Cutis

Identifying Characteristics and Disease Transmission

Cheyletiella are nonburrowing mites characterized by hooklike anterior palps (Figure 1) that have a worldwide distribution. Human dermatitis is the result of contact with an affected animal and may present as papular or bullous lesions. Cheyletiella blakei affects cats, Cheyletiella parasitovorax is found on rabbits, and Cheyletiella yasguri is found on dogs. The mites live in the outer layer of the epidermis of the host animal and feed on surface debris and tissue fluids.¹ They complete an entire 35-day life cycle on a single animal host. The larval, nymph, and adult male mites die within 48 hours of separation from a host. The female mite and possibly the eggs can live up to 10 days off the host, which makes environmental decontamination a critical part of pest control.² In animals, the mite often produces a subtle dermatitis sometimes called walking dandruff (Figure 2).³ Affected animals also can be asymptomatic, and up to 50% of rabbits in commercial colonies may harbor Cheyletiella or other mites.⁴

The typical human patient with Cheyletiella-associated dermatitis is a female 40 years or younger who presents with grouped pruritic papules.⁵ Although papules usually are grouped on exposed areas, they also may be widespread.^6,7 Bullous eruptions caused by Cheyletiella mites may mimic those found in immunobullous diseases (Figure 3).⁸ Children may experience widespread dermatitis after taking a nap where a dog has slept.⁹ Pet owners, farmers, and veterinarians frequently present with zoonotic mite-induced dermatitis.¹⁰ Arthralgia and peripheral eosinophilia caused by Cheyletiella infestation also has been reported.¹¹

Management of Affected Pets

In a case of human infestation resulting from an affected pet, the implicated pet should be evaluated by a qualified veterinarian. Various diagnostic techniques for animals have been used, including adhesive tape preparations.¹² A rapid knockdown insecticidal spray marketed for use on animals has been used to facilitate collection of mites, but some pets may be susceptible to toxicity from insecticides. The scaly area should be carefully brushed with a toothbrush or fine-tooth comb, and all scales, crust, and hair collected should be placed in a resealable plastic storage bag. When alcohol is added to the bag, most contents will sink, but the mites tend to float. Vacuum cleaners fitted with in-line filters also have been used to collect mites. The filter samples can be treated with hot potassium hydroxide, then floated in a concentrated sugar solution to collect the ectoparasites.¹³ Often, a straightforward approach using a #10 blade to provide a skin scraping from the animal in question is effective.¹⁴

Various treatment modalities may be employed by the veterinarian, including dips or shampoos, as well as fipronil.^15,16 A single application of fipronil 10% has been shown to be highly effective in the elimination of mites after a single application in cats.¹⁷ Oral ivermectin and topical amitraz also have been used.^18,19 A veterinarian should treat the animals, as some are more susceptible to toxicity from topical or systemic agents.

Treatment in Humans

Cheyletiella infestations in humans usually are self-limited and resolve within a few weeks after treatment of the source animal. Symptomatic treatment with antipruritic medications and topical steroids may be of use while awaiting resolution. Identification and treatment of the vector is key to eliminating the infestation and preventing recurrence.

Identifying Characteristics and Disease Transmission

Cheyletiella are nonburrowing mites characterized by hooklike anterior palps (Figure 1) that have a worldwide distribution. Human dermatitis is the result of contact with an affected animal and may present as papular or bullous lesions. Cheyletiella blakei affects cats, Cheyletiella parasitovorax is found on rabbits, and Cheyletiella yasguri is found on dogs. The mites live in the outer layer of the epidermis of the host animal and feed on surface debris and tissue fluids.¹ They complete an entire 35-day life cycle on a single animal host. The larval, nymph, and adult male mites die within 48 hours of separation from a host. The female mite and possibly the eggs can live up to 10 days off the host, which makes environmental decontamination a critical part of pest control.² In animals, the mite often produces a subtle dermatitis sometimes called walking dandruff (Figure 2).³ Affected animals also can be asymptomatic, and up to 50% of rabbits in commercial colonies may harbor Cheyletiella or other mites.⁴

The typical human patient with Cheyletiella-associated dermatitis is a female 40 years or younger who presents with grouped pruritic papules.⁵ Although papules usually are grouped on exposed areas, they also may be widespread.^6,7 Bullous eruptions caused by Cheyletiella mites may mimic those found in immunobullous diseases (Figure 3).⁸ Children may experience widespread dermatitis after taking a nap where a dog has slept.⁹ Pet owners, farmers, and veterinarians frequently present with zoonotic mite-induced dermatitis.¹⁰ Arthralgia and peripheral eosinophilia caused by Cheyletiella infestation also has been reported.¹¹

Management of Affected Pets

In a case of human infestation resulting from an affected pet, the implicated pet should be evaluated by a qualified veterinarian. Various diagnostic techniques for animals have been used, including adhesive tape preparations.¹² A rapid knockdown insecticidal spray marketed for use on animals has been used to facilitate collection of mites, but some pets may be susceptible to toxicity from insecticides. The scaly area should be carefully brushed with a toothbrush or fine-tooth comb, and all scales, crust, and hair collected should be placed in a resealable plastic storage bag. When alcohol is added to the bag, most contents will sink, but the mites tend to float. Vacuum cleaners fitted with in-line filters also have been used to collect mites. The filter samples can be treated with hot potassium hydroxide, then floated in a concentrated sugar solution to collect the ectoparasites.¹³ Often, a straightforward approach using a #10 blade to provide a skin scraping from the animal in question is effective.¹⁴

Various treatment modalities may be employed by the veterinarian, including dips or shampoos, as well as fipronil.^15,16 A single application of fipronil 10% has been shown to be highly effective in the elimination of mites after a single application in cats.¹⁷ Oral ivermectin and topical amitraz also have been used.^18,19 A veterinarian should treat the animals, as some are more susceptible to toxicity from topical or systemic agents.

Treatment in Humans

Cheyletiella infestations in humans usually are self-limited and resolve within a few weeks after treatment of the source animal. Symptomatic treatment with antipruritic medications and topical steroids may be of use while awaiting resolution. Identification and treatment of the vector is key to eliminating the infestation and preventing recurrence.

Identifying Characteristics and Disease Transmission

Cheyletiella are nonburrowing mites characterized by hooklike anterior palps (Figure 1) that have a worldwide distribution. Human dermatitis is the result of contact with an affected animal and may present as papular or bullous lesions. Cheyletiella blakei affects cats, Cheyletiella parasitovorax is found on rabbits, and Cheyletiella yasguri is found on dogs. The mites live in the outer layer of the epidermis of the host animal and feed on surface debris and tissue fluids.¹ They complete an entire 35-day life cycle on a single animal host. The larval, nymph, and adult male mites die within 48 hours of separation from a host. The female mite and possibly the eggs can live up to 10 days off the host, which makes environmental decontamination a critical part of pest control.² In animals, the mite often produces a subtle dermatitis sometimes called walking dandruff (Figure 2).³ Affected animals also can be asymptomatic, and up to 50% of rabbits in commercial colonies may harbor Cheyletiella or other mites.⁴

The typical human patient with Cheyletiella-associated dermatitis is a female 40 years or younger who presents with grouped pruritic papules.⁵ Although papules usually are grouped on exposed areas, they also may be widespread.^6,7 Bullous eruptions caused by Cheyletiella mites may mimic those found in immunobullous diseases (Figure 3).⁸ Children may experience widespread dermatitis after taking a nap where a dog has slept.⁹ Pet owners, farmers, and veterinarians frequently present with zoonotic mite-induced dermatitis.¹⁰ Arthralgia and peripheral eosinophilia caused by Cheyletiella infestation also has been reported.¹¹

Management of Affected Pets

In a case of human infestation resulting from an affected pet, the implicated pet should be evaluated by a qualified veterinarian. Various diagnostic techniques for animals have been used, including adhesive tape preparations.¹² A rapid knockdown insecticidal spray marketed for use on animals has been used to facilitate collection of mites, but some pets may be susceptible to toxicity from insecticides. The scaly area should be carefully brushed with a toothbrush or fine-tooth comb, and all scales, crust, and hair collected should be placed in a resealable plastic storage bag. When alcohol is added to the bag, most contents will sink, but the mites tend to float. Vacuum cleaners fitted with in-line filters also have been used to collect mites. The filter samples can be treated with hot potassium hydroxide, then floated in a concentrated sugar solution to collect the ectoparasites.¹³ Often, a straightforward approach using a #10 blade to provide a skin scraping from the animal in question is effective.¹⁴

Various treatment modalities may be employed by the veterinarian, including dips or shampoos, as well as fipronil.^15,16 A single application of fipronil 10% has been shown to be highly effective in the elimination of mites after a single application in cats.¹⁷ Oral ivermectin and topical amitraz also have been used.^18,19 A veterinarian should treat the animals, as some are more susceptible to toxicity from topical or systemic agents.

Treatment in Humans

Cheyletiella infestations in humans usually are self-limited and resolve within a few weeks after treatment of the source animal. Symptomatic treatment with antipruritic medications and topical steroids may be of use while awaiting resolution. Identification and treatment of the vector is key to eliminating the infestation and preventing recurrence.

Psoriasis impacts the ability to perform activities, causes embarrassment and social discrimination, and leads to a severe emotional impact in both adult and pediatric patients, according to a public meeting hosted by the US Food and Drug Administration (FDA) to hear patient perspectives. A common source of distress in daily life among psoriasis patients was the lack of understanding of the disease in the general population with wrongful concerns that psoriasis is infectious or contagious.

Approximately 70 psoriasis patients or patient representatives attended the meeting in person and others attended through a live webcast. The impact of psoriasis on daily life was underscored throughout the meeting. Daily activities impacted by psoriasis included physical limitations such as an inability to participate in sports among children due to cracking of the hands and feet, or the impracticability of managing a household or going to work among adults. The inconsistency and unpredictability of the condition led patients to be viewed as unreliable. One participant explained, “If you join a team you can play this week but you can’t play next week.”

Patients and their loved ones often experienced embarrassment and social discrimination. A caregiver stated, “Specifically to a child, psoriasis means something different. It means hiding. It means feeling ashamed and it means being ashamed, and it means thinking twice before being yourself. No child should have to think twice before learning to express themselves.” Social isolation and bullying also were prominent in children, mostly because an uniformed parent or classmate did not understand the disease process.

These effects on the daily life of psoriasis patients often led to a severe emotional impact and social isolation. At a young age, psoriasis can have a devastating social and emotional toll. One caregiver shared that his/her child admitted to having thoughts of suicide. The FDA asked how many participants missed days from work and school because of the emotional toll of their psoriasis symptoms and the majority of participants raised their hands. Several participants also indicated that they had sought treatment for depression and anxiety. Many adult patients also noted that they reconsidered having children because of the destructive effects psoriasis has had on multiple generations of family members.

Dermatologists may use these patient insights to monitor the psychological impact of psoriasis on patients and refer them to a psychiatrist or psychologist when needed.

The psoriasis public meeting in March 2016 was the FDA’s 18th patient-focused drug development meeting. The FDA sought this information to have a greater understanding of the burden of psoriasis on patients and the treatments currently used to treat psoriasis and its symptoms. This information will help guide the FDA as they consider future drug approvals.

Psoriasis impacts the ability to perform activities, causes embarrassment and social discrimination, and leads to a severe emotional impact in both adult and pediatric patients, according to a public meeting hosted by the US Food and Drug Administration (FDA) to hear patient perspectives. A common source of distress in daily life among psoriasis patients was the lack of understanding of the disease in the general population with wrongful concerns that psoriasis is infectious or contagious.

Approximately 70 psoriasis patients or patient representatives attended the meeting in person and others attended through a live webcast. The impact of psoriasis on daily life was underscored throughout the meeting. Daily activities impacted by psoriasis included physical limitations such as an inability to participate in sports among children due to cracking of the hands and feet, or the impracticability of managing a household or going to work among adults. The inconsistency and unpredictability of the condition led patients to be viewed as unreliable. One participant explained, “If you join a team you can play this week but you can’t play next week.”

Patients and their loved ones often experienced embarrassment and social discrimination. A caregiver stated, “Specifically to a child, psoriasis means something different. It means hiding. It means feeling ashamed and it means being ashamed, and it means thinking twice before being yourself. No child should have to think twice before learning to express themselves.” Social isolation and bullying also were prominent in children, mostly because an uniformed parent or classmate did not understand the disease process.

These effects on the daily life of psoriasis patients often led to a severe emotional impact and social isolation. At a young age, psoriasis can have a devastating social and emotional toll. One caregiver shared that his/her child admitted to having thoughts of suicide. The FDA asked how many participants missed days from work and school because of the emotional toll of their psoriasis symptoms and the majority of participants raised their hands. Several participants also indicated that they had sought treatment for depression and anxiety. Many adult patients also noted that they reconsidered having children because of the destructive effects psoriasis has had on multiple generations of family members.

Dermatologists may use these patient insights to monitor the psychological impact of psoriasis on patients and refer them to a psychiatrist or psychologist when needed.

The psoriasis public meeting in March 2016 was the FDA’s 18th patient-focused drug development meeting. The FDA sought this information to have a greater understanding of the burden of psoriasis on patients and the treatments currently used to treat psoriasis and its symptoms. This information will help guide the FDA as they consider future drug approvals.

Psoriasis impacts the ability to perform activities, causes embarrassment and social discrimination, and leads to a severe emotional impact in both adult and pediatric patients, according to a public meeting hosted by the US Food and Drug Administration (FDA) to hear patient perspectives. A common source of distress in daily life among psoriasis patients was the lack of understanding of the disease in the general population with wrongful concerns that psoriasis is infectious or contagious.

Approximately 70 psoriasis patients or patient representatives attended the meeting in person and others attended through a live webcast. The impact of psoriasis on daily life was underscored throughout the meeting. Daily activities impacted by psoriasis included physical limitations such as an inability to participate in sports among children due to cracking of the hands and feet, or the impracticability of managing a household or going to work among adults. The inconsistency and unpredictability of the condition led patients to be viewed as unreliable. One participant explained, “If you join a team you can play this week but you can’t play next week.”

Patients and their loved ones often experienced embarrassment and social discrimination. A caregiver stated, “Specifically to a child, psoriasis means something different. It means hiding. It means feeling ashamed and it means being ashamed, and it means thinking twice before being yourself. No child should have to think twice before learning to express themselves.” Social isolation and bullying also were prominent in children, mostly because an uniformed parent or classmate did not understand the disease process.

These effects on the daily life of psoriasis patients often led to a severe emotional impact and social isolation. At a young age, psoriasis can have a devastating social and emotional toll. One caregiver shared that his/her child admitted to having thoughts of suicide. The FDA asked how many participants missed days from work and school because of the emotional toll of their psoriasis symptoms and the majority of participants raised their hands. Several participants also indicated that they had sought treatment for depression and anxiety. Many adult patients also noted that they reconsidered having children because of the destructive effects psoriasis has had on multiple generations of family members.

Dermatologists may use these patient insights to monitor the psychological impact of psoriasis on patients and refer them to a psychiatrist or psychologist when needed.

The psoriasis public meeting in March 2016 was the FDA’s 18th patient-focused drug development meeting. The FDA sought this information to have a greater understanding of the burden of psoriasis on patients and the treatments currently used to treat psoriasis and its symptoms. This information will help guide the FDA as they consider future drug approvals.

Blepharoplasty, or surgical manipulation of the upper and/or lower eyelids, is a commonly performed cosmetic procedure to improve the appearance and function of the eyelids by repositioning and/or removing excess skin and soft tissue from the eyelids, most often through external incisions that minimize scarring and maximize the aesthetic outcomes of the surgery. Therefore, the placement of the incisions is an important determinant of the surgical outcome, and the preoperative marking of the eyelids to indicate where the incisions should be placed is a crucial part of preparation for the surgery.

Preoperative marking has unique challenges due to the dynamicity of the eyelids and the delicate nature of the surgery. The mark must be narrow to minimize the risk of placing the incision higher or lower than intended. The mark also must dry quickly because the patient may blink and create multiple impressions of the marking on skinfolds in contact with the wet ink. Fast drying of the ink used to create the marks improves the efficiency and clarity of the presurgical planning.

We present data on the performance of the various blepharoplasty markers regarding drying time and ink spread width based on an evaluation of 13 surgical markers.

Methods

Eleven unique fine tip (FT) markers and 2 standard tip (ST) markers were obtained based on their accessibility at the researchers’ home institution and availability for direct purchase in small quantities from the distributors (Figure 1). Four markers were double tipped with one FT end and one ST end; for these markers, only the FT end was studied. The experiments were conducted on the bilateral upper eyelids and on hairless patches of skin of a single patient in a minor procedure room with surgical lighting and minimal draft of air. The sole experimenter (J.M.K.) conducting the study was not blinded.

The drying time of each marker was measured by marking 1-in lines on a patch of hairless skin that was first cleaned with an alcohol pad, then dried. Drying time for each marking was measured in increments of 5 seconds; at each time point, the markings were wiped with a single-ply, light-duty tissue under the weight of 10 US quarters to ensure that the same weight/pressure was applied when wiping the skin. Smudges observed with the naked eye on either the wipe or the patients’ skin were interpreted as nondry status of the marking. The first time point at which a marking was found to have no visible smudges either on the skin or the wipe was recorded as the drying time of the respective marker.

Ink spread was measured on clean eyelid skin by drawing curved lines along the natural crease as would be done for actual blepharoplasty planning. Each line was allowed to dry for 2 minutes. The greatest perpendicular spread width along the line observed with the naked eye was measured using a digital Vernier caliper with 0.01-mm graduations. Three measurements were obtained per marker and the values averaged to arrive at the final spread width.

Results

Drying time among the 13 total markers (11 FT and 2 ST) ranged from 5 to 70 seconds, with a mean of 20.8 seconds and median of 5 seconds (Table). The drying time for the DERMarker E-Z Removable Ink Mini Skin Marker (Delasco, LLC) with an ST was 5 seconds, while the drying time for the other ST marker, WriteSite Plus Surgical Skin Marker (Aspen Surgical, Inc), was 70 seconds. The FT markers spanned the entire range of drying times. The ink spread width among the markers ranged from 0.53 to 2.27 mm with a median of 0.9 mm and mean of 1.13 mm (Table). The 2 ST markers were found to make some of the widest marks measured, including the WriteSite Plus Surgical Skin Marker, a nonsterile ST marker that created the widest ink marks. The second widest mark was made by an FT marker (Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker [Viscot Medical, LLC]).

To prioritize short drying time coupled with minimal ink spread width, the values associated with each marker were averaged to arrive at the overall score for each marker. The smaller the overall score, the higher we ranked the marker. The Devon Surgical Skin Marker, Dual Tip (Medtronic) ranked the highest among the 13 markers with a final score of 2.78. Runner-up markers included the Sterile Devon Surgical Skin marker, Fine Tip (Medtronic)(final score, 2.86); the Sterile Dual Tip Skin/Utility Marker (Medline Industries, Inc)(final score, 2.86); and the Skin Marker, Fine Tip (Cardinal Health)(final score, 2.89). The 2 lowest-ranking markers were the WriteSite Plus Surgical Skin Marker, an ST marker (final score, 36.13), followed by the Sterile BlephMarker (Viscot Medical, LLC)(final score, 35.27).

Figure 2 shows the drying time and ink spread width for all 13 markers.

Comment

Blepharoplasty surgeons generally agree that meticulous presurgical planning with marking of the eyelids is critical for successful surgical outcomes.^1,2 Fine tip markers have been recommended for this purpose due to the relative precision of the marks, but the prerequisite of these markers is that the marks must have minimal ink spread through skinfolds to allow for precision as well as short drying time to avoid unintentional duplication of the ink on overlapping skin, especially with the likely chance of reflexive blinking by the patient. The associated assumption is that FT markers automatically leave precise marks with minimal drying time. This study systemically compared these 2 qualities for 13 markers, and the results are notable for the unexpected wide range of performance. Although most of the FT markers had ink spread width of less than 1 mm, the Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker was an outlier among FT markers, with ink spread greater than 2 mm, making it too broad and imprecise for practical use. This result indicates that not every FT marker actually makes fine marks. The 2 ST markers in the study—DERMarker E-Z Removable Ink Mini Skin Marker and WriteSite Plus Surgical Skin Marker—left broad marks as anticipated.

The drying time of the markers also ranged from 5 to 70 seconds among both FT and ST markers. Indeed, most of the FT markers were dry at or before 5 seconds of marking, but 2 FT markers—Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker and Sterile BlephMarker—dried at 65 and 70 seconds, respectively. Such a long drying time would be considered impractical for use in blepharoplasty marking and also unexpected of FT markers, which usually are marketed for their precision and efficiency. Notable in the discussion of drying time is that one of the 2 ST markers in the study, the DERMarker E-Z Removable Ink Mini Skin Marker, had the shortest possible drying time of 5 seconds, while the other ST marker, WriteSite Plus Surgical Skin Marker, dried at 70 seconds. This observation coupled with the unexpected results of broad marks and long drying time for some of the FT markers indicates that a surgeon cannot simply assume that a FT marker would provide marks with precision and fast drying time, or that an ST marker would be the opposite.

Future directions for study include the addition of other markers and the extent of resistance to antiseptic routines that can fade the markings.

Conclusion

Among the 13 markers studied, FT markers typically had the shortest drying time and least ink spread on skin. Markers with these qualities rather than those with longer drying times or greater ink spread may be preferred by blepharoplasty surgeons. The dual- and fine-tipped Devon Surgical Skin Markers and the Sterile Dual Tip Skin/Utility Marker had the most favorable scores among the markers included in the study.

Acknowledgement

The authors would like to thank Laura B. Hall, MD (New Haven, Connecticut), for her participation as the volunteer in this study.

Blepharoplasty, or surgical manipulation of the upper and/or lower eyelids, is a commonly performed cosmetic procedure to improve the appearance and function of the eyelids by repositioning and/or removing excess skin and soft tissue from the eyelids, most often through external incisions that minimize scarring and maximize the aesthetic outcomes of the surgery. Therefore, the placement of the incisions is an important determinant of the surgical outcome, and the preoperative marking of the eyelids to indicate where the incisions should be placed is a crucial part of preparation for the surgery.

Preoperative marking has unique challenges due to the dynamicity of the eyelids and the delicate nature of the surgery. The mark must be narrow to minimize the risk of placing the incision higher or lower than intended. The mark also must dry quickly because the patient may blink and create multiple impressions of the marking on skinfolds in contact with the wet ink. Fast drying of the ink used to create the marks improves the efficiency and clarity of the presurgical planning.

We present data on the performance of the various blepharoplasty markers regarding drying time and ink spread width based on an evaluation of 13 surgical markers.

Methods

Eleven unique fine tip (FT) markers and 2 standard tip (ST) markers were obtained based on their accessibility at the researchers’ home institution and availability for direct purchase in small quantities from the distributors (Figure 1). Four markers were double tipped with one FT end and one ST end; for these markers, only the FT end was studied. The experiments were conducted on the bilateral upper eyelids and on hairless patches of skin of a single patient in a minor procedure room with surgical lighting and minimal draft of air. The sole experimenter (J.M.K.) conducting the study was not blinded.

The drying time of each marker was measured by marking 1-in lines on a patch of hairless skin that was first cleaned with an alcohol pad, then dried. Drying time for each marking was measured in increments of 5 seconds; at each time point, the markings were wiped with a single-ply, light-duty tissue under the weight of 10 US quarters to ensure that the same weight/pressure was applied when wiping the skin. Smudges observed with the naked eye on either the wipe or the patients’ skin were interpreted as nondry status of the marking. The first time point at which a marking was found to have no visible smudges either on the skin or the wipe was recorded as the drying time of the respective marker.

Ink spread was measured on clean eyelid skin by drawing curved lines along the natural crease as would be done for actual blepharoplasty planning. Each line was allowed to dry for 2 minutes. The greatest perpendicular spread width along the line observed with the naked eye was measured using a digital Vernier caliper with 0.01-mm graduations. Three measurements were obtained per marker and the values averaged to arrive at the final spread width.

Results

Drying time among the 13 total markers (11 FT and 2 ST) ranged from 5 to 70 seconds, with a mean of 20.8 seconds and median of 5 seconds (Table). The drying time for the DERMarker E-Z Removable Ink Mini Skin Marker (Delasco, LLC) with an ST was 5 seconds, while the drying time for the other ST marker, WriteSite Plus Surgical Skin Marker (Aspen Surgical, Inc), was 70 seconds. The FT markers spanned the entire range of drying times. The ink spread width among the markers ranged from 0.53 to 2.27 mm with a median of 0.9 mm and mean of 1.13 mm (Table). The 2 ST markers were found to make some of the widest marks measured, including the WriteSite Plus Surgical Skin Marker, a nonsterile ST marker that created the widest ink marks. The second widest mark was made by an FT marker (Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker [Viscot Medical, LLC]).

To prioritize short drying time coupled with minimal ink spread width, the values associated with each marker were averaged to arrive at the overall score for each marker. The smaller the overall score, the higher we ranked the marker. The Devon Surgical Skin Marker, Dual Tip (Medtronic) ranked the highest among the 13 markers with a final score of 2.78. Runner-up markers included the Sterile Devon Surgical Skin marker, Fine Tip (Medtronic)(final score, 2.86); the Sterile Dual Tip Skin/Utility Marker (Medline Industries, Inc)(final score, 2.86); and the Skin Marker, Fine Tip (Cardinal Health)(final score, 2.89). The 2 lowest-ranking markers were the WriteSite Plus Surgical Skin Marker, an ST marker (final score, 36.13), followed by the Sterile BlephMarker (Viscot Medical, LLC)(final score, 35.27).

Figure 2 shows the drying time and ink spread width for all 13 markers.

Comment

Blepharoplasty surgeons generally agree that meticulous presurgical planning with marking of the eyelids is critical for successful surgical outcomes.^1,2 Fine tip markers have been recommended for this purpose due to the relative precision of the marks, but the prerequisite of these markers is that the marks must have minimal ink spread through skinfolds to allow for precision as well as short drying time to avoid unintentional duplication of the ink on overlapping skin, especially with the likely chance of reflexive blinking by the patient. The associated assumption is that FT markers automatically leave precise marks with minimal drying time. This study systemically compared these 2 qualities for 13 markers, and the results are notable for the unexpected wide range of performance. Although most of the FT markers had ink spread width of less than 1 mm, the Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker was an outlier among FT markers, with ink spread greater than 2 mm, making it too broad and imprecise for practical use. This result indicates that not every FT marker actually makes fine marks. The 2 ST markers in the study—DERMarker E-Z Removable Ink Mini Skin Marker and WriteSite Plus Surgical Skin Marker—left broad marks as anticipated.

The drying time of the markers also ranged from 5 to 70 seconds among both FT and ST markers. Indeed, most of the FT markers were dry at or before 5 seconds of marking, but 2 FT markers—Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker and Sterile BlephMarker—dried at 65 and 70 seconds, respectively. Such a long drying time would be considered impractical for use in blepharoplasty marking and also unexpected of FT markers, which usually are marketed for their precision and efficiency. Notable in the discussion of drying time is that one of the 2 ST markers in the study, the DERMarker E-Z Removable Ink Mini Skin Marker, had the shortest possible drying time of 5 seconds, while the other ST marker, WriteSite Plus Surgical Skin Marker, dried at 70 seconds. This observation coupled with the unexpected results of broad marks and long drying time for some of the FT markers indicates that a surgeon cannot simply assume that a FT marker would provide marks with precision and fast drying time, or that an ST marker would be the opposite.

Future directions for study include the addition of other markers and the extent of resistance to antiseptic routines that can fade the markings.

Conclusion

Among the 13 markers studied, FT markers typically had the shortest drying time and least ink spread on skin. Markers with these qualities rather than those with longer drying times or greater ink spread may be preferred by blepharoplasty surgeons. The dual- and fine-tipped Devon Surgical Skin Markers and the Sterile Dual Tip Skin/Utility Marker had the most favorable scores among the markers included in the study.

Acknowledgement

The authors would like to thank Laura B. Hall, MD (New Haven, Connecticut), for her participation as the volunteer in this study.

Blepharoplasty, or surgical manipulation of the upper and/or lower eyelids, is a commonly performed cosmetic procedure to improve the appearance and function of the eyelids by repositioning and/or removing excess skin and soft tissue from the eyelids, most often through external incisions that minimize scarring and maximize the aesthetic outcomes of the surgery. Therefore, the placement of the incisions is an important determinant of the surgical outcome, and the preoperative marking of the eyelids to indicate where the incisions should be placed is a crucial part of preparation for the surgery.

Preoperative marking has unique challenges due to the dynamicity of the eyelids and the delicate nature of the surgery. The mark must be narrow to minimize the risk of placing the incision higher or lower than intended. The mark also must dry quickly because the patient may blink and create multiple impressions of the marking on skinfolds in contact with the wet ink. Fast drying of the ink used to create the marks improves the efficiency and clarity of the presurgical planning.

We present data on the performance of the various blepharoplasty markers regarding drying time and ink spread width based on an evaluation of 13 surgical markers.

Methods

Eleven unique fine tip (FT) markers and 2 standard tip (ST) markers were obtained based on their accessibility at the researchers’ home institution and availability for direct purchase in small quantities from the distributors (Figure 1). Four markers were double tipped with one FT end and one ST end; for these markers, only the FT end was studied. The experiments were conducted on the bilateral upper eyelids and on hairless patches of skin of a single patient in a minor procedure room with surgical lighting and minimal draft of air. The sole experimenter (J.M.K.) conducting the study was not blinded.

The drying time of each marker was measured by marking 1-in lines on a patch of hairless skin that was first cleaned with an alcohol pad, then dried. Drying time for each marking was measured in increments of 5 seconds; at each time point, the markings were wiped with a single-ply, light-duty tissue under the weight of 10 US quarters to ensure that the same weight/pressure was applied when wiping the skin. Smudges observed with the naked eye on either the wipe or the patients’ skin were interpreted as nondry status of the marking. The first time point at which a marking was found to have no visible smudges either on the skin or the wipe was recorded as the drying time of the respective marker.

Ink spread was measured on clean eyelid skin by drawing curved lines along the natural crease as would be done for actual blepharoplasty planning. Each line was allowed to dry for 2 minutes. The greatest perpendicular spread width along the line observed with the naked eye was measured using a digital Vernier caliper with 0.01-mm graduations. Three measurements were obtained per marker and the values averaged to arrive at the final spread width.

Results

Drying time among the 13 total markers (11 FT and 2 ST) ranged from 5 to 70 seconds, with a mean of 20.8 seconds and median of 5 seconds (Table). The drying time for the DERMarker E-Z Removable Ink Mini Skin Marker (Delasco, LLC) with an ST was 5 seconds, while the drying time for the other ST marker, WriteSite Plus Surgical Skin Marker (Aspen Surgical, Inc), was 70 seconds. The FT markers spanned the entire range of drying times. The ink spread width among the markers ranged from 0.53 to 2.27 mm with a median of 0.9 mm and mean of 1.13 mm (Table). The 2 ST markers were found to make some of the widest marks measured, including the WriteSite Plus Surgical Skin Marker, a nonsterile ST marker that created the widest ink marks. The second widest mark was made by an FT marker (Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker [Viscot Medical, LLC]).

To prioritize short drying time coupled with minimal ink spread width, the values associated with each marker were averaged to arrive at the overall score for each marker. The smaller the overall score, the higher we ranked the marker. The Devon Surgical Skin Marker, Dual Tip (Medtronic) ranked the highest among the 13 markers with a final score of 2.78. Runner-up markers included the Sterile Devon Surgical Skin marker, Fine Tip (Medtronic)(final score, 2.86); the Sterile Dual Tip Skin/Utility Marker (Medline Industries, Inc)(final score, 2.86); and the Skin Marker, Fine Tip (Cardinal Health)(final score, 2.89). The 2 lowest-ranking markers were the WriteSite Plus Surgical Skin Marker, an ST marker (final score, 36.13), followed by the Sterile BlephMarker (Viscot Medical, LLC)(final score, 35.27).

Figure 2 shows the drying time and ink spread width for all 13 markers.

Comment

Blepharoplasty surgeons generally agree that meticulous presurgical planning with marking of the eyelids is critical for successful surgical outcomes.^1,2 Fine tip markers have been recommended for this purpose due to the relative precision of the marks, but the prerequisite of these markers is that the marks must have minimal ink spread through skinfolds to allow for precision as well as short drying time to avoid unintentional duplication of the ink on overlapping skin, especially with the likely chance of reflexive blinking by the patient. The associated assumption is that FT markers automatically leave precise marks with minimal drying time. This study systemically compared these 2 qualities for 13 markers, and the results are notable for the unexpected wide range of performance. Although most of the FT markers had ink spread width of less than 1 mm, the Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker was an outlier among FT markers, with ink spread greater than 2 mm, making it too broad and imprecise for practical use. This result indicates that not every FT marker actually makes fine marks. The 2 ST markers in the study—DERMarker E-Z Removable Ink Mini Skin Marker and WriteSite Plus Surgical Skin Marker—left broad marks as anticipated.

The drying time of the markers also ranged from 5 to 70 seconds among both FT and ST markers. Indeed, most of the FT markers were dry at or before 5 seconds of marking, but 2 FT markers—Sterile Mini Ultrafine Tip XL Prep Resistant Ink Marker and Sterile BlephMarker—dried at 65 and 70 seconds, respectively. Such a long drying time would be considered impractical for use in blepharoplasty marking and also unexpected of FT markers, which usually are marketed for their precision and efficiency. Notable in the discussion of drying time is that one of the 2 ST markers in the study, the DERMarker E-Z Removable Ink Mini Skin Marker, had the shortest possible drying time of 5 seconds, while the other ST marker, WriteSite Plus Surgical Skin Marker, dried at 70 seconds. This observation coupled with the unexpected results of broad marks and long drying time for some of the FT markers indicates that a surgeon cannot simply assume that a FT marker would provide marks with precision and fast drying time, or that an ST marker would be the opposite.

Future directions for study include the addition of other markers and the extent of resistance to antiseptic routines that can fade the markings.

Conclusion

Among the 13 markers studied, FT markers typically had the shortest drying time and least ink spread on skin. Markers with these qualities rather than those with longer drying times or greater ink spread may be preferred by blepharoplasty surgeons. The dual- and fine-tipped Devon Surgical Skin Markers and the Sterile Dual Tip Skin/Utility Marker had the most favorable scores among the markers included in the study.

Acknowledgement

The authors would like to thank Laura B. Hall, MD (New Haven, Connecticut), for her participation as the volunteer in this study.

To the Editor:

Both alopecia areata (AA) and psoriasis vulgaris are chronic relapsing autoimmune diseases, with AA causing nonscarring hair loss in approximately 0.1% to 0.2%¹ of the population with a lifetime risk of 1.7%,² and psoriasis more broadly impacting 1.5% to 2% of the population.³ The helper T cell (T_H1) cytokine milieu is pathogenic in both conditions.^4-6 IFN-γ knockout mice, unlike their wild-type counterparts, do not exhibit AA.⁷ Psoriasis is notably improved by IL-10 injections, which dampen the T_H1 response.⁸ Distinct from AA, T_H17 and T_H22 cells have been implicated as key players in psoriasis pathogenesis, along with the associated IL-17 and IL-22 cytokines.^9-12

Few cases of patients with concurrent AA and psoriasis have been described. Interestingly, these cases document normal hair regrowth in the areas of psoriasis.^13-16 These cases may offer unique insight into the immune factors driving each disease. We describe a case of a man with both alopecia universalis (AU) and psoriasis who developed hair regrowth in some of the psoriatic plaques.

A 34-year-old man with concurrent AU and psoriasis who had not used any systemic or topical medication for either condition in the last year presented to our clinic seeking treatment. The patient had a history of alopecia totalis as a toddler that completely resolved by 4 years of age with the use of squaric acid dibutylester (SADBE). At 31 years of age, the alopecia recurred and was localized to the scalp. It was partially responsive to intralesional triamcinolone acetonide. The patient’s alopecia worsened over the 2 years following recurrence, ultimately progressing to AU. Two months after the alopecia recurrence, he developed the first psoriatic plaques. As the plaque psoriasis progressed, systemic therapy was initiated, first methotrexate and then etanercept. Shortly after developing AU, he lost his health insurance and discontinued all therapy. The patient’s psoriasis began to recur approximately 3 months after stopping etanercept. He was not using any other psoriasis medications. At that time, he noted terminal hair regrowth within some of the psoriatic plaques. No terminal hairs grew outside of the psoriatic plaques, and all regions with growth had previously been without hair for an extended period of time. The patient presented to our clinic approximately 1 year later. He had no other medical conditions and no relevant family history.

On initial physical examination, he had nonscarring hair loss involving nearly 100% of the body with psoriatic plaques on approximately 30% of the body surface area. Regions of terminal hair growth were confined to some but not all of the psoriatic plaques (Figure). Interestingly, the terminal hairs were primarily localized to the thickest central regions of the plaques. The patient’s psoriasis was treated with a combination of topical clobetasol and calcipotriene. In addition, he was started on tacrolimus ointment to the face and eyebrows for the AA. Maintenance of terminal hair within a region of topically treated psoriasis on the forearm persisted at the 2-month follow-up despite complete clearance of the corresponding psoriatic plaque. A small psoriatic plaque on the scalp cleared early with topical therapy without noticeable hair regrowth. The patient subsequently was started on contact immunotherapy with SADBE and intralesional triamcinolone acetonide for the scalp alopecia without satisfactory response. He decided to discontinue further attempts at treating the alopecia and requested to be restarted on etanercept therapy for recalcitrant psoriatic plaques. His psoriasis responded well to this therapy and he continues to be followed in our psoriasis clinic. One year after clearance of the treated psoriatic plaques, the corresponding terminal hairs persist.

Contact immunotherapy, most commonly with diphenylcyclopropenone or SADBE, is reported to have a 50% to 60% success rate in extensive AA, with a broad range of 9% to 87%¹⁷; however, randomized controlled trials testing the efficacy of contact immunotherapy are lacking. Although the mechanism of action of these topical sensitizers is not clearly delineated, it has been postulated that by inducing a new type of inflammatory response in the region, the immunologic milieu is changed, allowing the hair to grow. Some proposed mechanisms include promoting perifollicular lymphocyte apoptosis, preventing new recruitment of autoreactive lymphocytes, and allowing for the correction of aberrant major histocompatibility complex expression on the hair matrix epithelium to regain follicle immune privilege.^18-20

Iatrogenic immunotherapy may work analogously to the natural immune system deviation demonstrated in our patient. Psoriasis and AA are believed to form competing immune cells and cytokine milieus, thus explaining how an individual with AA could regain normal hair growth in areas of psoriasis.^15,16 The Renbök phenomenon, or reverse Köbner phenomenon, coined by Happle et al¹³ can be used to describe both the iatrogenic and natural cases of dermatologic disease improvement in response to secondary insults.¹⁴

A complex cascade of immune cells and cytokines coordinate AA pathogenesis. In the acute stage of AA, an inflammatory infiltrate of CD4⁺ T cells, CD8⁺ T cells, and antigen-presenting cells target anagen phase follicles, with a higher CD4⁺:CD8⁺ ratio in clinically active disease.^21-23 Subcutaneous injections of either CD4⁺ or CD8⁺ lymphocyte subsets from mice with AA into normal-haired mice induces disease. However, CD8⁺ T cell injections rapidly produce apparent hair loss, whereas CD4⁺ T cells cause hair loss after several weeks, suggesting that CD8⁺ T cells directly modulate AA hair loss and CD4⁺ T cells act as an aide.²⁴ The growth, differentiation, and survival of CD8⁺ T cells are stimulated by IL-2 and IFN-γ. Alopecia areata biopsies demonstrate a prevalence of T_H1 cytokines, and patients with localized AA, alopecia totalis, and AU have notably higher serum IFN-γ levels compared to controls.²⁵ In murine models, IL-1α and IL-1β increase during the catagen phase of the hair cycle and peak during the telogen phase.²⁶ Excessive IL-1β expression is detected in the early stages of human disease, and certain IL-1β polymorphisms are associated with severe forms of AA.²⁶ The role of tumor necrosis factor (TNF) α in AA is not well understood. In vitro studies show it inhibits hair growth, suggesting the cytokine may play a role in AA.²⁷ However, anti–TNF-α therapy is not effective in AA, and case reports propose these therapies rarely induce AA.^28-31

The T_H1 response is likewise critical to psoriatic plaque development. IFN-γ and TNF-α are overexpressed in psoriatic plaques.³² IFN-γ has an antiproliferative and differentiation-inducing effect on normal keratinocytes, but psoriatic epithelial cells in vitro respond differently to the cytokine with a notably diminished growth inhibition.^33,34 One explanation for the role of IFN-γ is that it stimulates dendritic cells to produce IL-1 and IL-23.³⁵ IL-23 activates T_H17 cells³⁶; T_H1 and T_H17 conditions produce IL-22 whose serum level correlates with disease severity.^37-39 IL-22 induces keratinocyte proliferation and migration and inhibits keratinocyte differentiation, helping account for hallmarks of the disease.⁴⁰ Patients with psoriasis have increased levels of T_H1, T_H17, and T_H22 cells, as well as their associated cytokines, in the skin and blood compared to controls.^{4,11,32,39,41}

Alopecia areata and psoriasis are regulated by complex and still not entirely understood immune interactions. The fact that many of the same therapies are used to treat both diseases emphasizes both their overlapping characteristics and the lack of targeted therapy. It is unclear if and how the topical or systemic therapies used in our patient to treat one disease affected the natural history of the other condition. It is important to highlight, however, that the patient had not been treated for months when he developed the psoriatic plaques with hair regrowth. Other case reports also document hair regrowth in untreated plaques,^13,16 making it unlikely to be a side effect of the medication regimen. For both psoriasis and AA, the immune cell composition and cytokine levels in the skin or serum vary throughout a patient’s disease course depending on severity of disease or response to treatment.^6,39,42,43 Therefore, we hypothesize that the 2 conditions interact in a similarly distinct manner based on each disease’s stage and intensity in the patient. Both our patient’s course thus far and the various presentations described by other groups support this hypothesis. Our patient had a small region of psoriasis on the scalp that cleared without any terminal hair growth. He also had larger plaques on the forearms that developed hair growth most predominantly within the thicker regions of the plaques. His unique presentation highlights the fluidity of the immune factors driving psoriasis vulgaris and AA.

To the Editor:

Both alopecia areata (AA) and psoriasis vulgaris are chronic relapsing autoimmune diseases, with AA causing nonscarring hair loss in approximately 0.1% to 0.2%¹ of the population with a lifetime risk of 1.7%,² and psoriasis more broadly impacting 1.5% to 2% of the population.³ The helper T cell (T_H1) cytokine milieu is pathogenic in both conditions.^4-6 IFN-γ knockout mice, unlike their wild-type counterparts, do not exhibit AA.⁷ Psoriasis is notably improved by IL-10 injections, which dampen the T_H1 response.⁸ Distinct from AA, T_H17 and T_H22 cells have been implicated as key players in psoriasis pathogenesis, along with the associated IL-17 and IL-22 cytokines.^9-12

Few cases of patients with concurrent AA and psoriasis have been described. Interestingly, these cases document normal hair regrowth in the areas of psoriasis.^13-16 These cases may offer unique insight into the immune factors driving each disease. We describe a case of a man with both alopecia universalis (AU) and psoriasis who developed hair regrowth in some of the psoriatic plaques.

A 34-year-old man with concurrent AU and psoriasis who had not used any systemic or topical medication for either condition in the last year presented to our clinic seeking treatment. The patient had a history of alopecia totalis as a toddler that completely resolved by 4 years of age with the use of squaric acid dibutylester (SADBE). At 31 years of age, the alopecia recurred and was localized to the scalp. It was partially responsive to intralesional triamcinolone acetonide. The patient’s alopecia worsened over the 2 years following recurrence, ultimately progressing to AU. Two months after the alopecia recurrence, he developed the first psoriatic plaques. As the plaque psoriasis progressed, systemic therapy was initiated, first methotrexate and then etanercept. Shortly after developing AU, he lost his health insurance and discontinued all therapy. The patient’s psoriasis began to recur approximately 3 months after stopping etanercept. He was not using any other psoriasis medications. At that time, he noted terminal hair regrowth within some of the psoriatic plaques. No terminal hairs grew outside of the psoriatic plaques, and all regions with growth had previously been without hair for an extended period of time. The patient presented to our clinic approximately 1 year later. He had no other medical conditions and no relevant family history.

On initial physical examination, he had nonscarring hair loss involving nearly 100% of the body with psoriatic plaques on approximately 30% of the body surface area. Regions of terminal hair growth were confined to some but not all of the psoriatic plaques (Figure). Interestingly, the terminal hairs were primarily localized to the thickest central regions of the plaques. The patient’s psoriasis was treated with a combination of topical clobetasol and calcipotriene. In addition, he was started on tacrolimus ointment to the face and eyebrows for the AA. Maintenance of terminal hair within a region of topically treated psoriasis on the forearm persisted at the 2-month follow-up despite complete clearance of the corresponding psoriatic plaque. A small psoriatic plaque on the scalp cleared early with topical therapy without noticeable hair regrowth. The patient subsequently was started on contact immunotherapy with SADBE and intralesional triamcinolone acetonide for the scalp alopecia without satisfactory response. He decided to discontinue further attempts at treating the alopecia and requested to be restarted on etanercept therapy for recalcitrant psoriatic plaques. His psoriasis responded well to this therapy and he continues to be followed in our psoriasis clinic. One year after clearance of the treated psoriatic plaques, the corresponding terminal hairs persist.

Contact immunotherapy, most commonly with diphenylcyclopropenone or SADBE, is reported to have a 50% to 60% success rate in extensive AA, with a broad range of 9% to 87%¹⁷; however, randomized controlled trials testing the efficacy of contact immunotherapy are lacking. Although the mechanism of action of these topical sensitizers is not clearly delineated, it has been postulated that by inducing a new type of inflammatory response in the region, the immunologic milieu is changed, allowing the hair to grow. Some proposed mechanisms include promoting perifollicular lymphocyte apoptosis, preventing new recruitment of autoreactive lymphocytes, and allowing for the correction of aberrant major histocompatibility complex expression on the hair matrix epithelium to regain follicle immune privilege.^18-20

Iatrogenic immunotherapy may work analogously to the natural immune system deviation demonstrated in our patient. Psoriasis and AA are believed to form competing immune cells and cytokine milieus, thus explaining how an individual with AA could regain normal hair growth in areas of psoriasis.^15,16 The Renbök phenomenon, or reverse Köbner phenomenon, coined by Happle et al¹³ can be used to describe both the iatrogenic and natural cases of dermatologic disease improvement in response to secondary insults.¹⁴

A complex cascade of immune cells and cytokines coordinate AA pathogenesis. In the acute stage of AA, an inflammatory infiltrate of CD4⁺ T cells, CD8⁺ T cells, and antigen-presenting cells target anagen phase follicles, with a higher CD4⁺:CD8⁺ ratio in clinically active disease.^21-23 Subcutaneous injections of either CD4⁺ or CD8⁺ lymphocyte subsets from mice with AA into normal-haired mice induces disease. However, CD8⁺ T cell injections rapidly produce apparent hair loss, whereas CD4⁺ T cells cause hair loss after several weeks, suggesting that CD8⁺ T cells directly modulate AA hair loss and CD4⁺ T cells act as an aide.²⁴ The growth, differentiation, and survival of CD8⁺ T cells are stimulated by IL-2 and IFN-γ. Alopecia areata biopsies demonstrate a prevalence of T_H1 cytokines, and patients with localized AA, alopecia totalis, and AU have notably higher serum IFN-γ levels compared to controls.²⁵ In murine models, IL-1α and IL-1β increase during the catagen phase of the hair cycle and peak during the telogen phase.²⁶ Excessive IL-1β expression is detected in the early stages of human disease, and certain IL-1β polymorphisms are associated with severe forms of AA.²⁶ The role of tumor necrosis factor (TNF) α in AA is not well understood. In vitro studies show it inhibits hair growth, suggesting the cytokine may play a role in AA.²⁷ However, anti–TNF-α therapy is not effective in AA, and case reports propose these therapies rarely induce AA.^28-31

The T_H1 response is likewise critical to psoriatic plaque development. IFN-γ and TNF-α are overexpressed in psoriatic plaques.³² IFN-γ has an antiproliferative and differentiation-inducing effect on normal keratinocytes, but psoriatic epithelial cells in vitro respond differently to the cytokine with a notably diminished growth inhibition.^33,34 One explanation for the role of IFN-γ is that it stimulates dendritic cells to produce IL-1 and IL-23.³⁵ IL-23 activates T_H17 cells³⁶; T_H1 and T_H17 conditions produce IL-22 whose serum level correlates with disease severity.^37-39 IL-22 induces keratinocyte proliferation and migration and inhibits keratinocyte differentiation, helping account for hallmarks of the disease.⁴⁰ Patients with psoriasis have increased levels of T_H1, T_H17, and T_H22 cells, as well as their associated cytokines, in the skin and blood compared to controls.^{4,11,32,39,41}

Alopecia areata and psoriasis are regulated by complex and still not entirely understood immune interactions. The fact that many of the same therapies are used to treat both diseases emphasizes both their overlapping characteristics and the lack of targeted therapy. It is unclear if and how the topical or systemic therapies used in our patient to treat one disease affected the natural history of the other condition. It is important to highlight, however, that the patient had not been treated for months when he developed the psoriatic plaques with hair regrowth. Other case reports also document hair regrowth in untreated plaques,^13,16 making it unlikely to be a side effect of the medication regimen. For both psoriasis and AA, the immune cell composition and cytokine levels in the skin or serum vary throughout a patient’s disease course depending on severity of disease or response to treatment.^6,39,42,43 Therefore, we hypothesize that the 2 conditions interact in a similarly distinct manner based on each disease’s stage and intensity in the patient. Both our patient’s course thus far and the various presentations described by other groups support this hypothesis. Our patient had a small region of psoriasis on the scalp that cleared without any terminal hair growth. He also had larger plaques on the forearms that developed hair growth most predominantly within the thicker regions of the plaques. His unique presentation highlights the fluidity of the immune factors driving psoriasis vulgaris and AA.

To the Editor:

Both alopecia areata (AA) and psoriasis vulgaris are chronic relapsing autoimmune diseases, with AA causing nonscarring hair loss in approximately 0.1% to 0.2%¹ of the population with a lifetime risk of 1.7%,² and psoriasis more broadly impacting 1.5% to 2% of the population.³ The helper T cell (T_H1) cytokine milieu is pathogenic in both conditions.^4-6 IFN-γ knockout mice, unlike their wild-type counterparts, do not exhibit AA.⁷ Psoriasis is notably improved by IL-10 injections, which dampen the T_H1 response.⁸ Distinct from AA, T_H17 and T_H22 cells have been implicated as key players in psoriasis pathogenesis, along with the associated IL-17 and IL-22 cytokines.^9-12

Few cases of patients with concurrent AA and psoriasis have been described. Interestingly, these cases document normal hair regrowth in the areas of psoriasis.^13-16 These cases may offer unique insight into the immune factors driving each disease. We describe a case of a man with both alopecia universalis (AU) and psoriasis who developed hair regrowth in some of the psoriatic plaques.

A 34-year-old man with concurrent AU and psoriasis who had not used any systemic or topical medication for either condition in the last year presented to our clinic seeking treatment. The patient had a history of alopecia totalis as a toddler that completely resolved by 4 years of age with the use of squaric acid dibutylester (SADBE). At 31 years of age, the alopecia recurred and was localized to the scalp. It was partially responsive to intralesional triamcinolone acetonide. The patient’s alopecia worsened over the 2 years following recurrence, ultimately progressing to AU. Two months after the alopecia recurrence, he developed the first psoriatic plaques. As the plaque psoriasis progressed, systemic therapy was initiated, first methotrexate and then etanercept. Shortly after developing AU, he lost his health insurance and discontinued all therapy. The patient’s psoriasis began to recur approximately 3 months after stopping etanercept. He was not using any other psoriasis medications. At that time, he noted terminal hair regrowth within some of the psoriatic plaques. No terminal hairs grew outside of the psoriatic plaques, and all regions with growth had previously been without hair for an extended period of time. The patient presented to our clinic approximately 1 year later. He had no other medical conditions and no relevant family history.

On initial physical examination, he had nonscarring hair loss involving nearly 100% of the body with psoriatic plaques on approximately 30% of the body surface area. Regions of terminal hair growth were confined to some but not all of the psoriatic plaques (Figure). Interestingly, the terminal hairs were primarily localized to the thickest central regions of the plaques. The patient’s psoriasis was treated with a combination of topical clobetasol and calcipotriene. In addition, he was started on tacrolimus ointment to the face and eyebrows for the AA. Maintenance of terminal hair within a region of topically treated psoriasis on the forearm persisted at the 2-month follow-up despite complete clearance of the corresponding psoriatic plaque. A small psoriatic plaque on the scalp cleared early with topical therapy without noticeable hair regrowth. The patient subsequently was started on contact immunotherapy with SADBE and intralesional triamcinolone acetonide for the scalp alopecia without satisfactory response. He decided to discontinue further attempts at treating the alopecia and requested to be restarted on etanercept therapy for recalcitrant psoriatic plaques. His psoriasis responded well to this therapy and he continues to be followed in our psoriasis clinic. One year after clearance of the treated psoriatic plaques, the corresponding terminal hairs persist.

Contact immunotherapy, most commonly with diphenylcyclopropenone or SADBE, is reported to have a 50% to 60% success rate in extensive AA, with a broad range of 9% to 87%¹⁷; however, randomized controlled trials testing the efficacy of contact immunotherapy are lacking. Although the mechanism of action of these topical sensitizers is not clearly delineated, it has been postulated that by inducing a new type of inflammatory response in the region, the immunologic milieu is changed, allowing the hair to grow. Some proposed mechanisms include promoting perifollicular lymphocyte apoptosis, preventing new recruitment of autoreactive lymphocytes, and allowing for the correction of aberrant major histocompatibility complex expression on the hair matrix epithelium to regain follicle immune privilege.^18-20

Iatrogenic immunotherapy may work analogously to the natural immune system deviation demonstrated in our patient. Psoriasis and AA are believed to form competing immune cells and cytokine milieus, thus explaining how an individual with AA could regain normal hair growth in areas of psoriasis.^15,16 The Renbök phenomenon, or reverse Köbner phenomenon, coined by Happle et al¹³ can be used to describe both the iatrogenic and natural cases of dermatologic disease improvement in response to secondary insults.¹⁴

A complex cascade of immune cells and cytokines coordinate AA pathogenesis. In the acute stage of AA, an inflammatory infiltrate of CD4⁺ T cells, CD8⁺ T cells, and antigen-presenting cells target anagen phase follicles, with a higher CD4⁺:CD8⁺ ratio in clinically active disease.^21-23 Subcutaneous injections of either CD4⁺ or CD8⁺ lymphocyte subsets from mice with AA into normal-haired mice induces disease. However, CD8⁺ T cell injections rapidly produce apparent hair loss, whereas CD4⁺ T cells cause hair loss after several weeks, suggesting that CD8⁺ T cells directly modulate AA hair loss and CD4⁺ T cells act as an aide.²⁴ The growth, differentiation, and survival of CD8⁺ T cells are stimulated by IL-2 and IFN-γ. Alopecia areata biopsies demonstrate a prevalence of T_H1 cytokines, and patients with localized AA, alopecia totalis, and AU have notably higher serum IFN-γ levels compared to controls.²⁵ In murine models, IL-1α and IL-1β increase during the catagen phase of the hair cycle and peak during the telogen phase.²⁶ Excessive IL-1β expression is detected in the early stages of human disease, and certain IL-1β polymorphisms are associated with severe forms of AA.²⁶ The role of tumor necrosis factor (TNF) α in AA is not well understood. In vitro studies show it inhibits hair growth, suggesting the cytokine may play a role in AA.²⁷ However, anti–TNF-α therapy is not effective in AA, and case reports propose these therapies rarely induce AA.^28-31

The T_H1 response is likewise critical to psoriatic plaque development. IFN-γ and TNF-α are overexpressed in psoriatic plaques.³² IFN-γ has an antiproliferative and differentiation-inducing effect on normal keratinocytes, but psoriatic epithelial cells in vitro respond differently to the cytokine with a notably diminished growth inhibition.^33,34 One explanation for the role of IFN-γ is that it stimulates dendritic cells to produce IL-1 and IL-23.³⁵ IL-23 activates T_H17 cells³⁶; T_H1 and T_H17 conditions produce IL-22 whose serum level correlates with disease severity.^37-39 IL-22 induces keratinocyte proliferation and migration and inhibits keratinocyte differentiation, helping account for hallmarks of the disease.⁴⁰ Patients with psoriasis have increased levels of T_H1, T_H17, and T_H22 cells, as well as their associated cytokines, in the skin and blood compared to controls.^{4,11,32,39,41}

Alopecia areata and psoriasis are regulated by complex and still not entirely understood immune interactions. The fact that many of the same therapies are used to treat both diseases emphasizes both their overlapping characteristics and the lack of targeted therapy. It is unclear if and how the topical or systemic therapies used in our patient to treat one disease affected the natural history of the other condition. It is important to highlight, however, that the patient had not been treated for months when he developed the psoriatic plaques with hair regrowth. Other case reports also document hair regrowth in untreated plaques,^13,16 making it unlikely to be a side effect of the medication regimen. For both psoriasis and AA, the immune cell composition and cytokine levels in the skin or serum vary throughout a patient’s disease course depending on severity of disease or response to treatment.^6,39,42,43 Therefore, we hypothesize that the 2 conditions interact in a similarly distinct manner based on each disease’s stage and intensity in the patient. Both our patient’s course thus far and the various presentations described by other groups support this hypothesis. Our patient had a small region of psoriasis on the scalp that cleared without any terminal hair growth. He also had larger plaques on the forearms that developed hair growth most predominantly within the thicker regions of the plaques. His unique presentation highlights the fluidity of the immune factors driving psoriasis vulgaris and AA.

To the Editor:

Atopic dermatitis (AD) is a common skin condition with an increasing prevalence, affecting up to 20% of children and 3% of adults.^1,2 More than 80% of patients with AD have elevated IgE levels.^3,4 IgE modulates the inflammatory response in AD in several ways including “a biphasic immediate/late phase reaction, allergen presentation by IgE-bearing Langerhans cells, allergen-induced activation of IgE-bearing macrophages, and IgE autoreactivity to human proteins.”⁵ Historically, most therapies have focused on mitigating the allergic symptoms caused by degranulated effector cells, such as antihistamines. However, a new class of biologically engineered medications (eg, anti-IgE [omalizumab]) aim to prevent the initiation of the allergic response.⁶ Variable success has been reported using omalizumab in the treatment of AD, though the majority of studies have shown improvement, especially when used in combination with conventional therapies.^4,5,7-22 Omalizumab dosage is determined by body weight and pretreatment serum total IgE levels and is administered via subcutaneous injections every 2 to 4 weeks.^6,7,23-26 However, the dosing tables are based on asthma therapy, in which serum IgE levels may be much lower than chronic AD,^7,24 and the appropriate dosage in AD patients with markedly elevated IgE is unclear. We report an interesting case of a 57-year-old man with erythroderma from long-standing severe chronic AD that was unresponsive to conventional therapy as well as an associated serum IgE level of 17,183 IU/mL who dramatically improved when omalizumab was added to his treatment regimen.

A 57-year-old man presented with essentially 100% body surface area involvement of AD with erythroderma and pruritus. Severe AD developed at infancy and cleared at 5 years of age; childhood onset of asthma was responsive to theophylline and oral inhalers. He developed recurrent AD and asthma at 38 years of age, which was progressive and developed into severe recalcitrant erythroderma by 50 years of age. His AD was unresponsive to multiple therapies, including topical steroids, antibiotics, tacrolimus, bleach baths, antihistamines, methotrexate (15 mg weekly for 1 year, then 12.5 mg weekly for 6 months), UVB phototherapy, and psoralen plus UVA photochemotherapy. He had minimal improvement with cyclosporine (200 mg daily for 4 weeks) and mycophenolate mofetil (3 g daily), and required systemic steroids for relief. The skin was violaceous and lichenified (Figure, A). Laboratory studies were normal, except for a serum IgE level of 17,183 IU/mL (reference range, <150 IU/mL) and peripheral blood eosinophilia up to 29.8% (reference range, 1%–5%) of the differential. Skin biopsies showed AD progressing to lichen simplex chronicus. Omalizumab was added to the therapeutic regimen at a dose of 375 mg every 2 weeks, with noticeable improvement after 3 months. The patient had approximately 80% to 90% clearing with resolution of erythroderma and pruritus, and only limited residual lichenification (Figure, B). The mycophenolate was tapered slowly, and the patient experienced a mild flare at 1 g daily. He is presently on 1 g of mycophenolate daily and omalizumab (375 mg every 2 weeks) and remains remarkably improved. His IgE level decreased to 11,983 IU/mL.

Omalizumab is a monoclonal IgG1 antibody that specifically binds to the FcεRI domain of serum IgE. It blocks binding to high-affinity receptors on effector cells, primarily mast cells, basophils, macrophages, and dendritic cells; it also decreases free IgE serum levels and downregulates the IgE receptor.^{4,6-10,23-25,27,28} Currently, omalizumab is US Food and Drug Administration approved for moderate to severe persistent asthma in patients 6 years or older with a positive aeroallergen skin test and IgE levels up to 700 IU/mL.^{6,7,23-25,27,28}

However, scattered case reports and small case series have described variable success in the treatment of severe AD that is unresponsive to conventional therapy in patients with markedly elevated serum IgE levels.^4,5,7-22 The majority of patients (approximately 80% of published cases yielded by a PubMed search of articles indexed for MEDLINE using the search terms omalizumab and atopic dermatitis) showed improvement when measured by clinical severity scores and quality of life improvement, especially when used in conjunction with conventional therapy. Possible reasons for reported treatment failure include insufficient dosage, lack of established treatment guidelines for markedly elevated serum IgE levels, severity of disease, or variable response with failure to lower IgE level below a required threshold.^7,9,23,24,27

Krathen and Hsu⁹ reported treatment failure with omalizumab for AD in 3 patients with serum IgE levels ranging from 5440 and 24,400 IU/mL, and one review indicated omalizumab may work best in patients with only moderately elevated serum IgE levels.²¹ However, Toledo et al¹⁸ reported efficacy of low-dose omalizumab for pretreatment IgE levels up to 30,000 IU/mL in 6 of 11 reported cases. The pretreatment serum IgE level is not predictive of response, and lowering the serum IgE level without normalization can be efficacious,^12,23 as in the current case. Serum IgE levels are not used for monitoring therapeutic response or calculating future dosing, given potential increases in serum IgE levels during and after therapy (for up to 12 months) secondary to the formation of anti-IgE:IgE complexes.^6,28 Omalizumab appears most effective when used in combination with conventional therapies. Hopefully ongoing studies will further elucidate the role of omalizumab in recalcitrant AD with elevated serum IgE levels.

To the Editor:

Atopic dermatitis (AD) is a common skin condition with an increasing prevalence, affecting up to 20% of children and 3% of adults.^1,2 More than 80% of patients with AD have elevated IgE levels.^3,4 IgE modulates the inflammatory response in AD in several ways including “a biphasic immediate/late phase reaction, allergen presentation by IgE-bearing Langerhans cells, allergen-induced activation of IgE-bearing macrophages, and IgE autoreactivity to human proteins.”⁵ Historically, most therapies have focused on mitigating the allergic symptoms caused by degranulated effector cells, such as antihistamines. However, a new class of biologically engineered medications (eg, anti-IgE [omalizumab]) aim to prevent the initiation of the allergic response.⁶ Variable success has been reported using omalizumab in the treatment of AD, though the majority of studies have shown improvement, especially when used in combination with conventional therapies.^4,5,7-22 Omalizumab dosage is determined by body weight and pretreatment serum total IgE levels and is administered via subcutaneous injections every 2 to 4 weeks.^6,7,23-26 However, the dosing tables are based on asthma therapy, in which serum IgE levels may be much lower than chronic AD,^7,24 and the appropriate dosage in AD patients with markedly elevated IgE is unclear. We report an interesting case of a 57-year-old man with erythroderma from long-standing severe chronic AD that was unresponsive to conventional therapy as well as an associated serum IgE level of 17,183 IU/mL who dramatically improved when omalizumab was added to his treatment regimen.

A 57-year-old man presented with essentially 100% body surface area involvement of AD with erythroderma and pruritus. Severe AD developed at infancy and cleared at 5 years of age; childhood onset of asthma was responsive to theophylline and oral inhalers. He developed recurrent AD and asthma at 38 years of age, which was progressive and developed into severe recalcitrant erythroderma by 50 years of age. His AD was unresponsive to multiple therapies, including topical steroids, antibiotics, tacrolimus, bleach baths, antihistamines, methotrexate (15 mg weekly for 1 year, then 12.5 mg weekly for 6 months), UVB phototherapy, and psoralen plus UVA photochemotherapy. He had minimal improvement with cyclosporine (200 mg daily for 4 weeks) and mycophenolate mofetil (3 g daily), and required systemic steroids for relief. The skin was violaceous and lichenified (Figure, A). Laboratory studies were normal, except for a serum IgE level of 17,183 IU/mL (reference range, <150 IU/mL) and peripheral blood eosinophilia up to 29.8% (reference range, 1%–5%) of the differential. Skin biopsies showed AD progressing to lichen simplex chronicus. Omalizumab was added to the therapeutic regimen at a dose of 375 mg every 2 weeks, with noticeable improvement after 3 months. The patient had approximately 80% to 90% clearing with resolution of erythroderma and pruritus, and only limited residual lichenification (Figure, B). The mycophenolate was tapered slowly, and the patient experienced a mild flare at 1 g daily. He is presently on 1 g of mycophenolate daily and omalizumab (375 mg every 2 weeks) and remains remarkably improved. His IgE level decreased to 11,983 IU/mL.

Omalizumab is a monoclonal IgG1 antibody that specifically binds to the FcεRI domain of serum IgE. It blocks binding to high-affinity receptors on effector cells, primarily mast cells, basophils, macrophages, and dendritic cells; it also decreases free IgE serum levels and downregulates the IgE receptor.^{4,6-10,23-25,27,28} Currently, omalizumab is US Food and Drug Administration approved for moderate to severe persistent asthma in patients 6 years or older with a positive aeroallergen skin test and IgE levels up to 700 IU/mL.^{6,7,23-25,27,28}

However, scattered case reports and small case series have described variable success in the treatment of severe AD that is unresponsive to conventional therapy in patients with markedly elevated serum IgE levels.^4,5,7-22 The majority of patients (approximately 80% of published cases yielded by a PubMed search of articles indexed for MEDLINE using the search terms omalizumab and atopic dermatitis) showed improvement when measured by clinical severity scores and quality of life improvement, especially when used in conjunction with conventional therapy. Possible reasons for reported treatment failure include insufficient dosage, lack of established treatment guidelines for markedly elevated serum IgE levels, severity of disease, or variable response with failure to lower IgE level below a required threshold.^7,9,23,24,27

Krathen and Hsu⁹ reported treatment failure with omalizumab for AD in 3 patients with serum IgE levels ranging from 5440 and 24,400 IU/mL, and one review indicated omalizumab may work best in patients with only moderately elevated serum IgE levels.²¹ However, Toledo et al¹⁸ reported efficacy of low-dose omalizumab for pretreatment IgE levels up to 30,000 IU/mL in 6 of 11 reported cases. The pretreatment serum IgE level is not predictive of response, and lowering the serum IgE level without normalization can be efficacious,^12,23 as in the current case. Serum IgE levels are not used for monitoring therapeutic response or calculating future dosing, given potential increases in serum IgE levels during and after therapy (for up to 12 months) secondary to the formation of anti-IgE:IgE complexes.^6,28 Omalizumab appears most effective when used in combination with conventional therapies. Hopefully ongoing studies will further elucidate the role of omalizumab in recalcitrant AD with elevated serum IgE levels.

To the Editor:

Atopic dermatitis (AD) is a common skin condition with an increasing prevalence, affecting up to 20% of children and 3% of adults.^1,2 More than 80% of patients with AD have elevated IgE levels.^3,4 IgE modulates the inflammatory response in AD in several ways including “a biphasic immediate/late phase reaction, allergen presentation by IgE-bearing Langerhans cells, allergen-induced activation of IgE-bearing macrophages, and IgE autoreactivity to human proteins.”⁵ Historically, most therapies have focused on mitigating the allergic symptoms caused by degranulated effector cells, such as antihistamines. However, a new class of biologically engineered medications (eg, anti-IgE [omalizumab]) aim to prevent the initiation of the allergic response.⁶ Variable success has been reported using omalizumab in the treatment of AD, though the majority of studies have shown improvement, especially when used in combination with conventional therapies.^4,5,7-22 Omalizumab dosage is determined by body weight and pretreatment serum total IgE levels and is administered via subcutaneous injections every 2 to 4 weeks.^6,7,23-26 However, the dosing tables are based on asthma therapy, in which serum IgE levels may be much lower than chronic AD,^7,24 and the appropriate dosage in AD patients with markedly elevated IgE is unclear. We report an interesting case of a 57-year-old man with erythroderma from long-standing severe chronic AD that was unresponsive to conventional therapy as well as an associated serum IgE level of 17,183 IU/mL who dramatically improved when omalizumab was added to his treatment regimen.

A 57-year-old man presented with essentially 100% body surface area involvement of AD with erythroderma and pruritus. Severe AD developed at infancy and cleared at 5 years of age; childhood onset of asthma was responsive to theophylline and oral inhalers. He developed recurrent AD and asthma at 38 years of age, which was progressive and developed into severe recalcitrant erythroderma by 50 years of age. His AD was unresponsive to multiple therapies, including topical steroids, antibiotics, tacrolimus, bleach baths, antihistamines, methotrexate (15 mg weekly for 1 year, then 12.5 mg weekly for 6 months), UVB phototherapy, and psoralen plus UVA photochemotherapy. He had minimal improvement with cyclosporine (200 mg daily for 4 weeks) and mycophenolate mofetil (3 g daily), and required systemic steroids for relief. The skin was violaceous and lichenified (Figure, A). Laboratory studies were normal, except for a serum IgE level of 17,183 IU/mL (reference range, <150 IU/mL) and peripheral blood eosinophilia up to 29.8% (reference range, 1%–5%) of the differential. Skin biopsies showed AD progressing to lichen simplex chronicus. Omalizumab was added to the therapeutic regimen at a dose of 375 mg every 2 weeks, with noticeable improvement after 3 months. The patient had approximately 80% to 90% clearing with resolution of erythroderma and pruritus, and only limited residual lichenification (Figure, B). The mycophenolate was tapered slowly, and the patient experienced a mild flare at 1 g daily. He is presently on 1 g of mycophenolate daily and omalizumab (375 mg every 2 weeks) and remains remarkably improved. His IgE level decreased to 11,983 IU/mL.

Omalizumab is a monoclonal IgG1 antibody that specifically binds to the FcεRI domain of serum IgE. It blocks binding to high-affinity receptors on effector cells, primarily mast cells, basophils, macrophages, and dendritic cells; it also decreases free IgE serum levels and downregulates the IgE receptor.^{4,6-10,23-25,27,28} Currently, omalizumab is US Food and Drug Administration approved for moderate to severe persistent asthma in patients 6 years or older with a positive aeroallergen skin test and IgE levels up to 700 IU/mL.^{6,7,23-25,27,28}

However, scattered case reports and small case series have described variable success in the treatment of severe AD that is unresponsive to conventional therapy in patients with markedly elevated serum IgE levels.^4,5,7-22 The majority of patients (approximately 80% of published cases yielded by a PubMed search of articles indexed for MEDLINE using the search terms omalizumab and atopic dermatitis) showed improvement when measured by clinical severity scores and quality of life improvement, especially when used in conjunction with conventional therapy. Possible reasons for reported treatment failure include insufficient dosage, lack of established treatment guidelines for markedly elevated serum IgE levels, severity of disease, or variable response with failure to lower IgE level below a required threshold.^7,9,23,24,27

Krathen and Hsu⁹ reported treatment failure with omalizumab for AD in 3 patients with serum IgE levels ranging from 5440 and 24,400 IU/mL, and one review indicated omalizumab may work best in patients with only moderately elevated serum IgE levels.²¹ However, Toledo et al¹⁸ reported efficacy of low-dose omalizumab for pretreatment IgE levels up to 30,000 IU/mL in 6 of 11 reported cases. The pretreatment serum IgE level is not predictive of response, and lowering the serum IgE level without normalization can be efficacious,^12,23 as in the current case. Serum IgE levels are not used for monitoring therapeutic response or calculating future dosing, given potential increases in serum IgE levels during and after therapy (for up to 12 months) secondary to the formation of anti-IgE:IgE complexes.^6,28 Omalizumab appears most effective when used in combination with conventional therapies. Hopefully ongoing studies will further elucidate the role of omalizumab in recalcitrant AD with elevated serum IgE levels.

On April 18, 2017, Gary Goldenberg, MD, took over the @CutisJournal Twitter account for 1 hour to answer reader questions about updates in cosmetic dermatology. Below is a transcript of the Twitter Q&A session (#AskCutisJournal).

@carriekovarik Aside from lightening agents & moisturizers, success with #microneedling. Go low & slow 2 prevent more hyperpigmentation.

RELATED ARTICLE:
Microneedling Therapy With and Without Platelet-Rich Plasma

@NailDoc12
What's new for treatment of melasma?

@NailDoc12 I recommend combo of prevention, sunscreen & lightening cream w/ microneedling w/ PRP or ktp laser such as #Cutera #ExcelV.

 

RELATED ARTICLE:
Dermatologists Weigh in on Skin-Lightening Agents

@NailDoc12
Is there good evidence for use of PRP for skin aging?

@NailDoc12 Pts swear by #PRP. Use after fillers/Botox & microneedling or laser. Pts say it improves skin quality, gives it a "glow" (1/2)
@NailDoc12 Growth factors in PRP improve tissue vascularity & help cells regenerate & normalize. Helps w/wound healing post procedure (2/2)

 

RELATED VIDEO:
Microneedling With Platelet-Rich Plasma

@anthonymrossi
@CutisJournal #AskCutisJournal What is your approach to global facial rejuvenation? Do you like to start with injectables or laser?

@anthonymrossi Total rejuvenation is just that. I rec combo tx 2 improve skin quality (laser and/or microneedling with PRP) (1/2)
@anthonymrossi Plus wrinkle relaxers for dynamic wrinkles, & fillers to address volume loss and deep wrinkles & lines (2/2)

 

RELATED VIDEO:
Facial Rejuvenation With Fractional Laser Resurfacing

@SkindocDLCC
@CutisJournal #AskCutisJournal Whats your favorite filler for cheek lifting?

@SkindocDLCC Filler naive pts: #RestylaneLyft or #JuvedermVoluma. Experienced pts: #Radiesse or #Bellafill

 

@SkindocDLCC
@CutisJournal @Goldenberg_Derm What filler do you like for a sharper jawline? #AskCutisJournal

@SkindocDLCC I prefer long-lasting fillers, such as #Radiesse or #Bellafill. This is true for both male & female pts

 

RELATED ARTICLE:
Efficacy and Safety of New Dermal Fillers

@SkindocDLCC
@CutisJournal @Goldenberg_Derm How do you get a smooth forehead with neurotoxin without a heavy brow? #AskCutisJournal

@SkindocDLCC Precise placement of product is important. Some pts may require more product to completely smooth out forehead (1/2)
@SkindocDLCC Those pts may need a combo tx with laser such as #CO2 or #microneedling with #PRP (2/2)

 

@SkindocDLCC
@CutisJournal @Goldenberg_Derm How do you combine PRP and fillers? #AskCutisJournal

@SkindocDLCC I regularly use #PRP with fillers 2 enhance the effect (1/3)
@SkindocDLCC PRP helps stimulate collagen & increase vascularity needed for collagen production (2/3)
@SkindocDLCC I use a mesotherapy needle to inject #PRP after injecting filler and/or neurotoxins (3/3)

 

@MilitelloDerm
@CutisJournal @Goldenberg_Derm What is your favorite filler for tear troughs?

@MilitelloDerm I prefer Restylane or Juvederm Ultra. These fillers give the best volume effect & last longer than other options in my hands

 

RELATED ARTICLE:
Periocular Fillers and Related Anatomy

On April 18, 2017, Gary Goldenberg, MD, took over the @CutisJournal Twitter account for 1 hour to answer reader questions about updates in cosmetic dermatology. Below is a transcript of the Twitter Q&A session (#AskCutisJournal).

@carriekovarik Aside from lightening agents & moisturizers, success with #microneedling. Go low & slow 2 prevent more hyperpigmentation.

RELATED ARTICLE:
Microneedling Therapy With and Without Platelet-Rich Plasma

@NailDoc12
What's new for treatment of melasma?

@NailDoc12 I recommend combo of prevention, sunscreen & lightening cream w/ microneedling w/ PRP or ktp laser such as #Cutera #ExcelV.

 

RELATED ARTICLE:
Dermatologists Weigh in on Skin-Lightening Agents

@NailDoc12
Is there good evidence for use of PRP for skin aging?

@NailDoc12 Pts swear by #PRP. Use after fillers/Botox & microneedling or laser. Pts say it improves skin quality, gives it a "glow" (1/2)
@NailDoc12 Growth factors in PRP improve tissue vascularity & help cells regenerate & normalize. Helps w/wound healing post procedure (2/2)

 

RELATED VIDEO:
Microneedling With Platelet-Rich Plasma

@anthonymrossi
@CutisJournal #AskCutisJournal What is your approach to global facial rejuvenation? Do you like to start with injectables or laser?

@anthonymrossi Total rejuvenation is just that. I rec combo tx 2 improve skin quality (laser and/or microneedling with PRP) (1/2)
@anthonymrossi Plus wrinkle relaxers for dynamic wrinkles, & fillers to address volume loss and deep wrinkles & lines (2/2)

 

RELATED VIDEO:
Facial Rejuvenation With Fractional Laser Resurfacing

@SkindocDLCC
@CutisJournal #AskCutisJournal Whats your favorite filler for cheek lifting?

@SkindocDLCC Filler naive pts: #RestylaneLyft or #JuvedermVoluma. Experienced pts: #Radiesse or #Bellafill

 

@SkindocDLCC
@CutisJournal @Goldenberg_Derm What filler do you like for a sharper jawline? #AskCutisJournal

@SkindocDLCC I prefer long-lasting fillers, such as #Radiesse or #Bellafill. This is true for both male & female pts

 

RELATED ARTICLE:
Efficacy and Safety of New Dermal Fillers

@SkindocDLCC
@CutisJournal @Goldenberg_Derm How do you get a smooth forehead with neurotoxin without a heavy brow? #AskCutisJournal

@SkindocDLCC Precise placement of product is important. Some pts may require more product to completely smooth out forehead (1/2)
@SkindocDLCC Those pts may need a combo tx with laser such as #CO2 or #microneedling with #PRP (2/2)

 

@SkindocDLCC
@CutisJournal @Goldenberg_Derm How do you combine PRP and fillers? #AskCutisJournal

@SkindocDLCC I regularly use #PRP with fillers 2 enhance the effect (1/3)
@SkindocDLCC PRP helps stimulate collagen & increase vascularity needed for collagen production (2/3)
@SkindocDLCC I use a mesotherapy needle to inject #PRP after injecting filler and/or neurotoxins (3/3)

 

@MilitelloDerm
@CutisJournal @Goldenberg_Derm What is your favorite filler for tear troughs?

@MilitelloDerm I prefer Restylane or Juvederm Ultra. These fillers give the best volume effect & last longer than other options in my hands

 

RELATED ARTICLE:
Periocular Fillers and Related Anatomy

On April 18, 2017, Gary Goldenberg, MD, took over the @CutisJournal Twitter account for 1 hour to answer reader questions about updates in cosmetic dermatology. Below is a transcript of the Twitter Q&A session (#AskCutisJournal).

@carriekovarik Aside from lightening agents & moisturizers, success with #microneedling. Go low & slow 2 prevent more hyperpigmentation.

RELATED ARTICLE:
Microneedling Therapy With and Without Platelet-Rich Plasma

@NailDoc12
What's new for treatment of melasma?

@NailDoc12 I recommend combo of prevention, sunscreen & lightening cream w/ microneedling w/ PRP or ktp laser such as #Cutera #ExcelV.

 

RELATED ARTICLE:
Dermatologists Weigh in on Skin-Lightening Agents

@NailDoc12
Is there good evidence for use of PRP for skin aging?

@NailDoc12 Pts swear by #PRP. Use after fillers/Botox & microneedling or laser. Pts say it improves skin quality, gives it a "glow" (1/2)
@NailDoc12 Growth factors in PRP improve tissue vascularity & help cells regenerate & normalize. Helps w/wound healing post procedure (2/2)

 

RELATED VIDEO:
Microneedling With Platelet-Rich Plasma

@anthonymrossi
@CutisJournal #AskCutisJournal What is your approach to global facial rejuvenation? Do you like to start with injectables or laser?

@anthonymrossi Total rejuvenation is just that. I rec combo tx 2 improve skin quality (laser and/or microneedling with PRP) (1/2)
@anthonymrossi Plus wrinkle relaxers for dynamic wrinkles, & fillers to address volume loss and deep wrinkles & lines (2/2)

 

RELATED VIDEO:
Facial Rejuvenation With Fractional Laser Resurfacing

@SkindocDLCC
@CutisJournal #AskCutisJournal Whats your favorite filler for cheek lifting?

@SkindocDLCC Filler naive pts: #RestylaneLyft or #JuvedermVoluma. Experienced pts: #Radiesse or #Bellafill

 

@SkindocDLCC
@CutisJournal @Goldenberg_Derm What filler do you like for a sharper jawline? #AskCutisJournal

@SkindocDLCC I prefer long-lasting fillers, such as #Radiesse or #Bellafill. This is true for both male & female pts

 

RELATED ARTICLE:
Efficacy and Safety of New Dermal Fillers

@SkindocDLCC
@CutisJournal @Goldenberg_Derm How do you get a smooth forehead with neurotoxin without a heavy brow? #AskCutisJournal

@SkindocDLCC Precise placement of product is important. Some pts may require more product to completely smooth out forehead (1/2)
@SkindocDLCC Those pts may need a combo tx with laser such as #CO2 or #microneedling with #PRP (2/2)

 

@SkindocDLCC
@CutisJournal @Goldenberg_Derm How do you combine PRP and fillers? #AskCutisJournal

@SkindocDLCC I regularly use #PRP with fillers 2 enhance the effect (1/3)
@SkindocDLCC PRP helps stimulate collagen & increase vascularity needed for collagen production (2/3)
@SkindocDLCC I use a mesotherapy needle to inject #PRP after injecting filler and/or neurotoxins (3/3)

 

@MilitelloDerm
@CutisJournal @Goldenberg_Derm What is your favorite filler for tear troughs?

@MilitelloDerm I prefer Restylane or Juvederm Ultra. These fillers give the best volume effect & last longer than other options in my hands

 

RELATED ARTICLE:
Periocular Fillers and Related Anatomy