken too much of a front row consideration in the conversations that parents sometimes want to have with their child’s health care providers,” Dr. Kimberlin said. “We have to stress this is a cancer vaccine. This is a vaccine that prevents the deaths of thousands of women and men. We simply need to get that message out more forcefully.”

In addition, there’s a need for joint action to debunk myths about the vaccine and work toward eliminating the stigma surrounding it, Dr. Dilley said.

“I talk to a lot parents about the HPV vaccine and there’s so much misinformation online,” she said. “But a lot of patients do look at websites of their ob.gyn. or their pediatrician, [and] if they see something reputable coming from one of those sites, they might listen. We have a lot of patients who are mothers or grandmothers of kids; that’s also an opportunity for us to say, ‘Hey while we’re screening you for cervical cancer, let’s talk about the HPV vaccine.’ That’s a really good opportunity to help our [pediatric] colleagues out.”

 

 

5 steps to increase HPV vaccination

Melissa Kottke, MD, director of the Jane Fonda Center for Adolescent Reproductive Health at Emory University offered her practice steps for increased HPV vaccination rates.

1. Be clear about your recommendation. For example, “I recommend the HPV vaccine. It can help prevent cancer.”

Dr. Melissa Kottke
2. Do not delay. From an immune response and potential HPV exposure standpoint, receiving the vaccine at a younger age is better than receiving it at an older age.

3. Educate the entire clinical team (front desk staff, nursing, medical assistants, etc.) about the HPV vaccine so there is consistent messaging and delivery.

4. Establish streamlined systems. The vaccine recommendation, order, and follow-up should be streamlined and automated, if possible. Systems should also ensure documentation of vaccine receipt.

5. Make time for conversations with patients who are mothers and grandmothers. Recommend the HPV vaccine for males and females aged 9-26 years old. Encourage parents/grandparents to follow-up with the child’s doctor or offer to provide the vaccine in your office.

*This story was updated 8/22/2017.
 

 

Despite widespread availability of the human papillomavirus vaccine over the last 11 years, vaccination rates continue to lag behind national targets and are far behind other vaccines routinely administered in adolescence, such as the meningococcal and tetanus vaccines.

Better collaboration among pediatricians and obstetrician-gynecologists to promote the HPV vaccine may be one answer to turning the tide, said David W. Kimberlin, MD, codirector of the division of pediatric infectious diseases at the University of Alabama at Birmingham and president of the Pediatric Infectious Diseases Society.

Courtesy Steve Wood/University of Alabama, Birmingham
Dr. David Kimberlin coauthored a paper on the importance of collaboration between ob.gyns. and pediatricians to raise HPV vaccination rates.
“Prevention of HPV-related cancers is in the pediatric period, but the disease being prevented [occurs] in women and men who are well into adulthood,” Dr. Kimberlin said in an interview. “We have to work together to raise awareness so that lives can be saved. Every patient encounter is an opportunity to do so, thereby the coordination between ob.gyn. and pediatrics that we are advocating is all the more important.”

As of 2015, just 63% of eligible U.S. girls completed the first dose of the HPV vaccination, 52% completed two doses, and 42% finished the three-dose series, according to a recent “Call to Action” paper in the American Journal of Obstetrics and Gynecology (doi: 10.1016/j.ajog.2017.02.026). Although the HPV vaccine has been recommended for boys since 2011, just half of eligible boys completed the first dose, 39% completed two doses, and 28% finished the full series. By contrast, 86% of adolescents received the tetanus, diphtheria, and acellular pertussis vaccine, and 81% received the first dose of the meningococcal vaccine. The federal government’s Office of Disease Prevention and Health Promotion aims for an 80% HPV vaccination completion rate for girls and boys aged 13-15 years by 2020.

[polldaddy:{"method":"iframe","type":"survey","src":"//newspolls2017.polldaddy.com/s/how-to-raise-hpv-vaccine-rates?iframe=1"}]The CDC now recommends that 11- to 12-year-olds get two doses of the HPV vaccine, rather than three, with the second dose given 6-12 months after the first (MMWR. 2016;65:1405-8).

The common ways in which the HPV vaccine is introduced to parents likely contributes to the low vaccination rates, said Beth Auslander, PhD, a clinical psychologist and associate professor in the department of pediatrics at the University of Texas Medical Branch in Galveston. Some pediatricians may tell parents about school-mandated vaccines first and then as a side note, mention the HPV vaccine.

“The way it’s presented at times is being separate from the other vaccines,” Dr. Auslander said. “Sometimes it sounds optional.”

Parents often are uncertain about the safety and efficacy of the HPV vaccine, she added, and some wrongly assume the vaccine will lead to sexual activity among their children.

Dr. Jennie Yoost
Both ob.gyns. and pediatricians could do a better job of giving stronger recommendations about the HPV vaccine, said Jennie Yoost, MD, a Huntington, W.Va.–based pediatric and adolescent gynecologist and a member of the American Congress of Obstetricians and Gynecologists’ (ACOG) Immunization Expert Work Group. She is also an assistant professor of ob.gyn. at Marshall University in Huntington, W.Va.* 

“Sometimes it can take a little longer to talk about,” Dr. Yoost said in an interview. “A lot of times, parents will bring up questions or concerns about the HPV vaccine. If physicians aren’t comfortable talking about those topics, they may not give the best recommendation. Pediatricians are not dealing with cervical cancer, so they may have a harder time recommending a vaccine based on outcomes they don’t deal with.”

Ob.gyns. are in a unique position to reach out to their pediatric counterparts and discuss strategies for catching more patients eligible for the HPV vaccine, said Sarah Dilley, MD, a gynecologic oncology fellow at the University of Alabama at Birmingham and the lead author of the recent Call to Action paper.

“We offer a unique perspective in that we are treating the conditions that the HPV vaccine is preventing, so we have more of a sense of urgency and an understanding of why that is so important,” Dr. Dilley said in an interview. “Obviously, pediatricians understand this as well, but it’s not something they see every day in their practice. We, as ob.gyns., have the opportunity to talk to our pediatric colleagues about the importance and really how devastating these conditions can be and how important it is to prevent them.”

In the recent paper, Dr. Dilley and her colleagues recommend that ob.gyns. speak to pediatricians and primary care physicians in their community to promote the vaccine and encourage them to view the Centers for Disease Control and Prevention’s You Are the Key presentation. The CDC resources include tips for how to discuss the burden of HPV-related diseases and effective communication with parents, an update on state vaccination rates, and the latest HPV vaccination recommendations.

Dr. Dilley encourages ob.gyns. and pediatricians to find different opportunities and venues to discuss the HPV vaccine. Ask about the pediatrician’s current approach to the vaccine, the doctor’s communication with parents, and how such practices could be improved, she said.

“People like to hear from their colleagues,” Dr. Dilley said. “Hearing from ob.gyns. [about] their experiences could be really helpful, whether it’s doing lunch and learns, formal education, grand rounds, or even more informal talks at the hospital.”

Ob.gyns. and pediatricians also need to better coordinate their messaging so that there is more consistent emphasis during each patient encounter about the need of the HPV vaccination, Dr. Kimberlin said. There needs to be a renewed focus on the vaccine as a cancer vaccination, he said.

“The nuances of HPV and the way that HPV is acquired, namely sexually transmitted, has taken too much of a front row consideration in the conversations that parents sometimes want to have with their child’s health care providers,” Dr. Kimberlin said. “We have to stress this is a cancer vaccine. This is a vaccine that prevents the deaths of thousands of women and men. We simply need to get that message out more forcefully.”

In addition, there’s a need for joint action to debunk myths about the vaccine and work toward eliminating the stigma surrounding it, Dr. Dilley said.

“I talk to a lot parents about the HPV vaccine and there’s so much misinformation online,” she said. “But a lot of patients do look at websites of their ob.gyn. or their pediatrician, [and] if they see something reputable coming from one of those sites, they might listen. We have a lot of patients who are mothers or grandmothers of kids; that’s also an opportunity for us to say, ‘Hey while we’re screening you for cervical cancer, let’s talk about the HPV vaccine.’ That’s a really good opportunity to help our [pediatric] colleagues out.”

 

 

5 steps to increase HPV vaccination

Melissa Kottke, MD, director of the Jane Fonda Center for Adolescent Reproductive Health at Emory University offered her practice steps for increased HPV vaccination rates.

1. Be clear about your recommendation. For example, “I recommend the HPV vaccine. It can help prevent cancer.”

Dr. Melissa Kottke
2. Do not delay. From an immune response and potential HPV exposure standpoint, receiving the vaccine at a younger age is better than receiving it at an older age.

3. Educate the entire clinical team (front desk staff, nursing, medical assistants, etc.) about the HPV vaccine so there is consistent messaging and delivery.

4. Establish streamlined systems. The vaccine recommendation, order, and follow-up should be streamlined and automated, if possible. Systems should also ensure documentation of vaccine receipt.

5. Make time for conversations with patients who are mothers and grandmothers. Recommend the HPV vaccine for males and females aged 9-26 years old. Encourage parents/grandparents to follow-up with the child’s doctor or offer to provide the vaccine in your office.

*This story was updated 8/22/2017.
 

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Start ART in first 3 months in infants with perinatal HIV

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– Infants with perinatal HIV infection are significantly more likely to achieve viral suppression by age 12 months if they start antiretroviral therapy (ART) before age 3 months than if physicians wait until 3-6 months of age, Paolo Palma, MD, reported at the annual meeting of the European Society for Paediatric Infectious Diseases.

He presented a study of the factors associated with time to virologic sup

Dr. Paolo Palma
pression in 420 perinatally HIV-infected children who began ART before age 6 months. The study was conducted by EPPICC, the European Pregnancy and Paediatric HIV Cohort Collaboration, a consortium of 25 research groups in 20 European countries and Thailand. To date, the EPPICC data base includes more than 30,000 HIV-positive pregnant women and more than 6,000 perinatally infected children.

The purpose of this study was to identify the key factors involved in attaining early virologic control of perinatally acquired HIV. This information is necessary to lay the groundwork for planned future investigations of immunotherapeutic strategies designed to achieve sustained ART-free remission. Such strategies are most likely to be successful in very young children who have not yet built up a massive viral load, explained Dr. Palma of Bambino Gesù Children’s Hospital in Rome.

“A major obstacle to curing HIV infection is persistence of virus as integrated proviral DNA in long-lived cells even after many years on ART. ART-free HIV remission is more likely to occur if viral suppression is achieved very early in infection,” he said.

The median age of the 420 subjects at the time ART was initiated was 2.9 months. Their CD4 cell percentage was 34%, with a median CD4 cell count of 1,780 and an average viral load at baseline of 316,228 copies/mL.

At 12 months of age, 84% of patients had achieved viral suppression. In multivariate analyses adjusted for initial ART regimen and geographic location, three factors were associated with this outcome: younger age at ART onset, a lower baseline viral load, and a higher per
xrender/thinkstockphotos.com
This image is a 3D illustration of the HIV virus.
centage of CD4 cells.

Indeed, for each 1-month increase in age at onset of ART, the likelihood of virologic response at age 12 months decreased by 16%. Similarly, the rate of virologic response at 1 year of age decreased by 15% for each 10 copies/mL increase in viral load at the start of ART. In contrast, the likelihood of virologic suppression at age 12 months increased by 10% for each 10% increase in CD4 cell percentage at the start of treatment.

Among the variables that proved unrelated to virologic suppression at 1 year of age were gender, AIDS status, feeding style (breastfed versus bottle-fed), and ethnicity.

Dr. Palma reported having no relevant financial disclosures.

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– Infants with perinatal HIV infection are significantly more likely to achieve viral suppression by age 12 months if they start antiretroviral therapy (ART) before age 3 months than if physicians wait until 3-6 months of age, Paolo Palma, MD, reported at the annual meeting of the European Society for Paediatric Infectious Diseases.

He presented a study of the factors associated with time to virologic sup

Dr. Paolo Palma
pression in 420 perinatally HIV-infected children who began ART before age 6 months. The study was conducted by EPPICC, the European Pregnancy and Paediatric HIV Cohort Collaboration, a consortium of 25 research groups in 20 European countries and Thailand. To date, the EPPICC data base includes more than 30,000 HIV-positive pregnant women and more than 6,000 perinatally infected children.

The purpose of this study was to identify the key factors involved in attaining early virologic control of perinatally acquired HIV. This information is necessary to lay the groundwork for planned future investigations of immunotherapeutic strategies designed to achieve sustained ART-free remission. Such strategies are most likely to be successful in very young children who have not yet built up a massive viral load, explained Dr. Palma of Bambino Gesù Children’s Hospital in Rome.

“A major obstacle to curing HIV infection is persistence of virus as integrated proviral DNA in long-lived cells even after many years on ART. ART-free HIV remission is more likely to occur if viral suppression is achieved very early in infection,” he said.

The median age of the 420 subjects at the time ART was initiated was 2.9 months. Their CD4 cell percentage was 34%, with a median CD4 cell count of 1,780 and an average viral load at baseline of 316,228 copies/mL.

At 12 months of age, 84% of patients had achieved viral suppression. In multivariate analyses adjusted for initial ART regimen and geographic location, three factors were associated with this outcome: younger age at ART onset, a lower baseline viral load, and a higher per
xrender/thinkstockphotos.com
This image is a 3D illustration of the HIV virus.
centage of CD4 cells.

Indeed, for each 1-month increase in age at onset of ART, the likelihood of virologic response at age 12 months decreased by 16%. Similarly, the rate of virologic response at 1 year of age decreased by 15% for each 10 copies/mL increase in viral load at the start of ART. In contrast, the likelihood of virologic suppression at age 12 months increased by 10% for each 10% increase in CD4 cell percentage at the start of treatment.

Among the variables that proved unrelated to virologic suppression at 1 year of age were gender, AIDS status, feeding style (breastfed versus bottle-fed), and ethnicity.

Dr. Palma reported having no relevant financial disclosures.

 

– Infants with perinatal HIV infection are significantly more likely to achieve viral suppression by age 12 months if they start antiretroviral therapy (ART) before age 3 months than if physicians wait until 3-6 months of age, Paolo Palma, MD, reported at the annual meeting of the European Society for Paediatric Infectious Diseases.

He presented a study of the factors associated with time to virologic sup

Dr. Paolo Palma
pression in 420 perinatally HIV-infected children who began ART before age 6 months. The study was conducted by EPPICC, the European Pregnancy and Paediatric HIV Cohort Collaboration, a consortium of 25 research groups in 20 European countries and Thailand. To date, the EPPICC data base includes more than 30,000 HIV-positive pregnant women and more than 6,000 perinatally infected children.

The purpose of this study was to identify the key factors involved in attaining early virologic control of perinatally acquired HIV. This information is necessary to lay the groundwork for planned future investigations of immunotherapeutic strategies designed to achieve sustained ART-free remission. Such strategies are most likely to be successful in very young children who have not yet built up a massive viral load, explained Dr. Palma of Bambino Gesù Children’s Hospital in Rome.

“A major obstacle to curing HIV infection is persistence of virus as integrated proviral DNA in long-lived cells even after many years on ART. ART-free HIV remission is more likely to occur if viral suppression is achieved very early in infection,” he said.

The median age of the 420 subjects at the time ART was initiated was 2.9 months. Their CD4 cell percentage was 34%, with a median CD4 cell count of 1,780 and an average viral load at baseline of 316,228 copies/mL.

At 12 months of age, 84% of patients had achieved viral suppression. In multivariate analyses adjusted for initial ART regimen and geographic location, three factors were associated with this outcome: younger age at ART onset, a lower baseline viral load, and a higher per
xrender/thinkstockphotos.com
This image is a 3D illustration of the HIV virus.
centage of CD4 cells.

Indeed, for each 1-month increase in age at onset of ART, the likelihood of virologic response at age 12 months decreased by 16%. Similarly, the rate of virologic response at 1 year of age decreased by 15% for each 10 copies/mL increase in viral load at the start of ART. In contrast, the likelihood of virologic suppression at age 12 months increased by 10% for each 10% increase in CD4 cell percentage at the start of treatment.

Among the variables that proved unrelated to virologic suppression at 1 year of age were gender, AIDS status, feeding style (breastfed versus bottle-fed), and ethnicity.

Dr. Palma reported having no relevant financial disclosures.

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Key clinical point: Start antiretroviral therapy in the first month or 2 of life in babies infected with HIV in utero.

Major finding: With each 1-month delay in starting antiretroviral therapy, the likelihood of attaining viral suppression by age 12 months drops by 16%.

Data source: This observational study included 420 infants with perinatally acquired HIV infection who began antiretroviral therapy prior to age 6 months.

Disclosures: Dr. Palma reported having no relevant financial disclosures.

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Lack of Significant Anti-inflammatory Activity With Clindamycin in the Treatment of Rosacea: Results of 2 Randomized, Vehicle-Controlled Trials

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Lack of Significant Anti-inflammatory Activity With Clindamycin in the Treatment of Rosacea: Results of 2 Randomized, Vehicle-Controlled Trials

Rosacea is a chronic inflammatory skin disease characterized by central facial erythema with or without intermittent papules and pustules (described as the inflammatory lesions of rosacea). Although twice-daily clindamycin 1% solution or gel has been used in the treatment of acne, few studies have investigated the use of clindamycin in rosacea.1,2 In one study comparing twice-daily clindamycin lotion 1% with oral tetracycline in 43 rosacea patients, clindamycin was found to be superior in the eradication of pustules.3 A combination therapy of clindamycin 1% and benzoyl peroxide 5% was found to be more effective than the vehicle in inflammatory lesions and erythema of rosacea in a 12-week randomized controlled trial; however, a definitive advantage over US Food and Drug Administration-approved topical agents used to treat papulopustular rosacea was not established.4,5 Two further studies evaluated clindamycin phosphate 1.2%-tretinoin 0.025% combination gel in the treatment of rosacea, but only 1 showed any effect on papulopustular lesions.6-8 The objective of the studies reported here was to evaluate the efficacy and safety of clindamycin in the treatment of patients with moderate to severe rosacea.

Methods

Study Design

Two multicenter (study A, 20 centers; study B, 10 centers), randomized, investigator-blinded, vehicle-controlled studies were conducted in the United States between 1999 and 2002 in accordance with the Declaration of Helsinki, International Conference on Harmonisation Good Clinical Practice guidelines, and local regulatory requirements. The studies were reviewed and approved by the respective institutional review boards, and all participants provided written informed consent.

In study A, moderate to severe rosacea patients with erythema, telangiectasia, and at least 8 inflammatory lesions were randomized to receive clindamycin cream 1% or vehicle cream once (in the evening) or twice daily (in the morning and evening) or clindamycin cream 0.3% once daily (in the evening) for 12 weeks (1:1:1:1:1 ratio). All study treatments were supplied in identical tubes with blinded labels.

In study B, patients with moderate to severe rosacea and at least 8 inflammatory lesions were randomized in a 1:1 ratio with instructions to apply clindamycin gel 1% or vehicle gel to the affected areas twice daily (morning and evening) for 12 weeks.

Efficacy Evaluation

Evaluations were performed at baseline and weeks 2, 4, 8, and 12 on the intention-to-treat population with the last observation carried forward.

Efficacy assessments in both studies included inflammatory lesion counts (papules and pustules) of 5 facial regions--forehead, chin, nose, right cheek, left cheek--counted separately and then combined to give the total inflammatory lesion count (both studies), as well as improvement in the investigator global rosacea severity score (0=none/clear; 1=mild, detectable erythema with ≤7 papules/pustules; 2=moderate, prominent erythema with ≥8 papules/pustules; 3=severe, intense erythema with ≥10 to <50 papules/pustules; 3.5 [study A] or 4 [study B]=very severe, intense erythema with >50 papules/pustules). In study B, the proportion of participants dichotomized to success (a score of 0 [none/clear] or 1 [mild/almost clear]) or failure (a score of ≥2) on the 5-point investigator global rosacea severity scale at week 12 was evaluated. In study A, investigator global improvement assessment at week 12, based on photographs taken at baseline, was graded on a 7-point scale (from -1 [worse], 0 [no change], and 1 [minimal improvement] to 5 [clear]). In both studies, erythema severity was graded on a 7-point scale in increments of 0.5 (from 0=no erythema to 3.5=very severe redness, very intense redness). Skin irritation also was graded as none, mild, moderate, or severe. 

Safety Evaluation

Safety was assessed by the incidence of adverse events (AEs).

Statistical Analysis

Studies were powered assuming 60% reduction in inflammatory lesion counts with active and 40% with vehicle, based on historical data from a prior study with metronidazole cream 0.75% versus vehicle; 64 participants were required in each treatment group to detect this effect using a 2-sided t test (&#945;=.017). Pairwise comparisons (clindamycin vs respective vehicle) were performed using the Cochran-Mantel-Haenszel test for combined lesion count percentage change.

 

 

Results

Participant Disposition and Baseline Characteristics

Overall, a total of 629 participants were randomized across both studies. In study A, a total of 416 participants were randomized into 5 treatment arms, with 369 participants (88.7%) completing the study; 47 (11.3%) participants discontinued study A, mainly due to participant request (19/47 [40.4%]) or lost to follow-up (11/47 [23.4%]). In study B, a total of 213 participants were randomized to receive either clindamycin gel 1% (n=109 [51.2%]) twice daily or vehicle gel (n=104 [48.8%]) twice daily, with 193 participants (90.6%) completing the study; 20 (9.4%) participants discontinued study B, mainly due to participant request (6/20 [30%]) or lost to follow-up (4/20 [20%]). Participants in studies A and B were similar in demographics and baseline disease characteristics (Table). The majority of participants were white females. 

Efficacy

No statistically significant difference was observed in all pairwise comparisons (clindamycin cream twice daily vs vehicle twice daily, clindamycin cream once daily vs vehicle once daily, clindamycin gel vs vehicle gel) for the primary end point of mean percentage change from baseline in inflammatory lesion counts at week 12 (Figure 1; P>.5 for all pairwise comparisons). 

Figure 1. Mean percentage decrease from baseline in total inflammatory lesion count for clindamycin cream 1% twice daily (n=81) versus vehicle cream twice daily (n=81)(A), clindamycin cream 1% once daily (n=87) and clindamycin cream 0.3% once daily (n=85) versus vehicle cream once daily (n=82)(B), and clindamycin gel 1% twice daily (n=109) versus vehicle gel twice daily (n=104)(C). All P values were not significant.

At week 12, the proportion of participants in study B deemed as a success (none/clear or mild/almost clear [investigator global rosacea severity score of 0 or 1]) in the clindamycin gel 1% and vehicle gel groups were 45% versus 38%, respectively (P=.347) (Figure 2). 

Figure 2. Study B success rate (score of 0 [none/clear] or 1 [mild/almost clear]) of participants after 12 weeks of treatment with clindamycin gel 1% twice daily or vehicle gel twice daily based on the 5-point investigator global rosacea severity score (P=.347).

For the secondary end point of mean investigator global rosacea severity assessment at week 12 (study A), there were no significant differences between the active and vehicle control groups (P>.5 for all pairwise comparisons)(Figure 3). Also, the proportion of participants with at least a moderate investigator global improvement assessment from baseline to week 12 ranged from 45% for clindamycin cream 1% twice daily to 56% for clindamycin cream 0.3% cream once daily and from 45% for vehicle cream once daily to 51% for vehicle cream twice daily (P>.5 for all pairwise comparisons).

Figure 3. Study A mean investigator global rosacea severity score at baseline and week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (A) and clindamycin cream 1% once daily and clindamycin cream 0.3% once daily versus vehicle cream once daily (B). All P values were not significant.

There were no significant differences in the mean total erythema severity scores at week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (6.3 vs 6.0; P>.5), clindamycin cream 1% once daily versus vehicle cream once daily (6.2 vs 6.0; P>.5), clindamycin cream 0.3% once daily versus vehicle cream once daily (5.9 vs 6.0; P>.5), and clindamycin gel 1% twice daily versus vehicle gel twice daily (6.7 vs 6.2; P>.5). 

There were no relevant differences between any of the clindamycin cream groups and their respective vehicle group at week 12 for skin irritation, including desquamation, edema, dryness, pruritus, and stinging/burning.

Safety

In study A, the majority of AEs in all 5 treatment arms were nondermatologic, mild in intensity, and not considered to be related to the study treatment by the investigator. Overall, 12 participants had AEs considered by the investigator as possibly or probably related to the study treatment: 4.9% in the clindamycin cream 1% twice daily group, 4.6% in the clindamycin cream 1% once daily group, 3.7% in the vehicle cream twice daily group, 1.2% in the clindamycin cream 0.3% once daily group, and 0% in the vehicle cream once daily group. Two treatment-related AEs led to treatment discontinuation, including dermatitis in 1 participant from the clindamycin cream 1% once daily group and contact dermatitis in 1 participant from the clindamycin cream 1% twice daily group.

Comment

No evidence of increased efficacy over the respective vehicles was observed with clindamycin cream or gel, whatever the regimen, in the treatment of rosacea patients in either of these well-designed and well-powered, blinded studies. Slight improvements in the various efficacy criteria were observed, even in the vehicle groups, highlighting the importance of using a good basic skin care regimen in the management of rosacea.9 In contrast to our observations of lack of efficacy in the treatment of rosacea, clinical efficacy of clindamycin has been demonstrated in acne,10-12 albeit with low efficacy for clindamycin monotherapy.13 It is noteworthy that oral or topical antibiotics are no longer recommended as monotherapy for acne to prevent and minimize antibiotic resistance and to preserve the therapeutic value of antibiotics.14

Acne and rosacea are both chronic inflammatory disorders of the skin associated with papules and pustules, and they share some common inflammatory patterns.15-19 Furthermore, the intrinsic anti-inflammatory activity of clindamycin in addition to its antibiotic effects has been suggested by some authors as the main reason for treating acne with clindamycin.20 However, the relative contributions of antibacterial and/or anti-inflammatory properties remain to be fully elucidated, and evidence for direct anti-inflammatory effects of clindamycin remains heterogeneous.21,22 Several pathophysiological factors have been implicated in acne, including hormonal effects, abnormal keratinocyte function, increased sebum production, and microbial components (eg, hypercolonization of the skin follicles by Propionibacterium acnes).23,24 The antibiotic activity of clindamycin against P acnes may be the key factor responsible for the clinical effects in acne.25,26 Although clindamycin may have anti-inflammatory effects in acne via a different inflammatory pathway not shared by rosacea, a purely antibiotic mechanism of action of clindamycin also could explain why we observed no evidence of efficacy in the treatment of rosacea, as no causative bacterial component has been clearly demonstrated in rosacea.27

Conclusion

In these studies, clindamycin cream 0.3% once daily, clindamycin cream 1% once or twice daily, and clindamycin gel 1% twice daily were all well tolerated; however, they were no more effective than the vehicles in the treatment of moderate to severe rosacea.  

Acknowledgment

The authors would like to thank Helen Simpson, PhD, of Galderma R&D (Sophia Antipolis, France), for editorial and medical writing assistance.

References
  1. Whitney KM, Ditre CM. Anti-inflammatory properties of clindamycin: a review of its use in the treatment of acne vulgaris. Clinical Medicine Insights: Dermatology. 2011;4:27-41.  
  2. Mays RM, Gordon RA, Wilson JM, et al. New antibiotic therapies for acne and rosacea. Dermatol Ther. 2012;25:23-37.
  3. Wilkin JK, DeWitt S. Treatment of rosacea: topical clindamycin versus oral tetracycline. Int J Dermatol. 1993;32:65-67.
  4. Breneman D, Savin R, VandePol C, et al. Double-blind, randomized, vehicle-controlled clinical trial of once-daily benzoyl peroxide/clindamycin topical gel in the treatment of patients with moderate to severe rosacea. Int J Dermatol. 2004;43:381-387.
  5. Leyden JJ, Thiboutot D, Shalita A. Photographic review of results from a clinical study comparing benzoyl peroxide 5%/clindamycin 1% topical gel with vehicle in the treatment of rosacea. Cutis. 2004;73(6 suppl):11-17.
  6. Chang AL, Alora-Palli M, Lima XT, et al. A randomized, double-blind, placebo-controlled, pilot study to assess the efficacy and safety of clindamycin 1.2% and tretinoin 0.025% combination gel for the treatment of acne rosacea over 12 weeks. J Drugs Dermatol. 2012;11:333-339.
  7. Freeman SA, Moon SD, Spencer JM. Clindamycin phosphate 1.2% and tretinoin 0.025% gel for rosacea: summary of a placebo-controlled, double-blind trial. J Drugs Dermatol. 2012;11:1410-1414.
  8. van Zuuren EJ, Fedorowicz Z, Carter B, et al. Interventions for rosacea. Cochrane Database Syst Rev. 2015;4:CD003262.
  9. Laquieze S, Czernielewski J, Baltas E. Beneficial use of Cetaphil moisturizing cream as part of a daily skin care regimen for individuals with rosacea. J Dermatolog Treat. 2007;18:158-162.
  10. Lookingbill DP, Chalker DK, Lindholm JS, et al. Treatment of acne with a combination clindamycin/benzoyl peroxide gel compared with clindamycin gel, benzoyl peroxide gel and vehicle gel: combined results of two double-blind investigations. J Am Acad Dermatol. 1997;37:590-595.
  11. Alirezaï M, Gerlach B, Horvath A, et al. Results of a randomised, multicentre study comparing a new water-based gel of clindamycin 1% versus clindamycin 1% topical solution in the treatment of acne vulgaris. Eur J Dermatol. 2005;15:274-278.
  12. Jarratt MT, Brundage T. Efficacy and safety of clindamycin-tretinoin gel versus clindamycin or tretinoin alone in acne vulgaris: a randomized, double-blind, vehicle-controlled study. J Drugs Dermatol. 2012;11:318-326.
  13. Benzaclin. Med Library website. http://medlibrary.org/lib/rx/meds/benzaclin-3. Updated May 8, 2013. Accessed January 24, 2017.
  14. Walsh TR, Efthimiou J, Dréno B. Systematic review of antibiotic resistance in acne: an increasing topical and oral threat. Lancet Infect Dis. 2016;16:E23-E33.
  15. Jeremy AH, Holland DB, Roberts SG, et al. Inflammatory events are involved in acne lesion initiation. J Invest Dermatol. 2003;121:20-27.  
  16. Kircik LH. Re-evaluating treatment targets in acne vulgaris: adapting to a new understanding of pathophysiology. J Drugs Dermatol. 2014;13:S57-S60.  
  17. Salzer S, Kresse S, Hirai Y, et al. Cathelicidin peptide LL-37 increases UVB-triggered inflammasome activation: possible implications for rosacea. J Dermatol Sci. 2014;76:173-179.
  18. Buhl T, Sulk M, Nowak P, et al. Molecular and morphological characterization of inflammatory infiltrate in rosacea reveals activation of Th1/Th17 pathways. J Invest Dermatol. 2015;135:2198-2208.
  19. Kistowska M, Meier B, Proust T, et al. Propionibacterium acnes promotes Th17 and Th17/Th1 responses in acne patients. J Invest Dermatol. 2015;135:110-118.  
  20. Zeichner JA. Inflammatory acne treatment: review of current and new topical therapeutic options. J Drugs Dermatol. 2016;15(1 suppl 1):S11-S16.  
  21. Nakano T, Hiramatsu K, Kishi K, et al. Clindamycin modulates inflammatory-cytokine induction in lipopolysaccharide-stimulated mouse peritoneal macrophages. Antimicrob Agents Chemother. 2003;47:363-367.
  22. Orman KL, English BK. Effects of antibiotic class on the macrophage inflammatory response to Streptococcus pneumoniae. J Infect Dis. 2000;182:1561-1565.
  23. Taylor M, Gonzalez M, Porter R. Pathways to inflammation: acne pathophysiology. Eur J Dermatol. 2011;21:323-333.
  24. Del Rosso JQ, Kircik LH. The sequence of inflammation, relevant biomarkers, and the pathogenesis of acne vulgaris: what does recent research show and what does it mean to the clinician? J Drugs Dermatol. 2013;12(8 suppl):S109-S115.  
  25. Leyden J, Kaidbey K, Levy SF. The combination formulation of clindamycin 1% plus benzoyl peroxide 5% versus 3 different formulations of topical clindamycin alone in the reduction of Propionibacterium acnes. an in vivo comparative study. Am J Clin Dermatol. 2001;2:263-266.
  26. Wang WL, Everett ED, Johnson M, et al. Susceptibility of Propionibacterium acnes to seventeen antibiotics. Antimicrob Agents Chemother. 1977;11:171-173.
  27. Steinhoff M, Schauber J, Leyden JJ. New insights into rosacea pathophysiology: a review of recent findings. J Am Acad Dermatol. 2013;69(6 suppl 1):S15-S26.  
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Author and Disclosure Information

Dr. Martel and Ms. Carlavan are from Galderma R&D, Sophia Antipolis, France. Dr. Jarratt is from DermResearch Inc, Austin, Texas. Dr. Weiss is from Gwinnett Dermatology, PC, and Gwinnett Clinical Research Center, Inc, Snellville, Georgia.

The studies were sponsored by Galderma R&D. Dr. Martel and Ms. Carlavan are employees of Galderma R&D. Dr. Jarratt has been a consultant, investigator, and received honoraria from Allergan; Galderma R&D; and Valeant Pharmaceuticals International, Inc. He also is a consultant for Athenex. Dr. Weiss has been an advisory board member and researcher for Foamix; Galderma R&D; and Valeant Pharmaceuticals International, Inc. He also has been a researcher for Allergan, Inc. 

Correspondence: Philippe Martel, MD, Galderma R&D, 2400 Route des Colles, F-06410 Biot, France ([email protected]).

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Author and Disclosure Information

Dr. Martel and Ms. Carlavan are from Galderma R&D, Sophia Antipolis, France. Dr. Jarratt is from DermResearch Inc, Austin, Texas. Dr. Weiss is from Gwinnett Dermatology, PC, and Gwinnett Clinical Research Center, Inc, Snellville, Georgia.

The studies were sponsored by Galderma R&D. Dr. Martel and Ms. Carlavan are employees of Galderma R&D. Dr. Jarratt has been a consultant, investigator, and received honoraria from Allergan; Galderma R&D; and Valeant Pharmaceuticals International, Inc. He also is a consultant for Athenex. Dr. Weiss has been an advisory board member and researcher for Foamix; Galderma R&D; and Valeant Pharmaceuticals International, Inc. He also has been a researcher for Allergan, Inc. 

Correspondence: Philippe Martel, MD, Galderma R&D, 2400 Route des Colles, F-06410 Biot, France ([email protected]).

Author and Disclosure Information

Dr. Martel and Ms. Carlavan are from Galderma R&D, Sophia Antipolis, France. Dr. Jarratt is from DermResearch Inc, Austin, Texas. Dr. Weiss is from Gwinnett Dermatology, PC, and Gwinnett Clinical Research Center, Inc, Snellville, Georgia.

The studies were sponsored by Galderma R&D. Dr. Martel and Ms. Carlavan are employees of Galderma R&D. Dr. Jarratt has been a consultant, investigator, and received honoraria from Allergan; Galderma R&D; and Valeant Pharmaceuticals International, Inc. He also is a consultant for Athenex. Dr. Weiss has been an advisory board member and researcher for Foamix; Galderma R&D; and Valeant Pharmaceuticals International, Inc. He also has been a researcher for Allergan, Inc. 

Correspondence: Philippe Martel, MD, Galderma R&D, 2400 Route des Colles, F-06410 Biot, France ([email protected]).

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Related Articles

Rosacea is a chronic inflammatory skin disease characterized by central facial erythema with or without intermittent papules and pustules (described as the inflammatory lesions of rosacea). Although twice-daily clindamycin 1% solution or gel has been used in the treatment of acne, few studies have investigated the use of clindamycin in rosacea.1,2 In one study comparing twice-daily clindamycin lotion 1% with oral tetracycline in 43 rosacea patients, clindamycin was found to be superior in the eradication of pustules.3 A combination therapy of clindamycin 1% and benzoyl peroxide 5% was found to be more effective than the vehicle in inflammatory lesions and erythema of rosacea in a 12-week randomized controlled trial; however, a definitive advantage over US Food and Drug Administration-approved topical agents used to treat papulopustular rosacea was not established.4,5 Two further studies evaluated clindamycin phosphate 1.2%-tretinoin 0.025% combination gel in the treatment of rosacea, but only 1 showed any effect on papulopustular lesions.6-8 The objective of the studies reported here was to evaluate the efficacy and safety of clindamycin in the treatment of patients with moderate to severe rosacea.

Methods

Study Design

Two multicenter (study A, 20 centers; study B, 10 centers), randomized, investigator-blinded, vehicle-controlled studies were conducted in the United States between 1999 and 2002 in accordance with the Declaration of Helsinki, International Conference on Harmonisation Good Clinical Practice guidelines, and local regulatory requirements. The studies were reviewed and approved by the respective institutional review boards, and all participants provided written informed consent.

In study A, moderate to severe rosacea patients with erythema, telangiectasia, and at least 8 inflammatory lesions were randomized to receive clindamycin cream 1% or vehicle cream once (in the evening) or twice daily (in the morning and evening) or clindamycin cream 0.3% once daily (in the evening) for 12 weeks (1:1:1:1:1 ratio). All study treatments were supplied in identical tubes with blinded labels.

In study B, patients with moderate to severe rosacea and at least 8 inflammatory lesions were randomized in a 1:1 ratio with instructions to apply clindamycin gel 1% or vehicle gel to the affected areas twice daily (morning and evening) for 12 weeks.

Efficacy Evaluation

Evaluations were performed at baseline and weeks 2, 4, 8, and 12 on the intention-to-treat population with the last observation carried forward.

Efficacy assessments in both studies included inflammatory lesion counts (papules and pustules) of 5 facial regions--forehead, chin, nose, right cheek, left cheek--counted separately and then combined to give the total inflammatory lesion count (both studies), as well as improvement in the investigator global rosacea severity score (0=none/clear; 1=mild, detectable erythema with ≤7 papules/pustules; 2=moderate, prominent erythema with ≥8 papules/pustules; 3=severe, intense erythema with ≥10 to <50 papules/pustules; 3.5 [study A] or 4 [study B]=very severe, intense erythema with >50 papules/pustules). In study B, the proportion of participants dichotomized to success (a score of 0 [none/clear] or 1 [mild/almost clear]) or failure (a score of ≥2) on the 5-point investigator global rosacea severity scale at week 12 was evaluated. In study A, investigator global improvement assessment at week 12, based on photographs taken at baseline, was graded on a 7-point scale (from -1 [worse], 0 [no change], and 1 [minimal improvement] to 5 [clear]). In both studies, erythema severity was graded on a 7-point scale in increments of 0.5 (from 0=no erythema to 3.5=very severe redness, very intense redness). Skin irritation also was graded as none, mild, moderate, or severe. 

Safety Evaluation

Safety was assessed by the incidence of adverse events (AEs).

Statistical Analysis

Studies were powered assuming 60% reduction in inflammatory lesion counts with active and 40% with vehicle, based on historical data from a prior study with metronidazole cream 0.75% versus vehicle; 64 participants were required in each treatment group to detect this effect using a 2-sided t test (&#945;=.017). Pairwise comparisons (clindamycin vs respective vehicle) were performed using the Cochran-Mantel-Haenszel test for combined lesion count percentage change.

 

 

Results

Participant Disposition and Baseline Characteristics

Overall, a total of 629 participants were randomized across both studies. In study A, a total of 416 participants were randomized into 5 treatment arms, with 369 participants (88.7%) completing the study; 47 (11.3%) participants discontinued study A, mainly due to participant request (19/47 [40.4%]) or lost to follow-up (11/47 [23.4%]). In study B, a total of 213 participants were randomized to receive either clindamycin gel 1% (n=109 [51.2%]) twice daily or vehicle gel (n=104 [48.8%]) twice daily, with 193 participants (90.6%) completing the study; 20 (9.4%) participants discontinued study B, mainly due to participant request (6/20 [30%]) or lost to follow-up (4/20 [20%]). Participants in studies A and B were similar in demographics and baseline disease characteristics (Table). The majority of participants were white females. 

Efficacy

No statistically significant difference was observed in all pairwise comparisons (clindamycin cream twice daily vs vehicle twice daily, clindamycin cream once daily vs vehicle once daily, clindamycin gel vs vehicle gel) for the primary end point of mean percentage change from baseline in inflammatory lesion counts at week 12 (Figure 1; P>.5 for all pairwise comparisons). 

Figure 1. Mean percentage decrease from baseline in total inflammatory lesion count for clindamycin cream 1% twice daily (n=81) versus vehicle cream twice daily (n=81)(A), clindamycin cream 1% once daily (n=87) and clindamycin cream 0.3% once daily (n=85) versus vehicle cream once daily (n=82)(B), and clindamycin gel 1% twice daily (n=109) versus vehicle gel twice daily (n=104)(C). All P values were not significant.

At week 12, the proportion of participants in study B deemed as a success (none/clear or mild/almost clear [investigator global rosacea severity score of 0 or 1]) in the clindamycin gel 1% and vehicle gel groups were 45% versus 38%, respectively (P=.347) (Figure 2). 

Figure 2. Study B success rate (score of 0 [none/clear] or 1 [mild/almost clear]) of participants after 12 weeks of treatment with clindamycin gel 1% twice daily or vehicle gel twice daily based on the 5-point investigator global rosacea severity score (P=.347).

For the secondary end point of mean investigator global rosacea severity assessment at week 12 (study A), there were no significant differences between the active and vehicle control groups (P>.5 for all pairwise comparisons)(Figure 3). Also, the proportion of participants with at least a moderate investigator global improvement assessment from baseline to week 12 ranged from 45% for clindamycin cream 1% twice daily to 56% for clindamycin cream 0.3% cream once daily and from 45% for vehicle cream once daily to 51% for vehicle cream twice daily (P>.5 for all pairwise comparisons).

Figure 3. Study A mean investigator global rosacea severity score at baseline and week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (A) and clindamycin cream 1% once daily and clindamycin cream 0.3% once daily versus vehicle cream once daily (B). All P values were not significant.

There were no significant differences in the mean total erythema severity scores at week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (6.3 vs 6.0; P>.5), clindamycin cream 1% once daily versus vehicle cream once daily (6.2 vs 6.0; P>.5), clindamycin cream 0.3% once daily versus vehicle cream once daily (5.9 vs 6.0; P>.5), and clindamycin gel 1% twice daily versus vehicle gel twice daily (6.7 vs 6.2; P>.5). 

There were no relevant differences between any of the clindamycin cream groups and their respective vehicle group at week 12 for skin irritation, including desquamation, edema, dryness, pruritus, and stinging/burning.

Safety

In study A, the majority of AEs in all 5 treatment arms were nondermatologic, mild in intensity, and not considered to be related to the study treatment by the investigator. Overall, 12 participants had AEs considered by the investigator as possibly or probably related to the study treatment: 4.9% in the clindamycin cream 1% twice daily group, 4.6% in the clindamycin cream 1% once daily group, 3.7% in the vehicle cream twice daily group, 1.2% in the clindamycin cream 0.3% once daily group, and 0% in the vehicle cream once daily group. Two treatment-related AEs led to treatment discontinuation, including dermatitis in 1 participant from the clindamycin cream 1% once daily group and contact dermatitis in 1 participant from the clindamycin cream 1% twice daily group.

Comment

No evidence of increased efficacy over the respective vehicles was observed with clindamycin cream or gel, whatever the regimen, in the treatment of rosacea patients in either of these well-designed and well-powered, blinded studies. Slight improvements in the various efficacy criteria were observed, even in the vehicle groups, highlighting the importance of using a good basic skin care regimen in the management of rosacea.9 In contrast to our observations of lack of efficacy in the treatment of rosacea, clinical efficacy of clindamycin has been demonstrated in acne,10-12 albeit with low efficacy for clindamycin monotherapy.13 It is noteworthy that oral or topical antibiotics are no longer recommended as monotherapy for acne to prevent and minimize antibiotic resistance and to preserve the therapeutic value of antibiotics.14

Acne and rosacea are both chronic inflammatory disorders of the skin associated with papules and pustules, and they share some common inflammatory patterns.15-19 Furthermore, the intrinsic anti-inflammatory activity of clindamycin in addition to its antibiotic effects has been suggested by some authors as the main reason for treating acne with clindamycin.20 However, the relative contributions of antibacterial and/or anti-inflammatory properties remain to be fully elucidated, and evidence for direct anti-inflammatory effects of clindamycin remains heterogeneous.21,22 Several pathophysiological factors have been implicated in acne, including hormonal effects, abnormal keratinocyte function, increased sebum production, and microbial components (eg, hypercolonization of the skin follicles by Propionibacterium acnes).23,24 The antibiotic activity of clindamycin against P acnes may be the key factor responsible for the clinical effects in acne.25,26 Although clindamycin may have anti-inflammatory effects in acne via a different inflammatory pathway not shared by rosacea, a purely antibiotic mechanism of action of clindamycin also could explain why we observed no evidence of efficacy in the treatment of rosacea, as no causative bacterial component has been clearly demonstrated in rosacea.27

Conclusion

In these studies, clindamycin cream 0.3% once daily, clindamycin cream 1% once or twice daily, and clindamycin gel 1% twice daily were all well tolerated; however, they were no more effective than the vehicles in the treatment of moderate to severe rosacea.  

Acknowledgment

The authors would like to thank Helen Simpson, PhD, of Galderma R&D (Sophia Antipolis, France), for editorial and medical writing assistance.

Rosacea is a chronic inflammatory skin disease characterized by central facial erythema with or without intermittent papules and pustules (described as the inflammatory lesions of rosacea). Although twice-daily clindamycin 1% solution or gel has been used in the treatment of acne, few studies have investigated the use of clindamycin in rosacea.1,2 In one study comparing twice-daily clindamycin lotion 1% with oral tetracycline in 43 rosacea patients, clindamycin was found to be superior in the eradication of pustules.3 A combination therapy of clindamycin 1% and benzoyl peroxide 5% was found to be more effective than the vehicle in inflammatory lesions and erythema of rosacea in a 12-week randomized controlled trial; however, a definitive advantage over US Food and Drug Administration-approved topical agents used to treat papulopustular rosacea was not established.4,5 Two further studies evaluated clindamycin phosphate 1.2%-tretinoin 0.025% combination gel in the treatment of rosacea, but only 1 showed any effect on papulopustular lesions.6-8 The objective of the studies reported here was to evaluate the efficacy and safety of clindamycin in the treatment of patients with moderate to severe rosacea.

Methods

Study Design

Two multicenter (study A, 20 centers; study B, 10 centers), randomized, investigator-blinded, vehicle-controlled studies were conducted in the United States between 1999 and 2002 in accordance with the Declaration of Helsinki, International Conference on Harmonisation Good Clinical Practice guidelines, and local regulatory requirements. The studies were reviewed and approved by the respective institutional review boards, and all participants provided written informed consent.

In study A, moderate to severe rosacea patients with erythema, telangiectasia, and at least 8 inflammatory lesions were randomized to receive clindamycin cream 1% or vehicle cream once (in the evening) or twice daily (in the morning and evening) or clindamycin cream 0.3% once daily (in the evening) for 12 weeks (1:1:1:1:1 ratio). All study treatments were supplied in identical tubes with blinded labels.

In study B, patients with moderate to severe rosacea and at least 8 inflammatory lesions were randomized in a 1:1 ratio with instructions to apply clindamycin gel 1% or vehicle gel to the affected areas twice daily (morning and evening) for 12 weeks.

Efficacy Evaluation

Evaluations were performed at baseline and weeks 2, 4, 8, and 12 on the intention-to-treat population with the last observation carried forward.

Efficacy assessments in both studies included inflammatory lesion counts (papules and pustules) of 5 facial regions--forehead, chin, nose, right cheek, left cheek--counted separately and then combined to give the total inflammatory lesion count (both studies), as well as improvement in the investigator global rosacea severity score (0=none/clear; 1=mild, detectable erythema with ≤7 papules/pustules; 2=moderate, prominent erythema with ≥8 papules/pustules; 3=severe, intense erythema with ≥10 to <50 papules/pustules; 3.5 [study A] or 4 [study B]=very severe, intense erythema with >50 papules/pustules). In study B, the proportion of participants dichotomized to success (a score of 0 [none/clear] or 1 [mild/almost clear]) or failure (a score of ≥2) on the 5-point investigator global rosacea severity scale at week 12 was evaluated. In study A, investigator global improvement assessment at week 12, based on photographs taken at baseline, was graded on a 7-point scale (from -1 [worse], 0 [no change], and 1 [minimal improvement] to 5 [clear]). In both studies, erythema severity was graded on a 7-point scale in increments of 0.5 (from 0=no erythema to 3.5=very severe redness, very intense redness). Skin irritation also was graded as none, mild, moderate, or severe. 

Safety Evaluation

Safety was assessed by the incidence of adverse events (AEs).

Statistical Analysis

Studies were powered assuming 60% reduction in inflammatory lesion counts with active and 40% with vehicle, based on historical data from a prior study with metronidazole cream 0.75% versus vehicle; 64 participants were required in each treatment group to detect this effect using a 2-sided t test (&#945;=.017). Pairwise comparisons (clindamycin vs respective vehicle) were performed using the Cochran-Mantel-Haenszel test for combined lesion count percentage change.

 

 

Results

Participant Disposition and Baseline Characteristics

Overall, a total of 629 participants were randomized across both studies. In study A, a total of 416 participants were randomized into 5 treatment arms, with 369 participants (88.7%) completing the study; 47 (11.3%) participants discontinued study A, mainly due to participant request (19/47 [40.4%]) or lost to follow-up (11/47 [23.4%]). In study B, a total of 213 participants were randomized to receive either clindamycin gel 1% (n=109 [51.2%]) twice daily or vehicle gel (n=104 [48.8%]) twice daily, with 193 participants (90.6%) completing the study; 20 (9.4%) participants discontinued study B, mainly due to participant request (6/20 [30%]) or lost to follow-up (4/20 [20%]). Participants in studies A and B were similar in demographics and baseline disease characteristics (Table). The majority of participants were white females. 

Efficacy

No statistically significant difference was observed in all pairwise comparisons (clindamycin cream twice daily vs vehicle twice daily, clindamycin cream once daily vs vehicle once daily, clindamycin gel vs vehicle gel) for the primary end point of mean percentage change from baseline in inflammatory lesion counts at week 12 (Figure 1; P>.5 for all pairwise comparisons). 

Figure 1. Mean percentage decrease from baseline in total inflammatory lesion count for clindamycin cream 1% twice daily (n=81) versus vehicle cream twice daily (n=81)(A), clindamycin cream 1% once daily (n=87) and clindamycin cream 0.3% once daily (n=85) versus vehicle cream once daily (n=82)(B), and clindamycin gel 1% twice daily (n=109) versus vehicle gel twice daily (n=104)(C). All P values were not significant.

At week 12, the proportion of participants in study B deemed as a success (none/clear or mild/almost clear [investigator global rosacea severity score of 0 or 1]) in the clindamycin gel 1% and vehicle gel groups were 45% versus 38%, respectively (P=.347) (Figure 2). 

Figure 2. Study B success rate (score of 0 [none/clear] or 1 [mild/almost clear]) of participants after 12 weeks of treatment with clindamycin gel 1% twice daily or vehicle gel twice daily based on the 5-point investigator global rosacea severity score (P=.347).

For the secondary end point of mean investigator global rosacea severity assessment at week 12 (study A), there were no significant differences between the active and vehicle control groups (P>.5 for all pairwise comparisons)(Figure 3). Also, the proportion of participants with at least a moderate investigator global improvement assessment from baseline to week 12 ranged from 45% for clindamycin cream 1% twice daily to 56% for clindamycin cream 0.3% cream once daily and from 45% for vehicle cream once daily to 51% for vehicle cream twice daily (P>.5 for all pairwise comparisons).

Figure 3. Study A mean investigator global rosacea severity score at baseline and week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (A) and clindamycin cream 1% once daily and clindamycin cream 0.3% once daily versus vehicle cream once daily (B). All P values were not significant.

There were no significant differences in the mean total erythema severity scores at week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (6.3 vs 6.0; P>.5), clindamycin cream 1% once daily versus vehicle cream once daily (6.2 vs 6.0; P>.5), clindamycin cream 0.3% once daily versus vehicle cream once daily (5.9 vs 6.0; P>.5), and clindamycin gel 1% twice daily versus vehicle gel twice daily (6.7 vs 6.2; P>.5). 

There were no relevant differences between any of the clindamycin cream groups and their respective vehicle group at week 12 for skin irritation, including desquamation, edema, dryness, pruritus, and stinging/burning.

Safety

In study A, the majority of AEs in all 5 treatment arms were nondermatologic, mild in intensity, and not considered to be related to the study treatment by the investigator. Overall, 12 participants had AEs considered by the investigator as possibly or probably related to the study treatment: 4.9% in the clindamycin cream 1% twice daily group, 4.6% in the clindamycin cream 1% once daily group, 3.7% in the vehicle cream twice daily group, 1.2% in the clindamycin cream 0.3% once daily group, and 0% in the vehicle cream once daily group. Two treatment-related AEs led to treatment discontinuation, including dermatitis in 1 participant from the clindamycin cream 1% once daily group and contact dermatitis in 1 participant from the clindamycin cream 1% twice daily group.

Comment

No evidence of increased efficacy over the respective vehicles was observed with clindamycin cream or gel, whatever the regimen, in the treatment of rosacea patients in either of these well-designed and well-powered, blinded studies. Slight improvements in the various efficacy criteria were observed, even in the vehicle groups, highlighting the importance of using a good basic skin care regimen in the management of rosacea.9 In contrast to our observations of lack of efficacy in the treatment of rosacea, clinical efficacy of clindamycin has been demonstrated in acne,10-12 albeit with low efficacy for clindamycin monotherapy.13 It is noteworthy that oral or topical antibiotics are no longer recommended as monotherapy for acne to prevent and minimize antibiotic resistance and to preserve the therapeutic value of antibiotics.14

Acne and rosacea are both chronic inflammatory disorders of the skin associated with papules and pustules, and they share some common inflammatory patterns.15-19 Furthermore, the intrinsic anti-inflammatory activity of clindamycin in addition to its antibiotic effects has been suggested by some authors as the main reason for treating acne with clindamycin.20 However, the relative contributions of antibacterial and/or anti-inflammatory properties remain to be fully elucidated, and evidence for direct anti-inflammatory effects of clindamycin remains heterogeneous.21,22 Several pathophysiological factors have been implicated in acne, including hormonal effects, abnormal keratinocyte function, increased sebum production, and microbial components (eg, hypercolonization of the skin follicles by Propionibacterium acnes).23,24 The antibiotic activity of clindamycin against P acnes may be the key factor responsible for the clinical effects in acne.25,26 Although clindamycin may have anti-inflammatory effects in acne via a different inflammatory pathway not shared by rosacea, a purely antibiotic mechanism of action of clindamycin also could explain why we observed no evidence of efficacy in the treatment of rosacea, as no causative bacterial component has been clearly demonstrated in rosacea.27

Conclusion

In these studies, clindamycin cream 0.3% once daily, clindamycin cream 1% once or twice daily, and clindamycin gel 1% twice daily were all well tolerated; however, they were no more effective than the vehicles in the treatment of moderate to severe rosacea.  

Acknowledgment

The authors would like to thank Helen Simpson, PhD, of Galderma R&D (Sophia Antipolis, France), for editorial and medical writing assistance.

References
  1. Whitney KM, Ditre CM. Anti-inflammatory properties of clindamycin: a review of its use in the treatment of acne vulgaris. Clinical Medicine Insights: Dermatology. 2011;4:27-41.  
  2. Mays RM, Gordon RA, Wilson JM, et al. New antibiotic therapies for acne and rosacea. Dermatol Ther. 2012;25:23-37.
  3. Wilkin JK, DeWitt S. Treatment of rosacea: topical clindamycin versus oral tetracycline. Int J Dermatol. 1993;32:65-67.
  4. Breneman D, Savin R, VandePol C, et al. Double-blind, randomized, vehicle-controlled clinical trial of once-daily benzoyl peroxide/clindamycin topical gel in the treatment of patients with moderate to severe rosacea. Int J Dermatol. 2004;43:381-387.
  5. Leyden JJ, Thiboutot D, Shalita A. Photographic review of results from a clinical study comparing benzoyl peroxide 5%/clindamycin 1% topical gel with vehicle in the treatment of rosacea. Cutis. 2004;73(6 suppl):11-17.
  6. Chang AL, Alora-Palli M, Lima XT, et al. A randomized, double-blind, placebo-controlled, pilot study to assess the efficacy and safety of clindamycin 1.2% and tretinoin 0.025% combination gel for the treatment of acne rosacea over 12 weeks. J Drugs Dermatol. 2012;11:333-339.
  7. Freeman SA, Moon SD, Spencer JM. Clindamycin phosphate 1.2% and tretinoin 0.025% gel for rosacea: summary of a placebo-controlled, double-blind trial. J Drugs Dermatol. 2012;11:1410-1414.
  8. van Zuuren EJ, Fedorowicz Z, Carter B, et al. Interventions for rosacea. Cochrane Database Syst Rev. 2015;4:CD003262.
  9. Laquieze S, Czernielewski J, Baltas E. Beneficial use of Cetaphil moisturizing cream as part of a daily skin care regimen for individuals with rosacea. J Dermatolog Treat. 2007;18:158-162.
  10. Lookingbill DP, Chalker DK, Lindholm JS, et al. Treatment of acne with a combination clindamycin/benzoyl peroxide gel compared with clindamycin gel, benzoyl peroxide gel and vehicle gel: combined results of two double-blind investigations. J Am Acad Dermatol. 1997;37:590-595.
  11. Alirezaï M, Gerlach B, Horvath A, et al. Results of a randomised, multicentre study comparing a new water-based gel of clindamycin 1% versus clindamycin 1% topical solution in the treatment of acne vulgaris. Eur J Dermatol. 2005;15:274-278.
  12. Jarratt MT, Brundage T. Efficacy and safety of clindamycin-tretinoin gel versus clindamycin or tretinoin alone in acne vulgaris: a randomized, double-blind, vehicle-controlled study. J Drugs Dermatol. 2012;11:318-326.
  13. Benzaclin. Med Library website. http://medlibrary.org/lib/rx/meds/benzaclin-3. Updated May 8, 2013. Accessed January 24, 2017.
  14. Walsh TR, Efthimiou J, Dréno B. Systematic review of antibiotic resistance in acne: an increasing topical and oral threat. Lancet Infect Dis. 2016;16:E23-E33.
  15. Jeremy AH, Holland DB, Roberts SG, et al. Inflammatory events are involved in acne lesion initiation. J Invest Dermatol. 2003;121:20-27.  
  16. Kircik LH. Re-evaluating treatment targets in acne vulgaris: adapting to a new understanding of pathophysiology. J Drugs Dermatol. 2014;13:S57-S60.  
  17. Salzer S, Kresse S, Hirai Y, et al. Cathelicidin peptide LL-37 increases UVB-triggered inflammasome activation: possible implications for rosacea. J Dermatol Sci. 2014;76:173-179.
  18. Buhl T, Sulk M, Nowak P, et al. Molecular and morphological characterization of inflammatory infiltrate in rosacea reveals activation of Th1/Th17 pathways. J Invest Dermatol. 2015;135:2198-2208.
  19. Kistowska M, Meier B, Proust T, et al. Propionibacterium acnes promotes Th17 and Th17/Th1 responses in acne patients. J Invest Dermatol. 2015;135:110-118.  
  20. Zeichner JA. Inflammatory acne treatment: review of current and new topical therapeutic options. J Drugs Dermatol. 2016;15(1 suppl 1):S11-S16.  
  21. Nakano T, Hiramatsu K, Kishi K, et al. Clindamycin modulates inflammatory-cytokine induction in lipopolysaccharide-stimulated mouse peritoneal macrophages. Antimicrob Agents Chemother. 2003;47:363-367.
  22. Orman KL, English BK. Effects of antibiotic class on the macrophage inflammatory response to Streptococcus pneumoniae. J Infect Dis. 2000;182:1561-1565.
  23. Taylor M, Gonzalez M, Porter R. Pathways to inflammation: acne pathophysiology. Eur J Dermatol. 2011;21:323-333.
  24. Del Rosso JQ, Kircik LH. The sequence of inflammation, relevant biomarkers, and the pathogenesis of acne vulgaris: what does recent research show and what does it mean to the clinician? J Drugs Dermatol. 2013;12(8 suppl):S109-S115.  
  25. Leyden J, Kaidbey K, Levy SF. The combination formulation of clindamycin 1% plus benzoyl peroxide 5% versus 3 different formulations of topical clindamycin alone in the reduction of Propionibacterium acnes. an in vivo comparative study. Am J Clin Dermatol. 2001;2:263-266.
  26. Wang WL, Everett ED, Johnson M, et al. Susceptibility of Propionibacterium acnes to seventeen antibiotics. Antimicrob Agents Chemother. 1977;11:171-173.
  27. Steinhoff M, Schauber J, Leyden JJ. New insights into rosacea pathophysiology: a review of recent findings. J Am Acad Dermatol. 2013;69(6 suppl 1):S15-S26.  
References
  1. Whitney KM, Ditre CM. Anti-inflammatory properties of clindamycin: a review of its use in the treatment of acne vulgaris. Clinical Medicine Insights: Dermatology. 2011;4:27-41.  
  2. Mays RM, Gordon RA, Wilson JM, et al. New antibiotic therapies for acne and rosacea. Dermatol Ther. 2012;25:23-37.
  3. Wilkin JK, DeWitt S. Treatment of rosacea: topical clindamycin versus oral tetracycline. Int J Dermatol. 1993;32:65-67.
  4. Breneman D, Savin R, VandePol C, et al. Double-blind, randomized, vehicle-controlled clinical trial of once-daily benzoyl peroxide/clindamycin topical gel in the treatment of patients with moderate to severe rosacea. Int J Dermatol. 2004;43:381-387.
  5. Leyden JJ, Thiboutot D, Shalita A. Photographic review of results from a clinical study comparing benzoyl peroxide 5%/clindamycin 1% topical gel with vehicle in the treatment of rosacea. Cutis. 2004;73(6 suppl):11-17.
  6. Chang AL, Alora-Palli M, Lima XT, et al. A randomized, double-blind, placebo-controlled, pilot study to assess the efficacy and safety of clindamycin 1.2% and tretinoin 0.025% combination gel for the treatment of acne rosacea over 12 weeks. J Drugs Dermatol. 2012;11:333-339.
  7. Freeman SA, Moon SD, Spencer JM. Clindamycin phosphate 1.2% and tretinoin 0.025% gel for rosacea: summary of a placebo-controlled, double-blind trial. J Drugs Dermatol. 2012;11:1410-1414.
  8. van Zuuren EJ, Fedorowicz Z, Carter B, et al. Interventions for rosacea. Cochrane Database Syst Rev. 2015;4:CD003262.
  9. Laquieze S, Czernielewski J, Baltas E. Beneficial use of Cetaphil moisturizing cream as part of a daily skin care regimen for individuals with rosacea. J Dermatolog Treat. 2007;18:158-162.
  10. Lookingbill DP, Chalker DK, Lindholm JS, et al. Treatment of acne with a combination clindamycin/benzoyl peroxide gel compared with clindamycin gel, benzoyl peroxide gel and vehicle gel: combined results of two double-blind investigations. J Am Acad Dermatol. 1997;37:590-595.
  11. Alirezaï M, Gerlach B, Horvath A, et al. Results of a randomised, multicentre study comparing a new water-based gel of clindamycin 1% versus clindamycin 1% topical solution in the treatment of acne vulgaris. Eur J Dermatol. 2005;15:274-278.
  12. Jarratt MT, Brundage T. Efficacy and safety of clindamycin-tretinoin gel versus clindamycin or tretinoin alone in acne vulgaris: a randomized, double-blind, vehicle-controlled study. J Drugs Dermatol. 2012;11:318-326.
  13. Benzaclin. Med Library website. http://medlibrary.org/lib/rx/meds/benzaclin-3. Updated May 8, 2013. Accessed January 24, 2017.
  14. Walsh TR, Efthimiou J, Dréno B. Systematic review of antibiotic resistance in acne: an increasing topical and oral threat. Lancet Infect Dis. 2016;16:E23-E33.
  15. Jeremy AH, Holland DB, Roberts SG, et al. Inflammatory events are involved in acne lesion initiation. J Invest Dermatol. 2003;121:20-27.  
  16. Kircik LH. Re-evaluating treatment targets in acne vulgaris: adapting to a new understanding of pathophysiology. J Drugs Dermatol. 2014;13:S57-S60.  
  17. Salzer S, Kresse S, Hirai Y, et al. Cathelicidin peptide LL-37 increases UVB-triggered inflammasome activation: possible implications for rosacea. J Dermatol Sci. 2014;76:173-179.
  18. Buhl T, Sulk M, Nowak P, et al. Molecular and morphological characterization of inflammatory infiltrate in rosacea reveals activation of Th1/Th17 pathways. J Invest Dermatol. 2015;135:2198-2208.
  19. Kistowska M, Meier B, Proust T, et al. Propionibacterium acnes promotes Th17 and Th17/Th1 responses in acne patients. J Invest Dermatol. 2015;135:110-118.  
  20. Zeichner JA. Inflammatory acne treatment: review of current and new topical therapeutic options. J Drugs Dermatol. 2016;15(1 suppl 1):S11-S16.  
  21. Nakano T, Hiramatsu K, Kishi K, et al. Clindamycin modulates inflammatory-cytokine induction in lipopolysaccharide-stimulated mouse peritoneal macrophages. Antimicrob Agents Chemother. 2003;47:363-367.
  22. Orman KL, English BK. Effects of antibiotic class on the macrophage inflammatory response to Streptococcus pneumoniae. J Infect Dis. 2000;182:1561-1565.
  23. Taylor M, Gonzalez M, Porter R. Pathways to inflammation: acne pathophysiology. Eur J Dermatol. 2011;21:323-333.
  24. Del Rosso JQ, Kircik LH. The sequence of inflammation, relevant biomarkers, and the pathogenesis of acne vulgaris: what does recent research show and what does it mean to the clinician? J Drugs Dermatol. 2013;12(8 suppl):S109-S115.  
  25. Leyden J, Kaidbey K, Levy SF. The combination formulation of clindamycin 1% plus benzoyl peroxide 5% versus 3 different formulations of topical clindamycin alone in the reduction of Propionibacterium acnes. an in vivo comparative study. Am J Clin Dermatol. 2001;2:263-266.
  26. Wang WL, Everett ED, Johnson M, et al. Susceptibility of Propionibacterium acnes to seventeen antibiotics. Antimicrob Agents Chemother. 1977;11:171-173.
  27. Steinhoff M, Schauber J, Leyden JJ. New insights into rosacea pathophysiology: a review of recent findings. J Am Acad Dermatol. 2013;69(6 suppl 1):S15-S26.  
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Practice Points

  • Clindamycin cream 0.3% and 1% and clindamycin gel 1% were no more effective than their respective vehicles in the treatment of moderate to severe rosacea.
  • Clindamycin may have no intrinsic anti-inflammatory activity in rosacea.
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Adult diabetes up 35% over 25 years

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The overall prevalence of diabetes increased 35% from 1988-1994 to 2011-2014 among adults aged 20 years and over, according the National Center for Health Statistics.

During 2011-2014, the age-adjusted prevalence of diabetes was 11.9% in adults aged 20 years and over, compared with 8.8% in 1988-1994. That 35% increase came despite a decrease in undiagnosed diabetes from 3.6% to 2.9% over that time period, which was not enough to offset a jump in physician-diagnosed disease from 5.2% to 9%, the NCHS reported in “Health, United States, 2016.”

Although diabetes prevalence was up for each of the largest racial/ethnic groups, only the increase from 7.7% to 9.6% in non-Hispanic whites was statistically significant. Prevalence in non-Hispanic blacks rose from 16.3% to 18% from 1988-1994 to 2011-2014, and adults of Mexican origin saw an increase from 15.6% to 18%. Neither change was statistically significant, the NCHS said.

Undiagnosed diabetes dropped from 2.9% to 2% in whites and from 7.2% to 4.6% in blacks, but adults of Mexican origin saw a slight increase from 5% in 1988-1994 to 5.1% in 2011-2014. The physician-diagnosed side of the equation rose from 4.8% to 7.6% in whites, 9.1% to 13.4% in blacks, and 10.7% to 13% in those of Mexican origin, according to data from the National Health and Nutrition Examination Survey, which combines interviews and physical examinations, including laboratory analysis of blood samples.

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The overall prevalence of diabetes increased 35% from 1988-1994 to 2011-2014 among adults aged 20 years and over, according the National Center for Health Statistics.

During 2011-2014, the age-adjusted prevalence of diabetes was 11.9% in adults aged 20 years and over, compared with 8.8% in 1988-1994. That 35% increase came despite a decrease in undiagnosed diabetes from 3.6% to 2.9% over that time period, which was not enough to offset a jump in physician-diagnosed disease from 5.2% to 9%, the NCHS reported in “Health, United States, 2016.”

Although diabetes prevalence was up for each of the largest racial/ethnic groups, only the increase from 7.7% to 9.6% in non-Hispanic whites was statistically significant. Prevalence in non-Hispanic blacks rose from 16.3% to 18% from 1988-1994 to 2011-2014, and adults of Mexican origin saw an increase from 15.6% to 18%. Neither change was statistically significant, the NCHS said.

Undiagnosed diabetes dropped from 2.9% to 2% in whites and from 7.2% to 4.6% in blacks, but adults of Mexican origin saw a slight increase from 5% in 1988-1994 to 5.1% in 2011-2014. The physician-diagnosed side of the equation rose from 4.8% to 7.6% in whites, 9.1% to 13.4% in blacks, and 10.7% to 13% in those of Mexican origin, according to data from the National Health and Nutrition Examination Survey, which combines interviews and physical examinations, including laboratory analysis of blood samples.

 

The overall prevalence of diabetes increased 35% from 1988-1994 to 2011-2014 among adults aged 20 years and over, according the National Center for Health Statistics.

During 2011-2014, the age-adjusted prevalence of diabetes was 11.9% in adults aged 20 years and over, compared with 8.8% in 1988-1994. That 35% increase came despite a decrease in undiagnosed diabetes from 3.6% to 2.9% over that time period, which was not enough to offset a jump in physician-diagnosed disease from 5.2% to 9%, the NCHS reported in “Health, United States, 2016.”

Although diabetes prevalence was up for each of the largest racial/ethnic groups, only the increase from 7.7% to 9.6% in non-Hispanic whites was statistically significant. Prevalence in non-Hispanic blacks rose from 16.3% to 18% from 1988-1994 to 2011-2014, and adults of Mexican origin saw an increase from 15.6% to 18%. Neither change was statistically significant, the NCHS said.

Undiagnosed diabetes dropped from 2.9% to 2% in whites and from 7.2% to 4.6% in blacks, but adults of Mexican origin saw a slight increase from 5% in 1988-1994 to 5.1% in 2011-2014. The physician-diagnosed side of the equation rose from 4.8% to 7.6% in whites, 9.1% to 13.4% in blacks, and 10.7% to 13% in those of Mexican origin, according to data from the National Health and Nutrition Examination Survey, which combines interviews and physical examinations, including laboratory analysis of blood samples.

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Cosmetic Corner: Dermatologists Weigh in on Redness-Reducing Products

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To improve patient care and outcomes, leading dermatologists offered their recommendations on redness-reducing products. Consideration must be given to:

  • Avène Antirougeurs FORT Relief Concentrate
    Pierre Fabre Dermo-Cosmetique USA
    “This formula has medical-grade ruscus extract to support microcirculation and soothe skin reactivity and redness, as well as soothing Avène Thermal Spring Water.” — Jeannette Graf, MD, New York, New York
     
  • Eucerin Redness Relief
    Beiersdorf Inc
    “Eucerin’s Redness Relief product line has worked well for some of my patients.” — Gary Goldenberg, MD, New York, New York
     
  • Redness Solutions Daily Protective Base Broad Spectrum SPF 15
    Clinique Laboratories, LLC
    “This oil-free makeup primer has a sheer green tint that camouflages redness while also protecting from UV rays.” — Shari Lipner, MD, PhD, New York, New York

 

Cutis invites readers to send us their recommendations. Athlete’s foot treatments, cleansing devices, and men’s products will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

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To improve patient care and outcomes, leading dermatologists offered their recommendations on redness-reducing products. Consideration must be given to:

  • Avène Antirougeurs FORT Relief Concentrate
    Pierre Fabre Dermo-Cosmetique USA
    “This formula has medical-grade ruscus extract to support microcirculation and soothe skin reactivity and redness, as well as soothing Avène Thermal Spring Water.” — Jeannette Graf, MD, New York, New York
     
  • Eucerin Redness Relief
    Beiersdorf Inc
    “Eucerin’s Redness Relief product line has worked well for some of my patients.” — Gary Goldenberg, MD, New York, New York
     
  • Redness Solutions Daily Protective Base Broad Spectrum SPF 15
    Clinique Laboratories, LLC
    “This oil-free makeup primer has a sheer green tint that camouflages redness while also protecting from UV rays.” — Shari Lipner, MD, PhD, New York, New York

 

Cutis invites readers to send us their recommendations. Athlete’s foot treatments, cleansing devices, and men’s products will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on redness-reducing products. Consideration must be given to:

  • Avène Antirougeurs FORT Relief Concentrate
    Pierre Fabre Dermo-Cosmetique USA
    “This formula has medical-grade ruscus extract to support microcirculation and soothe skin reactivity and redness, as well as soothing Avène Thermal Spring Water.” — Jeannette Graf, MD, New York, New York
     
  • Eucerin Redness Relief
    Beiersdorf Inc
    “Eucerin’s Redness Relief product line has worked well for some of my patients.” — Gary Goldenberg, MD, New York, New York
     
  • Redness Solutions Daily Protective Base Broad Spectrum SPF 15
    Clinique Laboratories, LLC
    “This oil-free makeup primer has a sheer green tint that camouflages redness while also protecting from UV rays.” — Shari Lipner, MD, PhD, New York, New York

 

Cutis invites readers to send us their recommendations. Athlete’s foot treatments, cleansing devices, and men’s products will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

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Foreign Body Insertions: A Review

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Foreign Body Insertions: A Review
Treating patients who present with foreign body insertions requires a nonjudgmental and open-minded approach.

Anorectal and urethral foreign body insertions (polyembolokoilamania) are not infrequent presentations to the ED. The motivations behind these insertions vary, ranging from autoeroticism to reckless behavior. These insertions can lead to major complications and even death. Though ED staff members are used to the unpredictability of human behavior, foreign body insertions bring a mixture of responses from the staff, ranging from awe and incredulousness to anger and frustration. A knowledge and comfort in managing these cases includes a nonjudgmental triage assessment, collective professionalism, and self-awareness of the staff’s reaction.

Case 1

A 58-year-old man presented to the ED for evaluation of a foreign body in his rectum. He admitted to placing a beer bottle in his rectum, but was unable to remove it at home. The staff reported that the patient was previously seen in the ED for removal of a vibrator from his rectum.

Radiographic evaluation in the form of an acute abdominal series was obtained and confirmed a beer bottle in the rectum (Figures 1 and 2).

Figure 1.
This study was performed prior to the rectal examination to evaluate the orientation and integrity of the item, to prevent accidental injury from sharp objects.
Figure 2.
On examination, there was palpable glass in the rectum consistent with the rounded base of a bottle. The glass appeared intact and no gross bleeding was noted. Given the orientation of the bottle on the X-ray image, a surgical consultation was obtained and the patient was taken to the operating room (OR). The foreign body was successfully removed with manual extraction under general anesthesia. The patient did not experience any complications. He was offered psychiatric counseling in the ED, but he declined. He was discharged home with a referral to a psychiatrist for counseling.

Case 2

A 55-year-old man presented to the ED after he inserted a pen cap into his urethra to aid in obtaining an erection. A pelvic X-ray was obtained and showed a radiolucent structure in the penis (Figure 3).

Figure 3.
The patient had been seen in several different hospital EDs more than 20 times with similar presentations of penile foreign body insertion.
Figure 4.
The various items inserted included a dry wall screw (Figures 4 and 5) and ballpoint pen (Figure 6). The patient suffered from erectile dysfunction and had been offered multiple treatment options, ranging from medications to penile implant, but he refused these treatments.

The patient was admitted to the hospital and taken to the OR by the consulting urologist. Using a rigid cystoscope and flexible graspers, the pen cap was removed from the proximal urethra under monitored anesthesia control. The procedure went without any complications.

A psychiatrist was consulted, and during the encounter, the patient admitted that his behavior was pathological. He revealed that he was a victim of child abuse and reported he had been having mixed emotions of anxiety, guilt, and embarrassment because of his behavior.

Figure 5.
He consented to inpatient psychiatric treatment and was subsequently transferred to a psychiatric facility.

Discussion

Foreign body insertions are seen in patients with a wide variety of backgrounds, ages, and lifestyles. Approximately 80,000 cases of foreign body ingestion are seen annually in children under age 20 years. Young males have a higher predilection of swallowing foreign bodies when compared to young females,1 and rectal foreign body insertions are seen more commonly in males than in females.2 In this age group, intentional foreign body insertion may be an initial manifestation of psychiatric illness.

Figure 6.
It may also reflect risk-taking or attention-seeking behavior, or poor judgment—especially when combined with alcohol or drugs. Many of those who are evaluated for foreign object insertion have a history of similar prior presentation.1 In comparison, there is a much lower incidence for lower urinary tract foreign body insertions, and self-inflicted urethral foreign body insertions are considered rare, and much rarer in children.3-5 Information on the actual prevalence of foreign object insertions in the general population or in specific psychiatric populations, however, is lacking.1

Rectal Insertions

The earliest published report of a rectal foreign body insertion was in 1919 by Smiley.6 The typical age at presentation ranges from 20 to 90 years old, with a mean age of 44 years old.2 Household objects such as bottles and glasses are the most commonly seen, but a long list of other items have also been reported in the literature, including toothbrushes, knives, deodorant bottles, food articles, sports equipment, cell phones, flashlights, wooden rods, broomsticks, sex toys, light bulbs, construction tools, nails, ornaments, aerosol canisters, cocaine packets, jewelry, batteries, guitar picks, and many other items.1,2,7

 

 

In nearly half of the reported cases, the reasons for rectal insertion was for sexual arousal/stimulation.1,7 Other reasons include nonsuicidal injurious behavior (eg, borderline personality disorder); suicide attempt; psychosis; depression; factitious disorder; malingering; cognitive disorders, including dementia and delirium; treatment of constipation and hemorrhoids; concealment; attention-seeking behavior; “accidental”; assault; and the consequences of drunken wagers.1,2 Additionally, abuse should be considered, especially in patients with developmental delay and/or psychiatric illness.

Close to 20% of all traumatic rectal injuries are due to foreign body insertions. In most cases, foreign bodies fail to cause significant anorectal injuries. Complications, however, can result from the process of insertion, removal, or from the contents introduced into the orifice.1 Any rectal examination should be preceded by an anatomical survey utilizing radiographic modalities to evaluate the integrity and orientation of the object in question. Any sharp object can injure the examining physician if this is not done prior. All examinations should be chaperoned.2,7 The most obvious and dangerous complication is perforation, and the patient’s care should proceed in the same manner as any other trauma patient. Additionally, resulting sepsis should be managed with the same standards as any other septic patient.7

Treatment. The method of object removal is determined by the presence or absence of a surgical abdomen and the need for general anesthesia. The location and shape of the object, however, may not equate with successful retrieval. Objects placed in the sigmoid colon are more than twice as likely to require surgical intervention compared to items placed distally.2 Once it is determined that the patient is clinically stable and does not have an acute abdomen, attempts in removing the rectal foreign object can be done in the ED or, if anesthesia is needed, in the OR. Any attempts at transanal removal require optimal patient relaxation, which can be achieved via procedural sedation. The patient should be placed in a lithotomy or left lateral decubitus position to allow palpation of the object in the lower gastrointestinal tract. From here, several methods of removal can be employed. Blunt objects can be grasped and removed by a gloved hand or with a clamp. A Foley catheter can also be passed alongside the object and the balloon inflated above the foreign body to aid in extraction as the Foley is pulled out slowly. Sengstaken-Blakemore tubes, obstetric forceps, and vacuum extractors have also been utilized.7

While bedside extraction is advocated by many authors, Cawich et al8 recently reported that transanal extraction in the ED failed in 89% of cases. Additionally, these researchers reported that in 63% of the failed extractions, the objects were inadvertently pushed higher into the rectosigmoid region, and therefore recommended early mobilization of the OR team so that exploration under anesthesia can be performed under optimal conditions.8

Once the foreign body is successfully removed, follow-up imaging or postextraction endoscopy is warranted. Close observation in the hospital is recommended to facilitate serial abdominal examination.7

Urethral Insertions

Sexual exploration, efforts at contraception, transport of illicit drugs, assault or sexual violence, and accidental insertion have all been described as reasons for genitourinary (GU) insertion.1 The motives, however, mirror those who insert foreign bodies rectally.

Most presentations are due to pain or inability to void. Aggressive treatment should be undertaken because even when the penis appears dark or necrotic, salvage rates have been high. Complications include urinary tract infections, hematuria, urinary retention, urethral tears, abscess, ascending GU infections, and diverticula and fistula formations.1,3 In women, vaginal insertions can lead to pelvic pain and septic shock.1 Foreign bodies can also lead to a condition first described in the ancient literature as strangury—the process of slow and painful discharge of urine due to a significant inflammatory component or stricture. The term strangury has been replaced with the more general term bladder spasms.9

Treatment. Removal of urethral foreign bodies typically is done in conjunction with a urologist. A cystoscopic procedure is usually successful in removing the foreign body and is an effective method to minimize urethral and bladder injuries. However, more invasive surgical options, including perineal urethrotomy, suprapubic cystostomy, cystolithotomy, and external urethrotomy, have been used in more complicated cases or when the foreign body prevents urethral access of an endoscopic instrument.10

Patient and Staff Reactions

When patients realize they are unable to remove the inserted object, some present immediately to the ED for evaluation. Interestingly, others may wait up to 2 weeks after insertion before seeking help.2 Patients report feelings of being ashamed and report a feeling of being despised, frowned upon, and being talked about during the course of their ED evaluation. As a consequence, these patients may not readily come to the ED or if they do come, may not be open to conversation and hide the true reason of why they came in the first place.1,4 The amplified paranoia and perceived prejudice may delay diagnosis and lifesaving measures, or worse, lead patients to leave prior to a medical screening examination. Therefore, creating a nonjudgmental environment is essential, even when the presenting story appears to be fabricated.2

 

 

Once the patient’s foreign body is removed, and complications are excluded or properly managed, the goal is to understand the motivation behind the insertion, mitigate the consequences of the behavior, and prevent future recurrence. A psychiatric evaluation should be obtained in the ED, or if the patient is admitted, during hospitalization. Psychiatric behavior leading to insertions can be unmasked, treated, and harm-reduction strategies can be taught and instituted.1,3

Experienced ED staff members are used to the unpredictability of human behavior. However, patients who present with foreign body insertions can elicit a mixture of responses, ranging from awe and incredulousness to anger and frustration. It is not unusual for staff members to not understand or recognize their own reactions. The unique nature of the presentation, along with the astonishing radiographic images, can lead to a breach of privacy and dissemination of the digital photographs by cell phones and into social media sites.1 Staff members should be encouraged to foster open-mindedness and indifference. Ensuring privacy, professionalism, and empathy can go a long way to helping these patients. Moreover, ED staff members should be educated about countertransference reactions,1 as these actions are necessary to ensure the singular purpose of optimum patient-staff relationship.

Conclusion

Patients with foreign body insertions challenge the ED staff, as the presenting complaint not only tests the collective technical know-how of the staff, but also their emotional competencies. A nonjudgmental and open-minded approach is crucial, with the tone set during triage. Coordination with surgical specialties should be done early to ensure safe removal and to identify and manage complications. Psychiatric evaluation should be strongly considered prior to disposition in an attempt to prevent future recurrences.

References

1. Unruh BT, Nejad SH, Stern TW, Stern TA. Insertion of foreign bodies (polyembolokoilamania): underpinnings and management strategies. Prim Care Companion CNS Disord. 2012;14(1). doi:10.4088/PCC.11f01192.

2. Cologne KG, Ault GT. Rectal foreign bodies: what is the current standard? Clin Colon Rectal Surg. 2012;25(4):214-218. doi:10.1055/s-0032-1329392.3. Naidu K, Chung A, Mulcahy M. An unusual urethral foreign body. Int J Surg Case Rep. 2013;4(11):1052-1054. doi:10.1016/j.ijscr.2013.07.017.4. Rahman NU, Elliott SP, McAninch JW. Self-inflicted male urethral foreign body insertion: endoscopic management and complications. BJU Int. 2004;94(7):1051-1053. 10.1111/j.1464-410X.2004.05103.x.

5. SaiSwaroop Y, Darakh P, Amlani D. Self insertion of urethral foreign body in a child: a rare case report. Int J Curr Med Appl Sci. 2015;9(1):22-24.

6. Smiley O. A glass tumbler in the rectum. JAMA. 1919;72:1285.

7. Coskun A, Erkan N, Yakan S, Yıldirim M, Cengiz F. Management of rectal foreign bodies. World J Emerg Surg. 2013;8(1):11. doi:10.1186/1749-7922-8-11.

8. Cawich SO, Thomas DA, Mohammed F, Bobb NJ, Williams D, Naraynsingh V. A management algorithm for retained rectal foreign bodies. Am J Mens Health. 2017;11(3):684-692. doi:10.1177/1557988316680929.

9. Wright B, Husbands E. Strangury: the case of a symptom with ancient origins. BMJ Support Palliat Care. 2011;1(1):49-50. doi:10.1136/bmjspcare-2011-000030.

10. Moon SJ, Kim DH, Chung JH, et al. Unusual foreign bodies in the urinary bladder and urethra due to autoerotism. Int Neurourol J. 2010;14(3):186-189. doi:10.5213/inj.2010.14.3.186.

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Treating patients who present with foreign body insertions requires a nonjudgmental and open-minded approach.
Treating patients who present with foreign body insertions requires a nonjudgmental and open-minded approach.

Anorectal and urethral foreign body insertions (polyembolokoilamania) are not infrequent presentations to the ED. The motivations behind these insertions vary, ranging from autoeroticism to reckless behavior. These insertions can lead to major complications and even death. Though ED staff members are used to the unpredictability of human behavior, foreign body insertions bring a mixture of responses from the staff, ranging from awe and incredulousness to anger and frustration. A knowledge and comfort in managing these cases includes a nonjudgmental triage assessment, collective professionalism, and self-awareness of the staff’s reaction.

Case 1

A 58-year-old man presented to the ED for evaluation of a foreign body in his rectum. He admitted to placing a beer bottle in his rectum, but was unable to remove it at home. The staff reported that the patient was previously seen in the ED for removal of a vibrator from his rectum.

Radiographic evaluation in the form of an acute abdominal series was obtained and confirmed a beer bottle in the rectum (Figures 1 and 2).

Figure 1.
This study was performed prior to the rectal examination to evaluate the orientation and integrity of the item, to prevent accidental injury from sharp objects.
Figure 2.
On examination, there was palpable glass in the rectum consistent with the rounded base of a bottle. The glass appeared intact and no gross bleeding was noted. Given the orientation of the bottle on the X-ray image, a surgical consultation was obtained and the patient was taken to the operating room (OR). The foreign body was successfully removed with manual extraction under general anesthesia. The patient did not experience any complications. He was offered psychiatric counseling in the ED, but he declined. He was discharged home with a referral to a psychiatrist for counseling.

Case 2

A 55-year-old man presented to the ED after he inserted a pen cap into his urethra to aid in obtaining an erection. A pelvic X-ray was obtained and showed a radiolucent structure in the penis (Figure 3).

Figure 3.
The patient had been seen in several different hospital EDs more than 20 times with similar presentations of penile foreign body insertion.
Figure 4.
The various items inserted included a dry wall screw (Figures 4 and 5) and ballpoint pen (Figure 6). The patient suffered from erectile dysfunction and had been offered multiple treatment options, ranging from medications to penile implant, but he refused these treatments.

The patient was admitted to the hospital and taken to the OR by the consulting urologist. Using a rigid cystoscope and flexible graspers, the pen cap was removed from the proximal urethra under monitored anesthesia control. The procedure went without any complications.

A psychiatrist was consulted, and during the encounter, the patient admitted that his behavior was pathological. He revealed that he was a victim of child abuse and reported he had been having mixed emotions of anxiety, guilt, and embarrassment because of his behavior.

Figure 5.
He consented to inpatient psychiatric treatment and was subsequently transferred to a psychiatric facility.

Discussion

Foreign body insertions are seen in patients with a wide variety of backgrounds, ages, and lifestyles. Approximately 80,000 cases of foreign body ingestion are seen annually in children under age 20 years. Young males have a higher predilection of swallowing foreign bodies when compared to young females,1 and rectal foreign body insertions are seen more commonly in males than in females.2 In this age group, intentional foreign body insertion may be an initial manifestation of psychiatric illness.

Figure 6.
It may also reflect risk-taking or attention-seeking behavior, or poor judgment—especially when combined with alcohol or drugs. Many of those who are evaluated for foreign object insertion have a history of similar prior presentation.1 In comparison, there is a much lower incidence for lower urinary tract foreign body insertions, and self-inflicted urethral foreign body insertions are considered rare, and much rarer in children.3-5 Information on the actual prevalence of foreign object insertions in the general population or in specific psychiatric populations, however, is lacking.1

Rectal Insertions

The earliest published report of a rectal foreign body insertion was in 1919 by Smiley.6 The typical age at presentation ranges from 20 to 90 years old, with a mean age of 44 years old.2 Household objects such as bottles and glasses are the most commonly seen, but a long list of other items have also been reported in the literature, including toothbrushes, knives, deodorant bottles, food articles, sports equipment, cell phones, flashlights, wooden rods, broomsticks, sex toys, light bulbs, construction tools, nails, ornaments, aerosol canisters, cocaine packets, jewelry, batteries, guitar picks, and many other items.1,2,7

 

 

In nearly half of the reported cases, the reasons for rectal insertion was for sexual arousal/stimulation.1,7 Other reasons include nonsuicidal injurious behavior (eg, borderline personality disorder); suicide attempt; psychosis; depression; factitious disorder; malingering; cognitive disorders, including dementia and delirium; treatment of constipation and hemorrhoids; concealment; attention-seeking behavior; “accidental”; assault; and the consequences of drunken wagers.1,2 Additionally, abuse should be considered, especially in patients with developmental delay and/or psychiatric illness.

Close to 20% of all traumatic rectal injuries are due to foreign body insertions. In most cases, foreign bodies fail to cause significant anorectal injuries. Complications, however, can result from the process of insertion, removal, or from the contents introduced into the orifice.1 Any rectal examination should be preceded by an anatomical survey utilizing radiographic modalities to evaluate the integrity and orientation of the object in question. Any sharp object can injure the examining physician if this is not done prior. All examinations should be chaperoned.2,7 The most obvious and dangerous complication is perforation, and the patient’s care should proceed in the same manner as any other trauma patient. Additionally, resulting sepsis should be managed with the same standards as any other septic patient.7

Treatment. The method of object removal is determined by the presence or absence of a surgical abdomen and the need for general anesthesia. The location and shape of the object, however, may not equate with successful retrieval. Objects placed in the sigmoid colon are more than twice as likely to require surgical intervention compared to items placed distally.2 Once it is determined that the patient is clinically stable and does not have an acute abdomen, attempts in removing the rectal foreign object can be done in the ED or, if anesthesia is needed, in the OR. Any attempts at transanal removal require optimal patient relaxation, which can be achieved via procedural sedation. The patient should be placed in a lithotomy or left lateral decubitus position to allow palpation of the object in the lower gastrointestinal tract. From here, several methods of removal can be employed. Blunt objects can be grasped and removed by a gloved hand or with a clamp. A Foley catheter can also be passed alongside the object and the balloon inflated above the foreign body to aid in extraction as the Foley is pulled out slowly. Sengstaken-Blakemore tubes, obstetric forceps, and vacuum extractors have also been utilized.7

While bedside extraction is advocated by many authors, Cawich et al8 recently reported that transanal extraction in the ED failed in 89% of cases. Additionally, these researchers reported that in 63% of the failed extractions, the objects were inadvertently pushed higher into the rectosigmoid region, and therefore recommended early mobilization of the OR team so that exploration under anesthesia can be performed under optimal conditions.8

Once the foreign body is successfully removed, follow-up imaging or postextraction endoscopy is warranted. Close observation in the hospital is recommended to facilitate serial abdominal examination.7

Urethral Insertions

Sexual exploration, efforts at contraception, transport of illicit drugs, assault or sexual violence, and accidental insertion have all been described as reasons for genitourinary (GU) insertion.1 The motives, however, mirror those who insert foreign bodies rectally.

Most presentations are due to pain or inability to void. Aggressive treatment should be undertaken because even when the penis appears dark or necrotic, salvage rates have been high. Complications include urinary tract infections, hematuria, urinary retention, urethral tears, abscess, ascending GU infections, and diverticula and fistula formations.1,3 In women, vaginal insertions can lead to pelvic pain and septic shock.1 Foreign bodies can also lead to a condition first described in the ancient literature as strangury—the process of slow and painful discharge of urine due to a significant inflammatory component or stricture. The term strangury has been replaced with the more general term bladder spasms.9

Treatment. Removal of urethral foreign bodies typically is done in conjunction with a urologist. A cystoscopic procedure is usually successful in removing the foreign body and is an effective method to minimize urethral and bladder injuries. However, more invasive surgical options, including perineal urethrotomy, suprapubic cystostomy, cystolithotomy, and external urethrotomy, have been used in more complicated cases or when the foreign body prevents urethral access of an endoscopic instrument.10

Patient and Staff Reactions

When patients realize they are unable to remove the inserted object, some present immediately to the ED for evaluation. Interestingly, others may wait up to 2 weeks after insertion before seeking help.2 Patients report feelings of being ashamed and report a feeling of being despised, frowned upon, and being talked about during the course of their ED evaluation. As a consequence, these patients may not readily come to the ED or if they do come, may not be open to conversation and hide the true reason of why they came in the first place.1,4 The amplified paranoia and perceived prejudice may delay diagnosis and lifesaving measures, or worse, lead patients to leave prior to a medical screening examination. Therefore, creating a nonjudgmental environment is essential, even when the presenting story appears to be fabricated.2

 

 

Once the patient’s foreign body is removed, and complications are excluded or properly managed, the goal is to understand the motivation behind the insertion, mitigate the consequences of the behavior, and prevent future recurrence. A psychiatric evaluation should be obtained in the ED, or if the patient is admitted, during hospitalization. Psychiatric behavior leading to insertions can be unmasked, treated, and harm-reduction strategies can be taught and instituted.1,3

Experienced ED staff members are used to the unpredictability of human behavior. However, patients who present with foreign body insertions can elicit a mixture of responses, ranging from awe and incredulousness to anger and frustration. It is not unusual for staff members to not understand or recognize their own reactions. The unique nature of the presentation, along with the astonishing radiographic images, can lead to a breach of privacy and dissemination of the digital photographs by cell phones and into social media sites.1 Staff members should be encouraged to foster open-mindedness and indifference. Ensuring privacy, professionalism, and empathy can go a long way to helping these patients. Moreover, ED staff members should be educated about countertransference reactions,1 as these actions are necessary to ensure the singular purpose of optimum patient-staff relationship.

Conclusion

Patients with foreign body insertions challenge the ED staff, as the presenting complaint not only tests the collective technical know-how of the staff, but also their emotional competencies. A nonjudgmental and open-minded approach is crucial, with the tone set during triage. Coordination with surgical specialties should be done early to ensure safe removal and to identify and manage complications. Psychiatric evaluation should be strongly considered prior to disposition in an attempt to prevent future recurrences.

Anorectal and urethral foreign body insertions (polyembolokoilamania) are not infrequent presentations to the ED. The motivations behind these insertions vary, ranging from autoeroticism to reckless behavior. These insertions can lead to major complications and even death. Though ED staff members are used to the unpredictability of human behavior, foreign body insertions bring a mixture of responses from the staff, ranging from awe and incredulousness to anger and frustration. A knowledge and comfort in managing these cases includes a nonjudgmental triage assessment, collective professionalism, and self-awareness of the staff’s reaction.

Case 1

A 58-year-old man presented to the ED for evaluation of a foreign body in his rectum. He admitted to placing a beer bottle in his rectum, but was unable to remove it at home. The staff reported that the patient was previously seen in the ED for removal of a vibrator from his rectum.

Radiographic evaluation in the form of an acute abdominal series was obtained and confirmed a beer bottle in the rectum (Figures 1 and 2).

Figure 1.
This study was performed prior to the rectal examination to evaluate the orientation and integrity of the item, to prevent accidental injury from sharp objects.
Figure 2.
On examination, there was palpable glass in the rectum consistent with the rounded base of a bottle. The glass appeared intact and no gross bleeding was noted. Given the orientation of the bottle on the X-ray image, a surgical consultation was obtained and the patient was taken to the operating room (OR). The foreign body was successfully removed with manual extraction under general anesthesia. The patient did not experience any complications. He was offered psychiatric counseling in the ED, but he declined. He was discharged home with a referral to a psychiatrist for counseling.

Case 2

A 55-year-old man presented to the ED after he inserted a pen cap into his urethra to aid in obtaining an erection. A pelvic X-ray was obtained and showed a radiolucent structure in the penis (Figure 3).

Figure 3.
The patient had been seen in several different hospital EDs more than 20 times with similar presentations of penile foreign body insertion.
Figure 4.
The various items inserted included a dry wall screw (Figures 4 and 5) and ballpoint pen (Figure 6). The patient suffered from erectile dysfunction and had been offered multiple treatment options, ranging from medications to penile implant, but he refused these treatments.

The patient was admitted to the hospital and taken to the OR by the consulting urologist. Using a rigid cystoscope and flexible graspers, the pen cap was removed from the proximal urethra under monitored anesthesia control. The procedure went without any complications.

A psychiatrist was consulted, and during the encounter, the patient admitted that his behavior was pathological. He revealed that he was a victim of child abuse and reported he had been having mixed emotions of anxiety, guilt, and embarrassment because of his behavior.

Figure 5.
He consented to inpatient psychiatric treatment and was subsequently transferred to a psychiatric facility.

Discussion

Foreign body insertions are seen in patients with a wide variety of backgrounds, ages, and lifestyles. Approximately 80,000 cases of foreign body ingestion are seen annually in children under age 20 years. Young males have a higher predilection of swallowing foreign bodies when compared to young females,1 and rectal foreign body insertions are seen more commonly in males than in females.2 In this age group, intentional foreign body insertion may be an initial manifestation of psychiatric illness.

Figure 6.
It may also reflect risk-taking or attention-seeking behavior, or poor judgment—especially when combined with alcohol or drugs. Many of those who are evaluated for foreign object insertion have a history of similar prior presentation.1 In comparison, there is a much lower incidence for lower urinary tract foreign body insertions, and self-inflicted urethral foreign body insertions are considered rare, and much rarer in children.3-5 Information on the actual prevalence of foreign object insertions in the general population or in specific psychiatric populations, however, is lacking.1

Rectal Insertions

The earliest published report of a rectal foreign body insertion was in 1919 by Smiley.6 The typical age at presentation ranges from 20 to 90 years old, with a mean age of 44 years old.2 Household objects such as bottles and glasses are the most commonly seen, but a long list of other items have also been reported in the literature, including toothbrushes, knives, deodorant bottles, food articles, sports equipment, cell phones, flashlights, wooden rods, broomsticks, sex toys, light bulbs, construction tools, nails, ornaments, aerosol canisters, cocaine packets, jewelry, batteries, guitar picks, and many other items.1,2,7

 

 

In nearly half of the reported cases, the reasons for rectal insertion was for sexual arousal/stimulation.1,7 Other reasons include nonsuicidal injurious behavior (eg, borderline personality disorder); suicide attempt; psychosis; depression; factitious disorder; malingering; cognitive disorders, including dementia and delirium; treatment of constipation and hemorrhoids; concealment; attention-seeking behavior; “accidental”; assault; and the consequences of drunken wagers.1,2 Additionally, abuse should be considered, especially in patients with developmental delay and/or psychiatric illness.

Close to 20% of all traumatic rectal injuries are due to foreign body insertions. In most cases, foreign bodies fail to cause significant anorectal injuries. Complications, however, can result from the process of insertion, removal, or from the contents introduced into the orifice.1 Any rectal examination should be preceded by an anatomical survey utilizing radiographic modalities to evaluate the integrity and orientation of the object in question. Any sharp object can injure the examining physician if this is not done prior. All examinations should be chaperoned.2,7 The most obvious and dangerous complication is perforation, and the patient’s care should proceed in the same manner as any other trauma patient. Additionally, resulting sepsis should be managed with the same standards as any other septic patient.7

Treatment. The method of object removal is determined by the presence or absence of a surgical abdomen and the need for general anesthesia. The location and shape of the object, however, may not equate with successful retrieval. Objects placed in the sigmoid colon are more than twice as likely to require surgical intervention compared to items placed distally.2 Once it is determined that the patient is clinically stable and does not have an acute abdomen, attempts in removing the rectal foreign object can be done in the ED or, if anesthesia is needed, in the OR. Any attempts at transanal removal require optimal patient relaxation, which can be achieved via procedural sedation. The patient should be placed in a lithotomy or left lateral decubitus position to allow palpation of the object in the lower gastrointestinal tract. From here, several methods of removal can be employed. Blunt objects can be grasped and removed by a gloved hand or with a clamp. A Foley catheter can also be passed alongside the object and the balloon inflated above the foreign body to aid in extraction as the Foley is pulled out slowly. Sengstaken-Blakemore tubes, obstetric forceps, and vacuum extractors have also been utilized.7

While bedside extraction is advocated by many authors, Cawich et al8 recently reported that transanal extraction in the ED failed in 89% of cases. Additionally, these researchers reported that in 63% of the failed extractions, the objects were inadvertently pushed higher into the rectosigmoid region, and therefore recommended early mobilization of the OR team so that exploration under anesthesia can be performed under optimal conditions.8

Once the foreign body is successfully removed, follow-up imaging or postextraction endoscopy is warranted. Close observation in the hospital is recommended to facilitate serial abdominal examination.7

Urethral Insertions

Sexual exploration, efforts at contraception, transport of illicit drugs, assault or sexual violence, and accidental insertion have all been described as reasons for genitourinary (GU) insertion.1 The motives, however, mirror those who insert foreign bodies rectally.

Most presentations are due to pain or inability to void. Aggressive treatment should be undertaken because even when the penis appears dark or necrotic, salvage rates have been high. Complications include urinary tract infections, hematuria, urinary retention, urethral tears, abscess, ascending GU infections, and diverticula and fistula formations.1,3 In women, vaginal insertions can lead to pelvic pain and septic shock.1 Foreign bodies can also lead to a condition first described in the ancient literature as strangury—the process of slow and painful discharge of urine due to a significant inflammatory component or stricture. The term strangury has been replaced with the more general term bladder spasms.9

Treatment. Removal of urethral foreign bodies typically is done in conjunction with a urologist. A cystoscopic procedure is usually successful in removing the foreign body and is an effective method to minimize urethral and bladder injuries. However, more invasive surgical options, including perineal urethrotomy, suprapubic cystostomy, cystolithotomy, and external urethrotomy, have been used in more complicated cases or when the foreign body prevents urethral access of an endoscopic instrument.10

Patient and Staff Reactions

When patients realize they are unable to remove the inserted object, some present immediately to the ED for evaluation. Interestingly, others may wait up to 2 weeks after insertion before seeking help.2 Patients report feelings of being ashamed and report a feeling of being despised, frowned upon, and being talked about during the course of their ED evaluation. As a consequence, these patients may not readily come to the ED or if they do come, may not be open to conversation and hide the true reason of why they came in the first place.1,4 The amplified paranoia and perceived prejudice may delay diagnosis and lifesaving measures, or worse, lead patients to leave prior to a medical screening examination. Therefore, creating a nonjudgmental environment is essential, even when the presenting story appears to be fabricated.2

 

 

Once the patient’s foreign body is removed, and complications are excluded or properly managed, the goal is to understand the motivation behind the insertion, mitigate the consequences of the behavior, and prevent future recurrence. A psychiatric evaluation should be obtained in the ED, or if the patient is admitted, during hospitalization. Psychiatric behavior leading to insertions can be unmasked, treated, and harm-reduction strategies can be taught and instituted.1,3

Experienced ED staff members are used to the unpredictability of human behavior. However, patients who present with foreign body insertions can elicit a mixture of responses, ranging from awe and incredulousness to anger and frustration. It is not unusual for staff members to not understand or recognize their own reactions. The unique nature of the presentation, along with the astonishing radiographic images, can lead to a breach of privacy and dissemination of the digital photographs by cell phones and into social media sites.1 Staff members should be encouraged to foster open-mindedness and indifference. Ensuring privacy, professionalism, and empathy can go a long way to helping these patients. Moreover, ED staff members should be educated about countertransference reactions,1 as these actions are necessary to ensure the singular purpose of optimum patient-staff relationship.

Conclusion

Patients with foreign body insertions challenge the ED staff, as the presenting complaint not only tests the collective technical know-how of the staff, but also their emotional competencies. A nonjudgmental and open-minded approach is crucial, with the tone set during triage. Coordination with surgical specialties should be done early to ensure safe removal and to identify and manage complications. Psychiatric evaluation should be strongly considered prior to disposition in an attempt to prevent future recurrences.

References

1. Unruh BT, Nejad SH, Stern TW, Stern TA. Insertion of foreign bodies (polyembolokoilamania): underpinnings and management strategies. Prim Care Companion CNS Disord. 2012;14(1). doi:10.4088/PCC.11f01192.

2. Cologne KG, Ault GT. Rectal foreign bodies: what is the current standard? Clin Colon Rectal Surg. 2012;25(4):214-218. doi:10.1055/s-0032-1329392.3. Naidu K, Chung A, Mulcahy M. An unusual urethral foreign body. Int J Surg Case Rep. 2013;4(11):1052-1054. doi:10.1016/j.ijscr.2013.07.017.4. Rahman NU, Elliott SP, McAninch JW. Self-inflicted male urethral foreign body insertion: endoscopic management and complications. BJU Int. 2004;94(7):1051-1053. 10.1111/j.1464-410X.2004.05103.x.

5. SaiSwaroop Y, Darakh P, Amlani D. Self insertion of urethral foreign body in a child: a rare case report. Int J Curr Med Appl Sci. 2015;9(1):22-24.

6. Smiley O. A glass tumbler in the rectum. JAMA. 1919;72:1285.

7. Coskun A, Erkan N, Yakan S, Yıldirim M, Cengiz F. Management of rectal foreign bodies. World J Emerg Surg. 2013;8(1):11. doi:10.1186/1749-7922-8-11.

8. Cawich SO, Thomas DA, Mohammed F, Bobb NJ, Williams D, Naraynsingh V. A management algorithm for retained rectal foreign bodies. Am J Mens Health. 2017;11(3):684-692. doi:10.1177/1557988316680929.

9. Wright B, Husbands E. Strangury: the case of a symptom with ancient origins. BMJ Support Palliat Care. 2011;1(1):49-50. doi:10.1136/bmjspcare-2011-000030.

10. Moon SJ, Kim DH, Chung JH, et al. Unusual foreign bodies in the urinary bladder and urethra due to autoerotism. Int Neurourol J. 2010;14(3):186-189. doi:10.5213/inj.2010.14.3.186.

References

1. Unruh BT, Nejad SH, Stern TW, Stern TA. Insertion of foreign bodies (polyembolokoilamania): underpinnings and management strategies. Prim Care Companion CNS Disord. 2012;14(1). doi:10.4088/PCC.11f01192.

2. Cologne KG, Ault GT. Rectal foreign bodies: what is the current standard? Clin Colon Rectal Surg. 2012;25(4):214-218. doi:10.1055/s-0032-1329392.3. Naidu K, Chung A, Mulcahy M. An unusual urethral foreign body. Int J Surg Case Rep. 2013;4(11):1052-1054. doi:10.1016/j.ijscr.2013.07.017.4. Rahman NU, Elliott SP, McAninch JW. Self-inflicted male urethral foreign body insertion: endoscopic management and complications. BJU Int. 2004;94(7):1051-1053. 10.1111/j.1464-410X.2004.05103.x.

5. SaiSwaroop Y, Darakh P, Amlani D. Self insertion of urethral foreign body in a child: a rare case report. Int J Curr Med Appl Sci. 2015;9(1):22-24.

6. Smiley O. A glass tumbler in the rectum. JAMA. 1919;72:1285.

7. Coskun A, Erkan N, Yakan S, Yıldirim M, Cengiz F. Management of rectal foreign bodies. World J Emerg Surg. 2013;8(1):11. doi:10.1186/1749-7922-8-11.

8. Cawich SO, Thomas DA, Mohammed F, Bobb NJ, Williams D, Naraynsingh V. A management algorithm for retained rectal foreign bodies. Am J Mens Health. 2017;11(3):684-692. doi:10.1177/1557988316680929.

9. Wright B, Husbands E. Strangury: the case of a symptom with ancient origins. BMJ Support Palliat Care. 2011;1(1):49-50. doi:10.1136/bmjspcare-2011-000030.

10. Moon SJ, Kim DH, Chung JH, et al. Unusual foreign bodies in the urinary bladder and urethra due to autoerotism. Int Neurourol J. 2010;14(3):186-189. doi:10.5213/inj.2010.14.3.186.

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Telomere length predicts FCR response in CLL patients

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– Telomere length reliably predicts response to fludarabine-cyclophosphamide-rituximab (FCR) treatment in patients with chronic lymphocytic leukemia, according to an analysis of 278 samples from the ARCTIC and ADMIRE clinical trials of FCR in previously untreated CLL.

The findings were particularly pronounced in the immunoglobulin heavy-chain variable region gene (IGHV)–mutated patients and suggest a role for telomere measurement as a predictive tool in risk-adapted clinical trials, Kevin Norris reported in a poster at the annual International Workshop on Chronic Lymphocytic Leukemia.

Short telomere length was associated with quicker time to progression (median of 3.9 years vs. 5.5 years; hazard ratio[HR], 2.04) and reduced overall survival (OS) (median of 5.5 years vs. OS not reached; HR, 2.1), compared with long telomere length. IGHV-mutated patients with short telomeres were more than five times more likely to relapse (median progression-free survival 2.97 vs. PFS not reached; HR, 5.1), and more than four times more likely to die than were patients with long telomere length (median OS, 4.15 years vs. OS not reached; HR, 4.16), said Mr. Norris, a research associate at Cardiff (Wales) University.

The association between telomere length and FCR response was less pronounced among IGHV-unmutated patients, but those with short telomeres in this group still had an inferior response and shorter survival, compared with those with long telomeres (HR, 1.6 and 1.6, respectively), he noted.

Mr. Norris also noted that in contrast to the telomere length findings, CD38 expression and b2-microglobulin were not predictive of time to progression or OS.

“In multivariate analysis, telomere length was the dominant covariable for both PFS (HR, 2.58) and OS (HR, 2.84); when telomere length was entered into the model no other variable retained independent prognostic significance,” he and his colleagues wrote.

Telomere length in this analysis was assessed by use of the high throughput single telomere length analysis (HT-STELA) assay.

It has recently been shown that a proportion of IGHV-mutated CLL patients treated with FCR can achieve long-term remissions. The current findings demonstrate that these patients can be accurately identified by measuring telomere length, the investigators said, noting that they saw a similar pattern in patients in the UK CLL4 trial who were treated with fludarabine and cyclophosphamide

“Our results demonstrate that telomere length is the major determinant of response and survival following treatment with FCR,” they wrote. “IGHV-mutated patients with longer telomeres have a high probability of achieving a long-term remission following treatment with FCR (greater than 81% survival after 5 years). Equally, IGHV-mutated patients with short dysfunctional telomeres show a markedly inferior response to FCR and should be considered for alternative treatment options in the frontline setting.”

Patient material for this study was obtained from the UK CLL Trials Biobank, University of Liverpool, which is funded by Bloodwise. The authors reported having no other disclosures.

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– Telomere length reliably predicts response to fludarabine-cyclophosphamide-rituximab (FCR) treatment in patients with chronic lymphocytic leukemia, according to an analysis of 278 samples from the ARCTIC and ADMIRE clinical trials of FCR in previously untreated CLL.

The findings were particularly pronounced in the immunoglobulin heavy-chain variable region gene (IGHV)–mutated patients and suggest a role for telomere measurement as a predictive tool in risk-adapted clinical trials, Kevin Norris reported in a poster at the annual International Workshop on Chronic Lymphocytic Leukemia.

Short telomere length was associated with quicker time to progression (median of 3.9 years vs. 5.5 years; hazard ratio[HR], 2.04) and reduced overall survival (OS) (median of 5.5 years vs. OS not reached; HR, 2.1), compared with long telomere length. IGHV-mutated patients with short telomeres were more than five times more likely to relapse (median progression-free survival 2.97 vs. PFS not reached; HR, 5.1), and more than four times more likely to die than were patients with long telomere length (median OS, 4.15 years vs. OS not reached; HR, 4.16), said Mr. Norris, a research associate at Cardiff (Wales) University.

The association between telomere length and FCR response was less pronounced among IGHV-unmutated patients, but those with short telomeres in this group still had an inferior response and shorter survival, compared with those with long telomeres (HR, 1.6 and 1.6, respectively), he noted.

Mr. Norris also noted that in contrast to the telomere length findings, CD38 expression and b2-microglobulin were not predictive of time to progression or OS.

“In multivariate analysis, telomere length was the dominant covariable for both PFS (HR, 2.58) and OS (HR, 2.84); when telomere length was entered into the model no other variable retained independent prognostic significance,” he and his colleagues wrote.

Telomere length in this analysis was assessed by use of the high throughput single telomere length analysis (HT-STELA) assay.

It has recently been shown that a proportion of IGHV-mutated CLL patients treated with FCR can achieve long-term remissions. The current findings demonstrate that these patients can be accurately identified by measuring telomere length, the investigators said, noting that they saw a similar pattern in patients in the UK CLL4 trial who were treated with fludarabine and cyclophosphamide

“Our results demonstrate that telomere length is the major determinant of response and survival following treatment with FCR,” they wrote. “IGHV-mutated patients with longer telomeres have a high probability of achieving a long-term remission following treatment with FCR (greater than 81% survival after 5 years). Equally, IGHV-mutated patients with short dysfunctional telomeres show a markedly inferior response to FCR and should be considered for alternative treatment options in the frontline setting.”

Patient material for this study was obtained from the UK CLL Trials Biobank, University of Liverpool, which is funded by Bloodwise. The authors reported having no other disclosures.

 

– Telomere length reliably predicts response to fludarabine-cyclophosphamide-rituximab (FCR) treatment in patients with chronic lymphocytic leukemia, according to an analysis of 278 samples from the ARCTIC and ADMIRE clinical trials of FCR in previously untreated CLL.

The findings were particularly pronounced in the immunoglobulin heavy-chain variable region gene (IGHV)–mutated patients and suggest a role for telomere measurement as a predictive tool in risk-adapted clinical trials, Kevin Norris reported in a poster at the annual International Workshop on Chronic Lymphocytic Leukemia.

Short telomere length was associated with quicker time to progression (median of 3.9 years vs. 5.5 years; hazard ratio[HR], 2.04) and reduced overall survival (OS) (median of 5.5 years vs. OS not reached; HR, 2.1), compared with long telomere length. IGHV-mutated patients with short telomeres were more than five times more likely to relapse (median progression-free survival 2.97 vs. PFS not reached; HR, 5.1), and more than four times more likely to die than were patients with long telomere length (median OS, 4.15 years vs. OS not reached; HR, 4.16), said Mr. Norris, a research associate at Cardiff (Wales) University.

The association between telomere length and FCR response was less pronounced among IGHV-unmutated patients, but those with short telomeres in this group still had an inferior response and shorter survival, compared with those with long telomeres (HR, 1.6 and 1.6, respectively), he noted.

Mr. Norris also noted that in contrast to the telomere length findings, CD38 expression and b2-microglobulin were not predictive of time to progression or OS.

“In multivariate analysis, telomere length was the dominant covariable for both PFS (HR, 2.58) and OS (HR, 2.84); when telomere length was entered into the model no other variable retained independent prognostic significance,” he and his colleagues wrote.

Telomere length in this analysis was assessed by use of the high throughput single telomere length analysis (HT-STELA) assay.

It has recently been shown that a proportion of IGHV-mutated CLL patients treated with FCR can achieve long-term remissions. The current findings demonstrate that these patients can be accurately identified by measuring telomere length, the investigators said, noting that they saw a similar pattern in patients in the UK CLL4 trial who were treated with fludarabine and cyclophosphamide

“Our results demonstrate that telomere length is the major determinant of response and survival following treatment with FCR,” they wrote. “IGHV-mutated patients with longer telomeres have a high probability of achieving a long-term remission following treatment with FCR (greater than 81% survival after 5 years). Equally, IGHV-mutated patients with short dysfunctional telomeres show a markedly inferior response to FCR and should be considered for alternative treatment options in the frontline setting.”

Patient material for this study was obtained from the UK CLL Trials Biobank, University of Liverpool, which is funded by Bloodwise. The authors reported having no other disclosures.

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Key clinical point: Telomere length reliably predicts response to fludarabine-cyclophosphamide-rituximab (FCR) treatment in patients with chronic lymphocytic leukemia.

Major finding: Short vs. long telomere length was associated with quicker time to progression and reduced overall survival (hazard ratios, 2.04 and 2.1, respectively).

Data source: An analysis of 278 samples from the ARCTIC and ADMIRE trials.

Disclosures: Patient material for this study was obtained from the UK CLL Trials Biobank, University of Liverpool, which is funded by Bloodwise. The authors reported having no other disclosures.

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Glytone Sunscreen Lotion Broad Spectrum SPF 40

Pierre Fabre Dermo-Cosmetique USA introduces Glytone Sunscreen Lotion Broad Spectrum SPF 40, a mineral-based formula for face and body with micronized zinc oxide, octinoxate, and octisalate. The lightweight formula is water resistant for up to 40 minutes and contains hyaluronic acid to nourish the skin and help boost natural moisture levels to visibly reduce the appearance of fine lines and wrinkles. For more information, visit www.glytone-usa.com.

proactivMD

The Proactiv Company launches the proactivMD Essentials System, a 3-step acne regimen that has been reformulated to include the topical retinoid adapalene. Step 1 is the Deep Cleansing Face Wash formulated to help clear dirt and debris from deep within the pores. Step 2 is the Balancing Toner, an alcohol-free formula that contains a light astringent to sweep away impurities leaving the skin feeling fresh and balanced. Step 3 consists of the Daily Oil Control Moisturizer (morning), which protects the skin and controls shine, and Adapalene Gel 0.1% (evening) to speed acne healing and prevent new acne from forming. For more information, visit www.proactiv.com.

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Glytone Sunscreen Lotion Broad Spectrum SPF 40

Pierre Fabre Dermo-Cosmetique USA introduces Glytone Sunscreen Lotion Broad Spectrum SPF 40, a mineral-based formula for face and body with micronized zinc oxide, octinoxate, and octisalate. The lightweight formula is water resistant for up to 40 minutes and contains hyaluronic acid to nourish the skin and help boost natural moisture levels to visibly reduce the appearance of fine lines and wrinkles. For more information, visit www.glytone-usa.com.

proactivMD

The Proactiv Company launches the proactivMD Essentials System, a 3-step acne regimen that has been reformulated to include the topical retinoid adapalene. Step 1 is the Deep Cleansing Face Wash formulated to help clear dirt and debris from deep within the pores. Step 2 is the Balancing Toner, an alcohol-free formula that contains a light astringent to sweep away impurities leaving the skin feeling fresh and balanced. Step 3 consists of the Daily Oil Control Moisturizer (morning), which protects the skin and controls shine, and Adapalene Gel 0.1% (evening) to speed acne healing and prevent new acne from forming. For more information, visit www.proactiv.com.

If you would like your product included in Product News, please email a press release to the Editorial Office at [email protected].

Glytone Sunscreen Lotion Broad Spectrum SPF 40

Pierre Fabre Dermo-Cosmetique USA introduces Glytone Sunscreen Lotion Broad Spectrum SPF 40, a mineral-based formula for face and body with micronized zinc oxide, octinoxate, and octisalate. The lightweight formula is water resistant for up to 40 minutes and contains hyaluronic acid to nourish the skin and help boost natural moisture levels to visibly reduce the appearance of fine lines and wrinkles. For more information, visit www.glytone-usa.com.

proactivMD

The Proactiv Company launches the proactivMD Essentials System, a 3-step acne regimen that has been reformulated to include the topical retinoid adapalene. Step 1 is the Deep Cleansing Face Wash formulated to help clear dirt and debris from deep within the pores. Step 2 is the Balancing Toner, an alcohol-free formula that contains a light astringent to sweep away impurities leaving the skin feeling fresh and balanced. Step 3 consists of the Daily Oil Control Moisturizer (morning), which protects the skin and controls shine, and Adapalene Gel 0.1% (evening) to speed acne healing and prevent new acne from forming. For more information, visit www.proactiv.com.

If you would like your product included in Product News, please email a press release to the Editorial Office at [email protected].

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Hair and Scalp Disorders in Adult and Pediatric Patients With Skin of Color

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Hair and Scalp Disorders in Adult and Pediatric Patients With Skin of Color
In Collaboration with the Skin of Color Society

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.1 Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.2 Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.3 Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.6

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).8 Another study by Hall et al9 of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al6 investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al10 examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

 

 

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.11 Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.12 Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.13 Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.14 The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan15 revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.16

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling17 demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

 

 

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard22 shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.22 Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.25 Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.28 Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).8 Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

References
  1. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  2. Hickman JG, Cardin C, Dawson TL, et al. Dandruff, part I: scalp disease prevalence in Caucasians, African Americans, and Chinese and the effects of shampoo frequency on scalp health. Poster presented at: 60th Annual Meeting of the American Academy of Dermatology; February 22-27, 2002; New Orleans, LA.
  3. Swee W, Klontz KC, Lambert LA. A nationwide outbreak of alopecia associated with the use of a hair-relaxing formulation. Arch Dermatol. 2000;136:1104-1108.
  4. Nicholson AG, Harland CC, Bull RH, et al. Chemically induced cosmetic alopecia. Br J Dermatol. 1993;128:537-541.
  5. Detwiler SP, Carson JL, Woosley JT, et al. Bubble hair. case caused by an overheating hair dryer and reproducibility in normal hair with heat. J Am Acad Dermatol. 1994;30:54-60.
  6. Khumalo NP, Dawber RP, Ferguson DJ. Apparent fragility of African hair is unrelated to the cystine-rich protein distribution: a cytochemical electron microscopic study. Exp Dermatol. 2005;14:311-314.
  7. Robbins C. Hair breakage during combing. I. pathways of breakage. J Cosmet Sci. 2006;57:233-243.
  8. Lewallen R, Francis S, Fisher B, et al. Hair care practices and structural evaluation of scalp and hair shaft parameter in African American and Caucasian women. J Cosmet Dermatol. 2015;14:216-223.
  9. Hall RR, Francis S, Whitt-Glover M, et al. Hair care practices as a barrier to physical activity in African American women. JAMA Dermatol. 2013;149:310-314.
  10. Franbourg A, Hallegot P, Baltenneck F, et al. Current research on ethnic hair. J Am Acad Dermatol. 2003;48(6 suppl):S115-S119.
  11. Ogunbiyi A. Acne keloidalis nuchae: prevalence, impact, and management challenges. Clin Cosmet Investig Dermatol. 2016;9:483-489.
  12. Gray J, McMichael AJ. Pseudofolliculitis barbae: understanding the condition and the role of facial grooming. Int J Cosmet Sci. 2016;38(suppl 1):24-27.
  13. Kundu RV, Patterson S. Dermatologic conditions in skin of color: part II. disorders occurring predominately in skin of color. Am Fam Physician. 2013;87:859-865.
  14. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  15. Gathers RC, Mahan MG. African American women, hair care and health barriers. J Clin Aesthet Dermatol. 2014;7:26-29.
  16. Dlova NC, Fabbrocini G, Lauro C, et al. Quality of life in South African black women with alopecia: a pilot study. Int J Dermatol. 2016;55:875-881.
  17. Wohltmann WE, Sperling L. Histopathologic diagnosis of multifactorial alopecia. J Cutan Pathol. 2016;43:483-491.
  18. McDonald KA, Shelley AJ, Colantonio S, et al. Hair pull test: evidence-based update and revision of guidelines. J Am Acad Dermatol. 2017;76:472-477.
  19. Miteva M, Tosti A. Dermatoscopic features of central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2014;71:443-444.
  20. Coley MK, Bhanusali DG, Silverberg JI, et al. Scalp hyperkeratosis and alopecia in children of color. J Drugs Dermatol. 2011;10:511-516.
  21. Silverberg NB. Scalp hyperkeratosis in children with skin of color: diagnostic and therapeutic considerations. Cutis. 2015;95:199-204, 207.
  22. Hubbard TW. The predictive value of symptoms in diagnosing childhood tinea capitis. Arch Pediatr Adolesc Med. 1999;153:1150-1153.
  23. Kakourou T, Uksal U; European Society for Pediatric Dermatology. Guidelines for the management of tinea capitis in children. Pediatr Dermatol. 2010;27:226-228.
  24. Sethi A, Antanya R. Systemic antifungal therapy for cutaneous infections in children. Pediatr Infect Dis J. 2006;25:643-644.
  25. Gupta AK. Drummond-Main C. Meta-analysis of randomized, controlled trials comparing particular doses of griseofulvin and terbinafine for the treatment of tinea capitis. Pediatr Dermatol. 2013;30:1-6.
  26. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol 2000;39:302-304.
  27. Sharma V, Silverberg NB, Howard R, et al. Do hair care practices affect the acquisition of tinea capitis? a case-control study. Arch Pediatr Adolesc Med. 2001;155:818-821.
  28. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol. 2000;39:302-304.
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Drs. Taylor and Ogunleye are from the Department of Dermatology, University of Pennsylvania, Philadelphia. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland.

Dr. Taylor is an advisory board member for Allergan; Aqua Pharmaceuticals; Beiersdorf; and NeoStrata Company, Inc. She also is an investigator for Allergan; Alphaeon; Croma-Pharma; and Evolus, Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan; is a clinical research investigator for Aclaris Therapeutics, Cutanea Life Sciences, Foamix, and Revance; and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Allergan.

Presented in part at the 2017 American Academy of Dermatology Annual Meeting; March 3-7, 2017; Orlando, Florida.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 1050 BRB II/III, Philadelphia, PA 19104 ([email protected]).

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Drs. Taylor and Ogunleye are from the Department of Dermatology, University of Pennsylvania, Philadelphia. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland.

Dr. Taylor is an advisory board member for Allergan; Aqua Pharmaceuticals; Beiersdorf; and NeoStrata Company, Inc. She also is an investigator for Allergan; Alphaeon; Croma-Pharma; and Evolus, Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan; is a clinical research investigator for Aclaris Therapeutics, Cutanea Life Sciences, Foamix, and Revance; and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Allergan.

Presented in part at the 2017 American Academy of Dermatology Annual Meeting; March 3-7, 2017; Orlando, Florida.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 1050 BRB II/III, Philadelphia, PA 19104 ([email protected]).

Author and Disclosure Information

Drs. Taylor and Ogunleye are from the Department of Dermatology, University of Pennsylvania, Philadelphia. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland.

Dr. Taylor is an advisory board member for Allergan; Aqua Pharmaceuticals; Beiersdorf; and NeoStrata Company, Inc. She also is an investigator for Allergan; Alphaeon; Croma-Pharma; and Evolus, Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan; is a clinical research investigator for Aclaris Therapeutics, Cutanea Life Sciences, Foamix, and Revance; and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Allergan.

Presented in part at the 2017 American Academy of Dermatology Annual Meeting; March 3-7, 2017; Orlando, Florida.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 1050 BRB II/III, Philadelphia, PA 19104 ([email protected]).

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In Collaboration with the Skin of Color Society
In Collaboration with the Skin of Color Society

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.1 Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.2 Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.3 Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.6

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).8 Another study by Hall et al9 of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al6 investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al10 examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

 

 

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.11 Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.12 Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.13 Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.14 The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan15 revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.16

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling17 demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

 

 

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard22 shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.22 Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.25 Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.28 Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).8 Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.1 Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.2 Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.3 Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.6

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).8 Another study by Hall et al9 of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al6 investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al10 examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

 

 

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.11 Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.12 Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.13 Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.14 The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan15 revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.16

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling17 demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

 

 

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard22 shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.22 Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.25 Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.28 Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).8 Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

References
  1. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  2. Hickman JG, Cardin C, Dawson TL, et al. Dandruff, part I: scalp disease prevalence in Caucasians, African Americans, and Chinese and the effects of shampoo frequency on scalp health. Poster presented at: 60th Annual Meeting of the American Academy of Dermatology; February 22-27, 2002; New Orleans, LA.
  3. Swee W, Klontz KC, Lambert LA. A nationwide outbreak of alopecia associated with the use of a hair-relaxing formulation. Arch Dermatol. 2000;136:1104-1108.
  4. Nicholson AG, Harland CC, Bull RH, et al. Chemically induced cosmetic alopecia. Br J Dermatol. 1993;128:537-541.
  5. Detwiler SP, Carson JL, Woosley JT, et al. Bubble hair. case caused by an overheating hair dryer and reproducibility in normal hair with heat. J Am Acad Dermatol. 1994;30:54-60.
  6. Khumalo NP, Dawber RP, Ferguson DJ. Apparent fragility of African hair is unrelated to the cystine-rich protein distribution: a cytochemical electron microscopic study. Exp Dermatol. 2005;14:311-314.
  7. Robbins C. Hair breakage during combing. I. pathways of breakage. J Cosmet Sci. 2006;57:233-243.
  8. Lewallen R, Francis S, Fisher B, et al. Hair care practices and structural evaluation of scalp and hair shaft parameter in African American and Caucasian women. J Cosmet Dermatol. 2015;14:216-223.
  9. Hall RR, Francis S, Whitt-Glover M, et al. Hair care practices as a barrier to physical activity in African American women. JAMA Dermatol. 2013;149:310-314.
  10. Franbourg A, Hallegot P, Baltenneck F, et al. Current research on ethnic hair. J Am Acad Dermatol. 2003;48(6 suppl):S115-S119.
  11. Ogunbiyi A. Acne keloidalis nuchae: prevalence, impact, and management challenges. Clin Cosmet Investig Dermatol. 2016;9:483-489.
  12. Gray J, McMichael AJ. Pseudofolliculitis barbae: understanding the condition and the role of facial grooming. Int J Cosmet Sci. 2016;38(suppl 1):24-27.
  13. Kundu RV, Patterson S. Dermatologic conditions in skin of color: part II. disorders occurring predominately in skin of color. Am Fam Physician. 2013;87:859-865.
  14. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  15. Gathers RC, Mahan MG. African American women, hair care and health barriers. J Clin Aesthet Dermatol. 2014;7:26-29.
  16. Dlova NC, Fabbrocini G, Lauro C, et al. Quality of life in South African black women with alopecia: a pilot study. Int J Dermatol. 2016;55:875-881.
  17. Wohltmann WE, Sperling L. Histopathologic diagnosis of multifactorial alopecia. J Cutan Pathol. 2016;43:483-491.
  18. McDonald KA, Shelley AJ, Colantonio S, et al. Hair pull test: evidence-based update and revision of guidelines. J Am Acad Dermatol. 2017;76:472-477.
  19. Miteva M, Tosti A. Dermatoscopic features of central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2014;71:443-444.
  20. Coley MK, Bhanusali DG, Silverberg JI, et al. Scalp hyperkeratosis and alopecia in children of color. J Drugs Dermatol. 2011;10:511-516.
  21. Silverberg NB. Scalp hyperkeratosis in children with skin of color: diagnostic and therapeutic considerations. Cutis. 2015;95:199-204, 207.
  22. Hubbard TW. The predictive value of symptoms in diagnosing childhood tinea capitis. Arch Pediatr Adolesc Med. 1999;153:1150-1153.
  23. Kakourou T, Uksal U; European Society for Pediatric Dermatology. Guidelines for the management of tinea capitis in children. Pediatr Dermatol. 2010;27:226-228.
  24. Sethi A, Antanya R. Systemic antifungal therapy for cutaneous infections in children. Pediatr Infect Dis J. 2006;25:643-644.
  25. Gupta AK. Drummond-Main C. Meta-analysis of randomized, controlled trials comparing particular doses of griseofulvin and terbinafine for the treatment of tinea capitis. Pediatr Dermatol. 2013;30:1-6.
  26. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol 2000;39:302-304.
  27. Sharma V, Silverberg NB, Howard R, et al. Do hair care practices affect the acquisition of tinea capitis? a case-control study. Arch Pediatr Adolesc Med. 2001;155:818-821.
  28. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol. 2000;39:302-304.
References
  1. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  2. Hickman JG, Cardin C, Dawson TL, et al. Dandruff, part I: scalp disease prevalence in Caucasians, African Americans, and Chinese and the effects of shampoo frequency on scalp health. Poster presented at: 60th Annual Meeting of the American Academy of Dermatology; February 22-27, 2002; New Orleans, LA.
  3. Swee W, Klontz KC, Lambert LA. A nationwide outbreak of alopecia associated with the use of a hair-relaxing formulation. Arch Dermatol. 2000;136:1104-1108.
  4. Nicholson AG, Harland CC, Bull RH, et al. Chemically induced cosmetic alopecia. Br J Dermatol. 1993;128:537-541.
  5. Detwiler SP, Carson JL, Woosley JT, et al. Bubble hair. case caused by an overheating hair dryer and reproducibility in normal hair with heat. J Am Acad Dermatol. 1994;30:54-60.
  6. Khumalo NP, Dawber RP, Ferguson DJ. Apparent fragility of African hair is unrelated to the cystine-rich protein distribution: a cytochemical electron microscopic study. Exp Dermatol. 2005;14:311-314.
  7. Robbins C. Hair breakage during combing. I. pathways of breakage. J Cosmet Sci. 2006;57:233-243.
  8. Lewallen R, Francis S, Fisher B, et al. Hair care practices and structural evaluation of scalp and hair shaft parameter in African American and Caucasian women. J Cosmet Dermatol. 2015;14:216-223.
  9. Hall RR, Francis S, Whitt-Glover M, et al. Hair care practices as a barrier to physical activity in African American women. JAMA Dermatol. 2013;149:310-314.
  10. Franbourg A, Hallegot P, Baltenneck F, et al. Current research on ethnic hair. J Am Acad Dermatol. 2003;48(6 suppl):S115-S119.
  11. Ogunbiyi A. Acne keloidalis nuchae: prevalence, impact, and management challenges. Clin Cosmet Investig Dermatol. 2016;9:483-489.
  12. Gray J, McMichael AJ. Pseudofolliculitis barbae: understanding the condition and the role of facial grooming. Int J Cosmet Sci. 2016;38(suppl 1):24-27.
  13. Kundu RV, Patterson S. Dermatologic conditions in skin of color: part II. disorders occurring predominately in skin of color. Am Fam Physician. 2013;87:859-865.
  14. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  15. Gathers RC, Mahan MG. African American women, hair care and health barriers. J Clin Aesthet Dermatol. 2014;7:26-29.
  16. Dlova NC, Fabbrocini G, Lauro C, et al. Quality of life in South African black women with alopecia: a pilot study. Int J Dermatol. 2016;55:875-881.
  17. Wohltmann WE, Sperling L. Histopathologic diagnosis of multifactorial alopecia. J Cutan Pathol. 2016;43:483-491.
  18. McDonald KA, Shelley AJ, Colantonio S, et al. Hair pull test: evidence-based update and revision of guidelines. J Am Acad Dermatol. 2017;76:472-477.
  19. Miteva M, Tosti A. Dermatoscopic features of central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2014;71:443-444.
  20. Coley MK, Bhanusali DG, Silverberg JI, et al. Scalp hyperkeratosis and alopecia in children of color. J Drugs Dermatol. 2011;10:511-516.
  21. Silverberg NB. Scalp hyperkeratosis in children with skin of color: diagnostic and therapeutic considerations. Cutis. 2015;95:199-204, 207.
  22. Hubbard TW. The predictive value of symptoms in diagnosing childhood tinea capitis. Arch Pediatr Adolesc Med. 1999;153:1150-1153.
  23. Kakourou T, Uksal U; European Society for Pediatric Dermatology. Guidelines for the management of tinea capitis in children. Pediatr Dermatol. 2010;27:226-228.
  24. Sethi A, Antanya R. Systemic antifungal therapy for cutaneous infections in children. Pediatr Infect Dis J. 2006;25:643-644.
  25. Gupta AK. Drummond-Main C. Meta-analysis of randomized, controlled trials comparing particular doses of griseofulvin and terbinafine for the treatment of tinea capitis. Pediatr Dermatol. 2013;30:1-6.
  26. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol 2000;39:302-304.
  27. Sharma V, Silverberg NB, Howard R, et al. Do hair care practices affect the acquisition of tinea capitis? a case-control study. Arch Pediatr Adolesc Med. 2001;155:818-821.
  28. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol. 2000;39:302-304.
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Cutis - 100(1)
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Cutis - 100(1)
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31-35
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Hair and Scalp Disorders in Adult and Pediatric Patients With Skin of Color
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Hair and Scalp Disorders in Adult and Pediatric Patients With Skin of Color
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Practice Points

  • Instruct patients with acquired trichorrhexis nodosa to discontinue use of heat, colorants, and chemical relaxers on their hair.
  • Create a contract with your seborrheic dermatitis patients to have them shampoo at least weekly or every 2 weeks.
  • For children with treated tinea capitis that has not completely resolved, increase or extend the griseofulvin dosage, encourage ingestion of fatty foods to enhance absorption, and divide dosage of griseofulvin from once to twice daily.
  • Selection of a biopsy site at the periphery of an alopecic area that includes hair and hair follicles and evaluation by a dermatopathologist familiar with the features of central centrifugal cicatricial, traction, and traumatic alopecias will ensure an accurate diagnosis of alopecia.
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