In July, I had my annual physical with my primary care physician, whose practice is based out of a large urban academic medical center. As she concluded my visit and directed me to the lab to have my blood work done, she said, “You’ll be receiving an automatic notice from MyChart by 9 am tomorrow that your medical records from today’s visit are available. I apologize if I have not yet had the opportunity to review them and enter my note, but you’ll get access to all of that, as well, as soon as it is in the system.”

This sort of interaction is increasingly common across the United States as health care institutions implement policies and procedures to comply with new regulations promulgated by the Office of the National Coordinator for Health Information Technology (ONC), which went into effect on April 5, 2021. These rules were promulgated in accordance with the 21st Century Cures Act of 2016 (Cures Act).¹ The regulations, known as the Interoperability, Information Blocking, and the ONC Health IT Certification Program, implement provisions of the Cures Act intended to “support the access, exchange, and use of electronic health information.” The rule is considered a significant step in the “open notes” movement, which is intended to make health care more transparent by enabling patients to access their medical records. The drafters of the ONC regulations have carved out certain exceptions to the information blocking rule. For example, one exception allows some patient information to be withheld where making that information available might cause physical harm to the patient or another person.

Thus far, few patients have been informed about the new regulation.² By forbidding “information blocking,” the rule enables patients to more easily access and control their health information. Currently, the rule requires that physicians allow automatic access, without charge, to a patient’s own personal health information, including clinical notes, medication lists, laboratory results, and other diagnostic reports. Records must be provided “without delay,” or at least as soon as the physician’s office receives an electronic copy. In 2022, it will be required that access to even more of a patient’s personal electronic health record be provided in real-time through a patient portal and that electronic health information be shareable across third-party apps.

The Cures Act and the regulations governing its implementation highlight the inherent tension between two core principles of bioethical inquiry: autonomy and beneficence. The first principle, autonomy, champions allowing patient access and control over their own personal information. Beneficence, which is often expressed as paternalism, ensures that the experts are able to analyze and interpret data so that patients are in the best position to then make informed decisions.

With these principles in mind, arguments against open notes have generally fallen into three related categories. First, critics worry that immediate access to one’s medical record will increase patient anxiety caused by feelings of being inundated with complex medical information that patients may be ill-equipped to analyze and understand. This is a common refrain any time policies are implemented to improve medical information sharing. For example, critics of direct-to-consumer genetic testing caution that permitting unfettered access to complex information, particularly without an intermediary to interpret the data, could lead to confusion and poor medical choices.

There may be validity to this claim. One study found that 3% of patients reported feeling very confused when granted access to their medical notes.³ Another study concluded that direct release of medical test results “sometimes leads to unnecessary anxiety.”⁴ While the drafters of the ONC regulations have carved out certain exceptions to the information blocking rule, those exceptions do not allow for withholding of information because of concerns about patient anxiety or psychological harms.

The second common critique of open notes is that requiring release of all clinical notes will lead to clinician self-censorship, effectively muzzling or silencing the experts whose responsibility it is to objectively interpret results in order to provide the best care for their patients. Some have expressed concern that clinicians will be forced to “code” their records to avoid addressing “sensitive” subjects that might make patients feel offended or judged. This, in turn, might lead to less complete, reliable, or useful clinician communication.³

In fact, open notes has led to changes in the documentation process for some clinicians. They have reported modifying the way they document patient visits by changing their use of critical language and sensitive information.⁵ One study found that open notes led physicians to adjust “their language to avoid being perceived as critical of patients; omitting certain terms, such as ‘noncompliant’ and ‘patient denies’; and modifying how they document sensitive information.”³

In response, experts recommend focusing on precise and empathetic patient notes; in other words, the clinician should not write something in the note that they would not say directly to the patient. For example, they recommend that clinicians use precise language (for example, identifying the patient’s BMI) rather than using terms that could be offensive (for example, labeling the patient as “obese”).⁶ The shift to more empathetic note-taking could be seen less as a burden and more as a valuable tool in the shared decision-making endeavor: It could allow physicians to document both their clinical judgments and the patient’s values and preferences, which could lead to better medical decision-making.

Third, critics of open notes point to concerns about the burden it places on clinicians’ already limited time. The ONC rule requires automatic release of test results regardless of whether the clinician has had the opportunity to review them and offer their interpretation and insight. Because physician interpretation of results has known benefits,⁴ this puts additional pressure on clinicians to review results and enter notes in a timely manner. But physicians have reported that often open notes necessitates that they spend more time on documentation than they would otherwise.⁵

Despite critiques of open notes, the benefits of allowing patients access to their medical records have been repeatedly demonstrated. And research has shown that patients benefit from accessing open notes by allowing them to access and control their own personal medical information.⁵ Patients report that they understand and value the information provided to them in their medical records,⁷ and they feel empowered to participate in their medical decision-making. In surveys, patients report that reading their doctors’ notes is useful for taking care of their health and for remembering their care plans, understanding why a medication was prescribed, and reinforcing the need to take their medications and adhere to treatment plans.⁸

Importantly, open notes can increase patient engagement and patients’ trust in their physicians,⁹ thereby improving the doctor-patient relationship.³ And allowing patients to share their medical records with care partners enables supported decision-making, particularly for older and chronically ill individuals.³ Additionally, it is predicted that open notes may, in fact, decrease legal liability.⁹ By improving both trust in the doctor-patient relationship and safety, some experts expect that legal claims against clinicians will, in turn, decrease.¹⁰

The modern practice of medicine necessitates a more empathetic approach to clinical note-taking, even in the absence of regulation requiring it. As the regulations implementing the Cures Act roll out, patients will have easier, and more immediate, access to their medical records. Despite earlier hesitancy, clinicians are steadily beginning to support sharing access to notes with patients.⁵ Change can be hard. But the change expected of clinicians because of these new regulations appears to be less onerous than originally anticipated.

Prof. Koch is codirector of Health Law & Policy Institute and assistant professor at the University of Houston Law Center, as well as director of law and ethics at the MacLean Center for Clinical Medical Ethics at the University of Chicago. She has no disclosures.

This article was updated Sept. 9, 2021.

References

1. Fed Regist. 2020 May;85(85):25642-961.

2. The Petrie-Flom Center Staff. “New Rule Puts Medical Data in Patients’ Hands.” Bill of Health. July 12, 2021. Accessed August 30, 2021. https://blog.petrieflom.law.harvard.edu/2021/07/12/new-rule-puts-medical-data-in-patients-hands/.

3. Blease C et al. Ann Intern Med. 2021 Jan;174(1):101-2.

4. Pillemer F et al. PLoS One. 2016 Jun. doi: 10.1371/journal.pone.0154743.

5. DesRoches CM et al. JAMA Netw Open. 2020 Mar. doi: 10.1001/jamanetworkopen.2020.1753.

6. Heath S. “Most Patients Understand Clinical Notes, Patient Data Access.” Patient Engagement HIT. July 29, 2020. Accessed August 30, 2021. https://patientengagementhit.com/news/most-patients-understand-clinical-notes-patient-data-access

7. Leveille SG et al. J Gen Intern Med. 2020 Dec;35(12):3510-6.

8. Walker J et al. J Med Internet Res. 2019 May. doi: 10.2196/13876.

9. Bell SK et al. BMJ Qual Saf. 2017 Apr;26(4):262-70.

10. Kachalia A, Mello MM. N Engl J Med. 2011 Apr;364(16):1564-72.

In July, I had my annual physical with my primary care physician, whose practice is based out of a large urban academic medical center. As she concluded my visit and directed me to the lab to have my blood work done, she said, “You’ll be receiving an automatic notice from MyChart by 9 am tomorrow that your medical records from today’s visit are available. I apologize if I have not yet had the opportunity to review them and enter my note, but you’ll get access to all of that, as well, as soon as it is in the system.”

This sort of interaction is increasingly common across the United States as health care institutions implement policies and procedures to comply with new regulations promulgated by the Office of the National Coordinator for Health Information Technology (ONC), which went into effect on April 5, 2021. These rules were promulgated in accordance with the 21st Century Cures Act of 2016 (Cures Act).¹ The regulations, known as the Interoperability, Information Blocking, and the ONC Health IT Certification Program, implement provisions of the Cures Act intended to “support the access, exchange, and use of electronic health information.” The rule is considered a significant step in the “open notes” movement, which is intended to make health care more transparent by enabling patients to access their medical records. The drafters of the ONC regulations have carved out certain exceptions to the information blocking rule. For example, one exception allows some patient information to be withheld where making that information available might cause physical harm to the patient or another person.

Thus far, few patients have been informed about the new regulation.² By forbidding “information blocking,” the rule enables patients to more easily access and control their health information. Currently, the rule requires that physicians allow automatic access, without charge, to a patient’s own personal health information, including clinical notes, medication lists, laboratory results, and other diagnostic reports. Records must be provided “without delay,” or at least as soon as the physician’s office receives an electronic copy. In 2022, it will be required that access to even more of a patient’s personal electronic health record be provided in real-time through a patient portal and that electronic health information be shareable across third-party apps.

The Cures Act and the regulations governing its implementation highlight the inherent tension between two core principles of bioethical inquiry: autonomy and beneficence. The first principle, autonomy, champions allowing patient access and control over their own personal information. Beneficence, which is often expressed as paternalism, ensures that the experts are able to analyze and interpret data so that patients are in the best position to then make informed decisions.

With these principles in mind, arguments against open notes have generally fallen into three related categories. First, critics worry that immediate access to one’s medical record will increase patient anxiety caused by feelings of being inundated with complex medical information that patients may be ill-equipped to analyze and understand. This is a common refrain any time policies are implemented to improve medical information sharing. For example, critics of direct-to-consumer genetic testing caution that permitting unfettered access to complex information, particularly without an intermediary to interpret the data, could lead to confusion and poor medical choices.

There may be validity to this claim. One study found that 3% of patients reported feeling very confused when granted access to their medical notes.³ Another study concluded that direct release of medical test results “sometimes leads to unnecessary anxiety.”⁴ While the drafters of the ONC regulations have carved out certain exceptions to the information blocking rule, those exceptions do not allow for withholding of information because of concerns about patient anxiety or psychological harms.

The second common critique of open notes is that requiring release of all clinical notes will lead to clinician self-censorship, effectively muzzling or silencing the experts whose responsibility it is to objectively interpret results in order to provide the best care for their patients. Some have expressed concern that clinicians will be forced to “code” their records to avoid addressing “sensitive” subjects that might make patients feel offended or judged. This, in turn, might lead to less complete, reliable, or useful clinician communication.³

In fact, open notes has led to changes in the documentation process for some clinicians. They have reported modifying the way they document patient visits by changing their use of critical language and sensitive information.⁵ One study found that open notes led physicians to adjust “their language to avoid being perceived as critical of patients; omitting certain terms, such as ‘noncompliant’ and ‘patient denies’; and modifying how they document sensitive information.”³

In response, experts recommend focusing on precise and empathetic patient notes; in other words, the clinician should not write something in the note that they would not say directly to the patient. For example, they recommend that clinicians use precise language (for example, identifying the patient’s BMI) rather than using terms that could be offensive (for example, labeling the patient as “obese”).⁶ The shift to more empathetic note-taking could be seen less as a burden and more as a valuable tool in the shared decision-making endeavor: It could allow physicians to document both their clinical judgments and the patient’s values and preferences, which could lead to better medical decision-making.

Third, critics of open notes point to concerns about the burden it places on clinicians’ already limited time. The ONC rule requires automatic release of test results regardless of whether the clinician has had the opportunity to review them and offer their interpretation and insight. Because physician interpretation of results has known benefits,⁴ this puts additional pressure on clinicians to review results and enter notes in a timely manner. But physicians have reported that often open notes necessitates that they spend more time on documentation than they would otherwise.⁵

Despite critiques of open notes, the benefits of allowing patients access to their medical records have been repeatedly demonstrated. And research has shown that patients benefit from accessing open notes by allowing them to access and control their own personal medical information.⁵ Patients report that they understand and value the information provided to them in their medical records,⁷ and they feel empowered to participate in their medical decision-making. In surveys, patients report that reading their doctors’ notes is useful for taking care of their health and for remembering their care plans, understanding why a medication was prescribed, and reinforcing the need to take their medications and adhere to treatment plans.⁸

Importantly, open notes can increase patient engagement and patients’ trust in their physicians,⁹ thereby improving the doctor-patient relationship.³ And allowing patients to share their medical records with care partners enables supported decision-making, particularly for older and chronically ill individuals.³ Additionally, it is predicted that open notes may, in fact, decrease legal liability.⁹ By improving both trust in the doctor-patient relationship and safety, some experts expect that legal claims against clinicians will, in turn, decrease.¹⁰

The modern practice of medicine necessitates a more empathetic approach to clinical note-taking, even in the absence of regulation requiring it. As the regulations implementing the Cures Act roll out, patients will have easier, and more immediate, access to their medical records. Despite earlier hesitancy, clinicians are steadily beginning to support sharing access to notes with patients.⁵ Change can be hard. But the change expected of clinicians because of these new regulations appears to be less onerous than originally anticipated.

Prof. Koch is codirector of Health Law & Policy Institute and assistant professor at the University of Houston Law Center, as well as director of law and ethics at the MacLean Center for Clinical Medical Ethics at the University of Chicago. She has no disclosures.

This article was updated Sept. 9, 2021.

References

1. Fed Regist. 2020 May;85(85):25642-961.

2. The Petrie-Flom Center Staff. “New Rule Puts Medical Data in Patients’ Hands.” Bill of Health. July 12, 2021. Accessed August 30, 2021. https://blog.petrieflom.law.harvard.edu/2021/07/12/new-rule-puts-medical-data-in-patients-hands/.

3. Blease C et al. Ann Intern Med. 2021 Jan;174(1):101-2.

4. Pillemer F et al. PLoS One. 2016 Jun. doi: 10.1371/journal.pone.0154743.

5. DesRoches CM et al. JAMA Netw Open. 2020 Mar. doi: 10.1001/jamanetworkopen.2020.1753.

6. Heath S. “Most Patients Understand Clinical Notes, Patient Data Access.” Patient Engagement HIT. July 29, 2020. Accessed August 30, 2021. https://patientengagementhit.com/news/most-patients-understand-clinical-notes-patient-data-access

7. Leveille SG et al. J Gen Intern Med. 2020 Dec;35(12):3510-6.

8. Walker J et al. J Med Internet Res. 2019 May. doi: 10.2196/13876.

9. Bell SK et al. BMJ Qual Saf. 2017 Apr;26(4):262-70.

10. Kachalia A, Mello MM. N Engl J Med. 2011 Apr;364(16):1564-72.

In July, I had my annual physical with my primary care physician, whose practice is based out of a large urban academic medical center. As she concluded my visit and directed me to the lab to have my blood work done, she said, “You’ll be receiving an automatic notice from MyChart by 9 am tomorrow that your medical records from today’s visit are available. I apologize if I have not yet had the opportunity to review them and enter my note, but you’ll get access to all of that, as well, as soon as it is in the system.”

This sort of interaction is increasingly common across the United States as health care institutions implement policies and procedures to comply with new regulations promulgated by the Office of the National Coordinator for Health Information Technology (ONC), which went into effect on April 5, 2021. These rules were promulgated in accordance with the 21st Century Cures Act of 2016 (Cures Act).¹ The regulations, known as the Interoperability, Information Blocking, and the ONC Health IT Certification Program, implement provisions of the Cures Act intended to “support the access, exchange, and use of electronic health information.” The rule is considered a significant step in the “open notes” movement, which is intended to make health care more transparent by enabling patients to access their medical records. The drafters of the ONC regulations have carved out certain exceptions to the information blocking rule. For example, one exception allows some patient information to be withheld where making that information available might cause physical harm to the patient or another person.

Thus far, few patients have been informed about the new regulation.² By forbidding “information blocking,” the rule enables patients to more easily access and control their health information. Currently, the rule requires that physicians allow automatic access, without charge, to a patient’s own personal health information, including clinical notes, medication lists, laboratory results, and other diagnostic reports. Records must be provided “without delay,” or at least as soon as the physician’s office receives an electronic copy. In 2022, it will be required that access to even more of a patient’s personal electronic health record be provided in real-time through a patient portal and that electronic health information be shareable across third-party apps.

The Cures Act and the regulations governing its implementation highlight the inherent tension between two core principles of bioethical inquiry: autonomy and beneficence. The first principle, autonomy, champions allowing patient access and control over their own personal information. Beneficence, which is often expressed as paternalism, ensures that the experts are able to analyze and interpret data so that patients are in the best position to then make informed decisions.

With these principles in mind, arguments against open notes have generally fallen into three related categories. First, critics worry that immediate access to one’s medical record will increase patient anxiety caused by feelings of being inundated with complex medical information that patients may be ill-equipped to analyze and understand. This is a common refrain any time policies are implemented to improve medical information sharing. For example, critics of direct-to-consumer genetic testing caution that permitting unfettered access to complex information, particularly without an intermediary to interpret the data, could lead to confusion and poor medical choices.

There may be validity to this claim. One study found that 3% of patients reported feeling very confused when granted access to their medical notes.³ Another study concluded that direct release of medical test results “sometimes leads to unnecessary anxiety.”⁴ While the drafters of the ONC regulations have carved out certain exceptions to the information blocking rule, those exceptions do not allow for withholding of information because of concerns about patient anxiety or psychological harms.

The second common critique of open notes is that requiring release of all clinical notes will lead to clinician self-censorship, effectively muzzling or silencing the experts whose responsibility it is to objectively interpret results in order to provide the best care for their patients. Some have expressed concern that clinicians will be forced to “code” their records to avoid addressing “sensitive” subjects that might make patients feel offended or judged. This, in turn, might lead to less complete, reliable, or useful clinician communication.³

In fact, open notes has led to changes in the documentation process for some clinicians. They have reported modifying the way they document patient visits by changing their use of critical language and sensitive information.⁵ One study found that open notes led physicians to adjust “their language to avoid being perceived as critical of patients; omitting certain terms, such as ‘noncompliant’ and ‘patient denies’; and modifying how they document sensitive information.”³

In response, experts recommend focusing on precise and empathetic patient notes; in other words, the clinician should not write something in the note that they would not say directly to the patient. For example, they recommend that clinicians use precise language (for example, identifying the patient’s BMI) rather than using terms that could be offensive (for example, labeling the patient as “obese”).⁶ The shift to more empathetic note-taking could be seen less as a burden and more as a valuable tool in the shared decision-making endeavor: It could allow physicians to document both their clinical judgments and the patient’s values and preferences, which could lead to better medical decision-making.

Third, critics of open notes point to concerns about the burden it places on clinicians’ already limited time. The ONC rule requires automatic release of test results regardless of whether the clinician has had the opportunity to review them and offer their interpretation and insight. Because physician interpretation of results has known benefits,⁴ this puts additional pressure on clinicians to review results and enter notes in a timely manner. But physicians have reported that often open notes necessitates that they spend more time on documentation than they would otherwise.⁵

Despite critiques of open notes, the benefits of allowing patients access to their medical records have been repeatedly demonstrated. And research has shown that patients benefit from accessing open notes by allowing them to access and control their own personal medical information.⁵ Patients report that they understand and value the information provided to them in their medical records,⁷ and they feel empowered to participate in their medical decision-making. In surveys, patients report that reading their doctors’ notes is useful for taking care of their health and for remembering their care plans, understanding why a medication was prescribed, and reinforcing the need to take their medications and adhere to treatment plans.⁸

Importantly, open notes can increase patient engagement and patients’ trust in their physicians,⁹ thereby improving the doctor-patient relationship.³ And allowing patients to share their medical records with care partners enables supported decision-making, particularly for older and chronically ill individuals.³ Additionally, it is predicted that open notes may, in fact, decrease legal liability.⁹ By improving both trust in the doctor-patient relationship and safety, some experts expect that legal claims against clinicians will, in turn, decrease.¹⁰

The modern practice of medicine necessitates a more empathetic approach to clinical note-taking, even in the absence of regulation requiring it. As the regulations implementing the Cures Act roll out, patients will have easier, and more immediate, access to their medical records. Despite earlier hesitancy, clinicians are steadily beginning to support sharing access to notes with patients.⁵ Change can be hard. But the change expected of clinicians because of these new regulations appears to be less onerous than originally anticipated.

Prof. Koch is codirector of Health Law & Policy Institute and assistant professor at the University of Houston Law Center, as well as director of law and ethics at the MacLean Center for Clinical Medical Ethics at the University of Chicago. She has no disclosures.

This article was updated Sept. 9, 2021.

References

1. Fed Regist. 2020 May;85(85):25642-961.

2. The Petrie-Flom Center Staff. “New Rule Puts Medical Data in Patients’ Hands.” Bill of Health. July 12, 2021. Accessed August 30, 2021. https://blog.petrieflom.law.harvard.edu/2021/07/12/new-rule-puts-medical-data-in-patients-hands/.

3. Blease C et al. Ann Intern Med. 2021 Jan;174(1):101-2.

4. Pillemer F et al. PLoS One. 2016 Jun. doi: 10.1371/journal.pone.0154743.

5. DesRoches CM et al. JAMA Netw Open. 2020 Mar. doi: 10.1001/jamanetworkopen.2020.1753.

6. Heath S. “Most Patients Understand Clinical Notes, Patient Data Access.” Patient Engagement HIT. July 29, 2020. Accessed August 30, 2021. https://patientengagementhit.com/news/most-patients-understand-clinical-notes-patient-data-access

7. Leveille SG et al. J Gen Intern Med. 2020 Dec;35(12):3510-6.

8. Walker J et al. J Med Internet Res. 2019 May. doi: 10.2196/13876.

9. Bell SK et al. BMJ Qual Saf. 2017 Apr;26(4):262-70.

10. Kachalia A, Mello MM. N Engl J Med. 2011 Apr;364(16):1564-72.

The COVID-19 pandemic continues to impact child and adolescent mental health, and clinicians are learning as they go to develop strategies that address the challenges of providing both medical and mental health care to young patients, including those who test positive for COVID-19, according to Hani Talebi, PhD, director of pediatric psychology, and Jorge Ganem, MD, FAAP, director of pediatric hospital medicine, both of the University of Texas at Austin and Dell Children’s Medical Center.

In a presentation at the 2021 virtual Pediatric Hospital Medicine conference, Dr. Talebi and Dr. Ganem shared their experiences in identifying the impact of the pandemic on mental health services in a freestanding hospital, and synthesizing inpatient mental health care and medical care outside of a dedicated mental health unit.

Mental health is a significant pediatric issue; approximately one in five children have a diagnosable mental or behavioral health problem, but nearly two-thirds get little or no help, Dr. Talebi said. “COVID-19 has only exacerbated these mental health challenges,” he said.

He noted that beginning in April 2020, the proportion of children’s mental health-related emergency department visits increased and remained elevated through the spring, summer, and fall of 2020, as families fearful of COVID-19 avoided regular hospital visits.

Data suggest that up to 50% of all adolescent psychiatric crises that led to inpatient admissions were related in some way to COVID-19, Dr. Talebi said. In addition, “individuals with a recent diagnosis of a mental health disorder are at increased risk for COVID-19 infection,” and the risk is even higher among women and African Americans, he said.

The past year significantly impacted the mental wellbeing of parents and children, Dr. Talebi said. He cited a June 2020 study in Pediatrics in which 27% of parents reported worsening mental health for themselves, and 14% reported worsening behavioral health for their children. Ongoing issues including food insecurity, loss of regular child care, and an overall “very disorienting experience in the day-to-day” compromised the mental health of families, Dr. Talebi emphasized. Children isolated at home were not meeting developmental milestones that organically occur when socializing with peers, parents didn’t know how to handle some of their children’s issues without support from schools, and many people were struggling with other preexisting health conditions, he said.

This confluence of factors helped drive a surge in emergency department visits, meaning longer wait times and concerns about meeting urgent medical and mental health needs while maintaining safety, he added.

Parents and children waited longer to seek care, and community hospitals such as Dell Children’s Medical Center were faced with children in the emergency department with crisis-level mental health issues, along with children already waiting in the ED to address medical emergencies. All these patients had to be tested for COVID-19 and managed accordingly, Dr. Talebi noted.

Dr. Talebi emphasized the need for clinically robust care of the children who were in isolation for 10 days on the medical unit, waiting to test negative. New protocols were created for social workers to conduct daily safety checks, and to develop regular schedules for screening, “so they are having an experience on the medical floors similar to what they would have in a mental health unit,” he said.

Dr. Ganem reflected on the logistical challenges of managing mental health care while observing COVID-19 safety protocols. “COVID-19 added a new wrinkle of isolation,” he said. As institutional guidelines on testing and isolation evolved, negative COVID-19 tests were required for admission to the mental health units both in the hospital and throughout the region. Patients who tested positive had to be quarantined for 10 days, at which time they could be admitted to a mental health unit if necessary, he said.

Dr. Ganem shared details of some strategies adopted by Dell Children’s. He explained that the COVID-19 psychiatry patient workflow started with an ED evaluation, followed by medical clearance and consideration for admission.

“There was significant coordination between the social worker in the emergency department and the psychiatry social worker,” he said.

Key elements of the treatment plan for children with positive COVID-19 tests included an “interprofessional huddle” to coordinate the plan of care, goals for admission, and goals for safety, Dr. Ganem said.

Patients who required admission were expected to have an initial length of stay of 72 hours, and those who tested positive for COVID-19 were admitted to a medical unit with COVID-19 isolation, he said.

Once a patient is admitted, an RN activates a suicide prevention pathway, and an interprofessional team meets to determine what patients need for safe and effective discharge, said Dr. Ganem. He cited the SAFE-T protocol (Suicide Assessment Five-step Evaluation and Triage) as one of the tools used to determine safe discharge criteria. Considerations on the SAFE-T list include family support, an established outpatient therapist and psychiatrist, no suicide attempts prior to the current admission, or a low lethality attempt, and access to partial hospitalization or intensive outpatient programs.

Patients who could not be discharged because of suicidality or inadequate support or concerns about safety at home were considered for inpatient admission. Patients with COVID-19–positive tests who had continued need for inpatient mental health services could be transferred to an inpatient mental health unit after a 10-day quarantine.

Overall, “this has been a continuum of lessons learned, with some things we know now that we didn’t know in April or May of 2020,” Dr. Ganem said. Early in the pandemic, the focus was on minimizing risk, securing personal protective equipment, and determining who provided services in a patient’s room. “We developed new paradigms on the fly,” he said, including the use of virtual visits, which included securing and cleaning devices, as well as learning how to use them in this setting,” he said.

More recently, the emphasis has been on providing services to patients before they need to visit the hospital, rather than automatically admitting any patients with suicidal ideation and a positive COVID-19 test, Dr. Ganem said.

Dr. Talebi and Dr. Ganem had no financial conflicts to disclose. The conference was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.

The COVID-19 pandemic continues to impact child and adolescent mental health, and clinicians are learning as they go to develop strategies that address the challenges of providing both medical and mental health care to young patients, including those who test positive for COVID-19, according to Hani Talebi, PhD, director of pediatric psychology, and Jorge Ganem, MD, FAAP, director of pediatric hospital medicine, both of the University of Texas at Austin and Dell Children’s Medical Center.

In a presentation at the 2021 virtual Pediatric Hospital Medicine conference, Dr. Talebi and Dr. Ganem shared their experiences in identifying the impact of the pandemic on mental health services in a freestanding hospital, and synthesizing inpatient mental health care and medical care outside of a dedicated mental health unit.

Mental health is a significant pediatric issue; approximately one in five children have a diagnosable mental or behavioral health problem, but nearly two-thirds get little or no help, Dr. Talebi said. “COVID-19 has only exacerbated these mental health challenges,” he said.

He noted that beginning in April 2020, the proportion of children’s mental health-related emergency department visits increased and remained elevated through the spring, summer, and fall of 2020, as families fearful of COVID-19 avoided regular hospital visits.

Data suggest that up to 50% of all adolescent psychiatric crises that led to inpatient admissions were related in some way to COVID-19, Dr. Talebi said. In addition, “individuals with a recent diagnosis of a mental health disorder are at increased risk for COVID-19 infection,” and the risk is even higher among women and African Americans, he said.

The past year significantly impacted the mental wellbeing of parents and children, Dr. Talebi said. He cited a June 2020 study in Pediatrics in which 27% of parents reported worsening mental health for themselves, and 14% reported worsening behavioral health for their children. Ongoing issues including food insecurity, loss of regular child care, and an overall “very disorienting experience in the day-to-day” compromised the mental health of families, Dr. Talebi emphasized. Children isolated at home were not meeting developmental milestones that organically occur when socializing with peers, parents didn’t know how to handle some of their children’s issues without support from schools, and many people were struggling with other preexisting health conditions, he said.

This confluence of factors helped drive a surge in emergency department visits, meaning longer wait times and concerns about meeting urgent medical and mental health needs while maintaining safety, he added.

Parents and children waited longer to seek care, and community hospitals such as Dell Children’s Medical Center were faced with children in the emergency department with crisis-level mental health issues, along with children already waiting in the ED to address medical emergencies. All these patients had to be tested for COVID-19 and managed accordingly, Dr. Talebi noted.

Dr. Talebi emphasized the need for clinically robust care of the children who were in isolation for 10 days on the medical unit, waiting to test negative. New protocols were created for social workers to conduct daily safety checks, and to develop regular schedules for screening, “so they are having an experience on the medical floors similar to what they would have in a mental health unit,” he said.

Dr. Ganem reflected on the logistical challenges of managing mental health care while observing COVID-19 safety protocols. “COVID-19 added a new wrinkle of isolation,” he said. As institutional guidelines on testing and isolation evolved, negative COVID-19 tests were required for admission to the mental health units both in the hospital and throughout the region. Patients who tested positive had to be quarantined for 10 days, at which time they could be admitted to a mental health unit if necessary, he said.

Dr. Ganem shared details of some strategies adopted by Dell Children’s. He explained that the COVID-19 psychiatry patient workflow started with an ED evaluation, followed by medical clearance and consideration for admission.

“There was significant coordination between the social worker in the emergency department and the psychiatry social worker,” he said.

Key elements of the treatment plan for children with positive COVID-19 tests included an “interprofessional huddle” to coordinate the plan of care, goals for admission, and goals for safety, Dr. Ganem said.

Patients who required admission were expected to have an initial length of stay of 72 hours, and those who tested positive for COVID-19 were admitted to a medical unit with COVID-19 isolation, he said.

Once a patient is admitted, an RN activates a suicide prevention pathway, and an interprofessional team meets to determine what patients need for safe and effective discharge, said Dr. Ganem. He cited the SAFE-T protocol (Suicide Assessment Five-step Evaluation and Triage) as one of the tools used to determine safe discharge criteria. Considerations on the SAFE-T list include family support, an established outpatient therapist and psychiatrist, no suicide attempts prior to the current admission, or a low lethality attempt, and access to partial hospitalization or intensive outpatient programs.

Patients who could not be discharged because of suicidality or inadequate support or concerns about safety at home were considered for inpatient admission. Patients with COVID-19–positive tests who had continued need for inpatient mental health services could be transferred to an inpatient mental health unit after a 10-day quarantine.

Overall, “this has been a continuum of lessons learned, with some things we know now that we didn’t know in April or May of 2020,” Dr. Ganem said. Early in the pandemic, the focus was on minimizing risk, securing personal protective equipment, and determining who provided services in a patient’s room. “We developed new paradigms on the fly,” he said, including the use of virtual visits, which included securing and cleaning devices, as well as learning how to use them in this setting,” he said.

More recently, the emphasis has been on providing services to patients before they need to visit the hospital, rather than automatically admitting any patients with suicidal ideation and a positive COVID-19 test, Dr. Ganem said.

Dr. Talebi and Dr. Ganem had no financial conflicts to disclose. The conference was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.

The COVID-19 pandemic continues to impact child and adolescent mental health, and clinicians are learning as they go to develop strategies that address the challenges of providing both medical and mental health care to young patients, including those who test positive for COVID-19, according to Hani Talebi, PhD, director of pediatric psychology, and Jorge Ganem, MD, FAAP, director of pediatric hospital medicine, both of the University of Texas at Austin and Dell Children’s Medical Center.

In a presentation at the 2021 virtual Pediatric Hospital Medicine conference, Dr. Talebi and Dr. Ganem shared their experiences in identifying the impact of the pandemic on mental health services in a freestanding hospital, and synthesizing inpatient mental health care and medical care outside of a dedicated mental health unit.

Mental health is a significant pediatric issue; approximately one in five children have a diagnosable mental or behavioral health problem, but nearly two-thirds get little or no help, Dr. Talebi said. “COVID-19 has only exacerbated these mental health challenges,” he said.

He noted that beginning in April 2020, the proportion of children’s mental health-related emergency department visits increased and remained elevated through the spring, summer, and fall of 2020, as families fearful of COVID-19 avoided regular hospital visits.

Data suggest that up to 50% of all adolescent psychiatric crises that led to inpatient admissions were related in some way to COVID-19, Dr. Talebi said. In addition, “individuals with a recent diagnosis of a mental health disorder are at increased risk for COVID-19 infection,” and the risk is even higher among women and African Americans, he said.

The past year significantly impacted the mental wellbeing of parents and children, Dr. Talebi said. He cited a June 2020 study in Pediatrics in which 27% of parents reported worsening mental health for themselves, and 14% reported worsening behavioral health for their children. Ongoing issues including food insecurity, loss of regular child care, and an overall “very disorienting experience in the day-to-day” compromised the mental health of families, Dr. Talebi emphasized. Children isolated at home were not meeting developmental milestones that organically occur when socializing with peers, parents didn’t know how to handle some of their children’s issues without support from schools, and many people were struggling with other preexisting health conditions, he said.

This confluence of factors helped drive a surge in emergency department visits, meaning longer wait times and concerns about meeting urgent medical and mental health needs while maintaining safety, he added.

Parents and children waited longer to seek care, and community hospitals such as Dell Children’s Medical Center were faced with children in the emergency department with crisis-level mental health issues, along with children already waiting in the ED to address medical emergencies. All these patients had to be tested for COVID-19 and managed accordingly, Dr. Talebi noted.

Dr. Talebi emphasized the need for clinically robust care of the children who were in isolation for 10 days on the medical unit, waiting to test negative. New protocols were created for social workers to conduct daily safety checks, and to develop regular schedules for screening, “so they are having an experience on the medical floors similar to what they would have in a mental health unit,” he said.

Dr. Ganem reflected on the logistical challenges of managing mental health care while observing COVID-19 safety protocols. “COVID-19 added a new wrinkle of isolation,” he said. As institutional guidelines on testing and isolation evolved, negative COVID-19 tests were required for admission to the mental health units both in the hospital and throughout the region. Patients who tested positive had to be quarantined for 10 days, at which time they could be admitted to a mental health unit if necessary, he said.

Dr. Ganem shared details of some strategies adopted by Dell Children’s. He explained that the COVID-19 psychiatry patient workflow started with an ED evaluation, followed by medical clearance and consideration for admission.

“There was significant coordination between the social worker in the emergency department and the psychiatry social worker,” he said.

Key elements of the treatment plan for children with positive COVID-19 tests included an “interprofessional huddle” to coordinate the plan of care, goals for admission, and goals for safety, Dr. Ganem said.

Patients who required admission were expected to have an initial length of stay of 72 hours, and those who tested positive for COVID-19 were admitted to a medical unit with COVID-19 isolation, he said.

Once a patient is admitted, an RN activates a suicide prevention pathway, and an interprofessional team meets to determine what patients need for safe and effective discharge, said Dr. Ganem. He cited the SAFE-T protocol (Suicide Assessment Five-step Evaluation and Triage) as one of the tools used to determine safe discharge criteria. Considerations on the SAFE-T list include family support, an established outpatient therapist and psychiatrist, no suicide attempts prior to the current admission, or a low lethality attempt, and access to partial hospitalization or intensive outpatient programs.

Patients who could not be discharged because of suicidality or inadequate support or concerns about safety at home were considered for inpatient admission. Patients with COVID-19–positive tests who had continued need for inpatient mental health services could be transferred to an inpatient mental health unit after a 10-day quarantine.

Overall, “this has been a continuum of lessons learned, with some things we know now that we didn’t know in April or May of 2020,” Dr. Ganem said. Early in the pandemic, the focus was on minimizing risk, securing personal protective equipment, and determining who provided services in a patient’s room. “We developed new paradigms on the fly,” he said, including the use of virtual visits, which included securing and cleaning devices, as well as learning how to use them in this setting,” he said.

More recently, the emphasis has been on providing services to patients before they need to visit the hospital, rather than automatically admitting any patients with suicidal ideation and a positive COVID-19 test, Dr. Ganem said.

Dr. Talebi and Dr. Ganem had no financial conflicts to disclose. The conference was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.

Many pregnant patients are not being screened for iron deficiency despite it being a common cause of anemia in pregnancy that could increase the risk of maternal and infant death.

Researchers analyzed data from 44,552 pregnant patients in Ontario, Canada, collected between 2013 and 2018 to determine the prevalence of ferritin testing, the standard test for iron deficiency, over the course of 5 years.

Their study, published in Blood Advances, revealed that only 59.4% of pregnant persons received a ferritin test, the standard test for iron deficiency. Of those pregnant persons, 25.2% were iron insufficient and 52.8% were iron deficient at least once during pregnancy.

They also found that 71% of these iron tests were ordered during the first trimester, when the risk of iron deficiency is lowest.

“We are not only missing a very large proportion of women who are iron deficient going into pregnancy, but we’re missing those that become iron deficient later on in their pregnancies,” study author Dr. Jennifer Teichman, hematology resident at the University of Toronto, said in an interview. Researchers said iron deficiency during pregnancy is associated with maternal fatigue, cognitive dysfunction, depression, low birth weight, and poor brain development of the child.

Dr. Teichman explained that if iron deficiency during pregnancy is identified early enough, doctors would have enough time to treat the condition with iron supplements before the patient goes into delivery. She also explained prenatal vitamins, which contain some iron, do not contain enough of the mineral to fix iron deficiency.

“One really important point is that the amount of iron contained in a prenatal vitamin is really low,” Dr. Teichman explained. “It’s enough to make up the difference of the additional iron that she needs to sustain her pregnancy, but it’s not enough to treat a woman who’s already got low iron going into pregnancy. So there’s a difference between a prenatal vitamin and true iron supplementation.”

Researchers also found that those who came from a household with a low annual income were even less likely to receive a ferritin test, which was a troubling finding since women of lower socioeconomic status are more likely to be iron deficient in pregnancy. 

“[This] says something about how we as health care providers are contributing to this gap in care,” Dr. Teichman said. “Women of lower socioeconomic status sort of have a triple whammy: They’re more likely to be iron deficient, they’re less likely to have it diagnosed, and they’re less likely to have it corrected.”

Dr. Teichman and her colleagues took a unique approach by looking at isolated ferritin levels as opposed to complete blood counts, which is the typical screening for anemia in pregnancy, said Lissette Tanner, MD, MPH, FACOG, who was not involved with the study.

“Those who meet the criteria for anemia should be evaluated for the cause with initial suspicion for iron deficiency anemia, as that is the most common etiology,” said Dr. Tanner, assistant professor of gynecology and obstetrics at Emory University, Atlanta.

The Centers for Disease Control and Prevention recommends screening for iron deficiency anemia in pregnant persons, in addition to universal iron supplementation to meet the iron requirements of pregnancy.  

Additionally, the American College of Obstetricians and Gynecologists recommends that all pregnant persons be screened for anemia with a complete blood count in the first trimester and again between 24 and 28 weeks of pregnancy.

However, iron deficiency is completely missed by ACOG’s recommendations, said Michael Auerbach, MD, of the department of medicine, Georgetown University, Washington. 

“They recommend a [complete blood count] on all presenting pregnant women, but they do not recommend iron parameters, including a ferritin test, unless the mother is anemic,” said Dr. Auerbach, who was not involved in the study. “I think those guidelines are in need of revision.”

Dr. Teichman hopes her team’s findings will motivate change in obstetric and hematologic guidelines that recommend routine prenatal testing.

“I think ferritin should be a part of routine prenatal testing,” Dr. Teichman said. “And I also think that patients need to be empowered to ask what their iron levels are in pregnancy and providers need to know what a normal iron level is.”

None of the experts interviewed for this story had financial conflicts of interest.

Many pregnant patients are not being screened for iron deficiency despite it being a common cause of anemia in pregnancy that could increase the risk of maternal and infant death.

Researchers analyzed data from 44,552 pregnant patients in Ontario, Canada, collected between 2013 and 2018 to determine the prevalence of ferritin testing, the standard test for iron deficiency, over the course of 5 years.

Their study, published in Blood Advances, revealed that only 59.4% of pregnant persons received a ferritin test, the standard test for iron deficiency. Of those pregnant persons, 25.2% were iron insufficient and 52.8% were iron deficient at least once during pregnancy.

They also found that 71% of these iron tests were ordered during the first trimester, when the risk of iron deficiency is lowest.

“We are not only missing a very large proportion of women who are iron deficient going into pregnancy, but we’re missing those that become iron deficient later on in their pregnancies,” study author Dr. Jennifer Teichman, hematology resident at the University of Toronto, said in an interview. Researchers said iron deficiency during pregnancy is associated with maternal fatigue, cognitive dysfunction, depression, low birth weight, and poor brain development of the child.

Dr. Teichman explained that if iron deficiency during pregnancy is identified early enough, doctors would have enough time to treat the condition with iron supplements before the patient goes into delivery. She also explained prenatal vitamins, which contain some iron, do not contain enough of the mineral to fix iron deficiency.

“One really important point is that the amount of iron contained in a prenatal vitamin is really low,” Dr. Teichman explained. “It’s enough to make up the difference of the additional iron that she needs to sustain her pregnancy, but it’s not enough to treat a woman who’s already got low iron going into pregnancy. So there’s a difference between a prenatal vitamin and true iron supplementation.”

Researchers also found that those who came from a household with a low annual income were even less likely to receive a ferritin test, which was a troubling finding since women of lower socioeconomic status are more likely to be iron deficient in pregnancy. 

“[This] says something about how we as health care providers are contributing to this gap in care,” Dr. Teichman said. “Women of lower socioeconomic status sort of have a triple whammy: They’re more likely to be iron deficient, they’re less likely to have it diagnosed, and they’re less likely to have it corrected.”

Dr. Teichman and her colleagues took a unique approach by looking at isolated ferritin levels as opposed to complete blood counts, which is the typical screening for anemia in pregnancy, said Lissette Tanner, MD, MPH, FACOG, who was not involved with the study.

“Those who meet the criteria for anemia should be evaluated for the cause with initial suspicion for iron deficiency anemia, as that is the most common etiology,” said Dr. Tanner, assistant professor of gynecology and obstetrics at Emory University, Atlanta.

The Centers for Disease Control and Prevention recommends screening for iron deficiency anemia in pregnant persons, in addition to universal iron supplementation to meet the iron requirements of pregnancy.  

Additionally, the American College of Obstetricians and Gynecologists recommends that all pregnant persons be screened for anemia with a complete blood count in the first trimester and again between 24 and 28 weeks of pregnancy.

However, iron deficiency is completely missed by ACOG’s recommendations, said Michael Auerbach, MD, of the department of medicine, Georgetown University, Washington. 

“They recommend a [complete blood count] on all presenting pregnant women, but they do not recommend iron parameters, including a ferritin test, unless the mother is anemic,” said Dr. Auerbach, who was not involved in the study. “I think those guidelines are in need of revision.”

Dr. Teichman hopes her team’s findings will motivate change in obstetric and hematologic guidelines that recommend routine prenatal testing.

“I think ferritin should be a part of routine prenatal testing,” Dr. Teichman said. “And I also think that patients need to be empowered to ask what their iron levels are in pregnancy and providers need to know what a normal iron level is.”

None of the experts interviewed for this story had financial conflicts of interest.

Many pregnant patients are not being screened for iron deficiency despite it being a common cause of anemia in pregnancy that could increase the risk of maternal and infant death.

Researchers analyzed data from 44,552 pregnant patients in Ontario, Canada, collected between 2013 and 2018 to determine the prevalence of ferritin testing, the standard test for iron deficiency, over the course of 5 years.

Their study, published in Blood Advances, revealed that only 59.4% of pregnant persons received a ferritin test, the standard test for iron deficiency. Of those pregnant persons, 25.2% were iron insufficient and 52.8% were iron deficient at least once during pregnancy.

They also found that 71% of these iron tests were ordered during the first trimester, when the risk of iron deficiency is lowest.

“We are not only missing a very large proportion of women who are iron deficient going into pregnancy, but we’re missing those that become iron deficient later on in their pregnancies,” study author Dr. Jennifer Teichman, hematology resident at the University of Toronto, said in an interview. Researchers said iron deficiency during pregnancy is associated with maternal fatigue, cognitive dysfunction, depression, low birth weight, and poor brain development of the child.

Dr. Teichman explained that if iron deficiency during pregnancy is identified early enough, doctors would have enough time to treat the condition with iron supplements before the patient goes into delivery. She also explained prenatal vitamins, which contain some iron, do not contain enough of the mineral to fix iron deficiency.

“One really important point is that the amount of iron contained in a prenatal vitamin is really low,” Dr. Teichman explained. “It’s enough to make up the difference of the additional iron that she needs to sustain her pregnancy, but it’s not enough to treat a woman who’s already got low iron going into pregnancy. So there’s a difference between a prenatal vitamin and true iron supplementation.”

Researchers also found that those who came from a household with a low annual income were even less likely to receive a ferritin test, which was a troubling finding since women of lower socioeconomic status are more likely to be iron deficient in pregnancy. 

“[This] says something about how we as health care providers are contributing to this gap in care,” Dr. Teichman said. “Women of lower socioeconomic status sort of have a triple whammy: They’re more likely to be iron deficient, they’re less likely to have it diagnosed, and they’re less likely to have it corrected.”

Dr. Teichman and her colleagues took a unique approach by looking at isolated ferritin levels as opposed to complete blood counts, which is the typical screening for anemia in pregnancy, said Lissette Tanner, MD, MPH, FACOG, who was not involved with the study.

“Those who meet the criteria for anemia should be evaluated for the cause with initial suspicion for iron deficiency anemia, as that is the most common etiology,” said Dr. Tanner, assistant professor of gynecology and obstetrics at Emory University, Atlanta.

The Centers for Disease Control and Prevention recommends screening for iron deficiency anemia in pregnant persons, in addition to universal iron supplementation to meet the iron requirements of pregnancy.  

Additionally, the American College of Obstetricians and Gynecologists recommends that all pregnant persons be screened for anemia with a complete blood count in the first trimester and again between 24 and 28 weeks of pregnancy.

However, iron deficiency is completely missed by ACOG’s recommendations, said Michael Auerbach, MD, of the department of medicine, Georgetown University, Washington. 

“They recommend a [complete blood count] on all presenting pregnant women, but they do not recommend iron parameters, including a ferritin test, unless the mother is anemic,” said Dr. Auerbach, who was not involved in the study. “I think those guidelines are in need of revision.”

Dr. Teichman hopes her team’s findings will motivate change in obstetric and hematologic guidelines that recommend routine prenatal testing.

“I think ferritin should be a part of routine prenatal testing,” Dr. Teichman said. “And I also think that patients need to be empowered to ask what their iron levels are in pregnancy and providers need to know what a normal iron level is.”

None of the experts interviewed for this story had financial conflicts of interest.

With more than 300 genetic skin disorders involving more than 1,000 genes and hundreds of genetic tests available on the market, it can be daunting for health care providers and families of pediatric patients to navigate the landscape.

“Testing options range from targeted variant testing and single-gene testing to exome and genome sequencing,” Gabriele Richard, MD, said at the annual meeting of the Society for Pediatric Dermatology. “It is not always easy to determine which testing is right.”

Increasingly, clinical genomic tests, including exome and genome sequencing, are used for patients with complex phenotypes, and possibly multiple disorders, who might have no diagnosis despite extensive prior testing, said Dr. Richard, medical director at Gaithersburg, Md.–based GeneDx., a molecular diagnostic laboratory that performs comprehensive testing for rare genetic disorders. These tests are also being used more for first-line testing in critically ill patients in the neonatal and pediatric intensive care units, and “have heralded a whole new era of gene and disease discovery,” she added.

Targeted variant testing is used for known familial variants, to test family members for carrier status and segregation, and to make a prenatal diagnosis, she said. Single-gene testing is available for most genes and has its place for conditions that can be clinically well-recognized, such as ichthyosis vulgaris, Darier disease, or Papillon-Lefèvre syndrome.

Specific tests for identifying gene deletions or duplications are exon-level microarrays, multiplex ligation-dependent probe amplification (MLPA), and chromosomal microarray analysis. “The latter has been successful in identifying diseases causing chromosomal abnormalities in over 10% of cases overall,” Dr. Richard said. An example of a skin disorder is X-linked ichthyosis caused by a deletion of the steroid sulfatase locus in more than 95% of affected males, she said.

“However, the current staple of molecular diagnostic testing is multigene next-generation sequencing (NGS) panels, which allow you to interrogate two to hundreds of genes concurrently, including sequencing and deletion duplication testing.” These tests are the most cost effective, she said, and are available for almost any genodermatosis or group of disorders with overlapping phenotypes, such as albinism or ichthyosis, epidermolysis bullosa and skin fragility, ectodermal dysplasia, or porphyria. According to Dr. Richard, the diagnostic outcomes of NGS panels mainly depend on test indication, panel size and gene curation, age of onset, and prevailing inheritance pattern of disorders.

Her recommended criteria for distinguishing the myriad of available NGS panels include checking gene content, technical sensitivity of sequencing and deletion/duplication analysis, quality of variant interpretation and reporting, turn-around time, and available familial follow-up testing. “If a family might consider future prenatal diagnosis, choose the lab that performs prenatal and diagnostic testing,” Dr. Richard said. “Equally important are client services such as ease of ordering, insurance coverage, and the ability to determine out-of-pocket cost to patients.”

Resources that enable consumers to compare panel content, methodology, turnaround time, and other parameters include the Genetic Testing Registry (GTR) operated by the National Center for Biotechnology Information, and Concert Genetics, a genetic testing company. The National Society of Genetic Counselors also offers a searchable database for finding a genetic counselor.

Exome sequencing includes the coding sequences of about 20,000 genes and has an average depth of 50 to about 150 reads. “It is a phenotype-driven test where only select variants are being reported fitting the phenotype,” Dr. Richard said. “The outcome of exome and genome sequencing much depends on optimization of bioinformatic pipelines and tools.” Besides small sequence variants, exome sequencing is able to identify a variety of different types of disease-causing variants, such as gene copy number variants seen in about 6% of positive cases, mosaicism, regions of homozygosity, uniparental disomy, and other unusual events and is cost effective.

Whole-genome sequencing, meanwhile, includes the entire genome, particularly noncoding regions, and has an average depth of more than 30 reads. “It’s based on single-molecule sequencing, has longer reads and more uniform coverage, compared to exome sequencing,” she said. “Higher cost, variant interpretation, and lack of coverage by payers are still presenting challenges for genome sequencing.” Genome sequencing can be done in a day or less.

According to diagnostic outcomes based on 280,000 individuals including 125,000 probands from GeneDx data, a definitive diagnosis was made in 26% of probands, of which 2.8% had more than one diagnostic finding and 1.8% had actionable secondary findings. In addition, 7% of the variants were found in candidate genes; 31% of probands had variants of uncertain significance, while 36% tested negative. “Nevertheless, the diagnostic yield of exome sequencing depends on the phenotype and cohort studied,” Dr. Richard continued.

At her company, she said, the highest positive rate is for multiple congenital anomalies (34%), skeletal system abnormalities (30%), and nervous system abnormalities (29%). Trio testing – the concurrent analysis of both biological parents and proband for all genes – “is a critical factor for success,” she added. “It not only improves the variant calling because we have three times the data and increases test sensitivity, it also provides more certain results, determines inheritance and allows for detection of parental mosaicism.”

According to Dr. Richard, trio testing has a one-third higher diagnostic rate than sequencing of the proband alone. Citing a published prospective study that compiled data from eight different exome- and genome-sequencing studies in critically ill neonates and children, trio testing made it possible to make a genetic diagnosis in up to 58% of children.

Whole-genome sequencing is estimated to have a 5%-10% higher diagnostic rate than exome sequencing. “However, we are still a ways away from using it as a routine diagnostic test for all test indications,” Dr. Richard said. “Automation, special bioinformatics algorithms and databases, and combination of genome sequencing with mRNA sequencing are being explored and built to further improve the diagnostic yield.”

Dr. Richard had no disclosures other than being an employee of GeneDx.

[email protected]

With more than 300 genetic skin disorders involving more than 1,000 genes and hundreds of genetic tests available on the market, it can be daunting for health care providers and families of pediatric patients to navigate the landscape.

“Testing options range from targeted variant testing and single-gene testing to exome and genome sequencing,” Gabriele Richard, MD, said at the annual meeting of the Society for Pediatric Dermatology. “It is not always easy to determine which testing is right.”

Increasingly, clinical genomic tests, including exome and genome sequencing, are used for patients with complex phenotypes, and possibly multiple disorders, who might have no diagnosis despite extensive prior testing, said Dr. Richard, medical director at Gaithersburg, Md.–based GeneDx., a molecular diagnostic laboratory that performs comprehensive testing for rare genetic disorders. These tests are also being used more for first-line testing in critically ill patients in the neonatal and pediatric intensive care units, and “have heralded a whole new era of gene and disease discovery,” she added.

Targeted variant testing is used for known familial variants, to test family members for carrier status and segregation, and to make a prenatal diagnosis, she said. Single-gene testing is available for most genes and has its place for conditions that can be clinically well-recognized, such as ichthyosis vulgaris, Darier disease, or Papillon-Lefèvre syndrome.

Specific tests for identifying gene deletions or duplications are exon-level microarrays, multiplex ligation-dependent probe amplification (MLPA), and chromosomal microarray analysis. “The latter has been successful in identifying diseases causing chromosomal abnormalities in over 10% of cases overall,” Dr. Richard said. An example of a skin disorder is X-linked ichthyosis caused by a deletion of the steroid sulfatase locus in more than 95% of affected males, she said.

“However, the current staple of molecular diagnostic testing is multigene next-generation sequencing (NGS) panels, which allow you to interrogate two to hundreds of genes concurrently, including sequencing and deletion duplication testing.” These tests are the most cost effective, she said, and are available for almost any genodermatosis or group of disorders with overlapping phenotypes, such as albinism or ichthyosis, epidermolysis bullosa and skin fragility, ectodermal dysplasia, or porphyria. According to Dr. Richard, the diagnostic outcomes of NGS panels mainly depend on test indication, panel size and gene curation, age of onset, and prevailing inheritance pattern of disorders.

Her recommended criteria for distinguishing the myriad of available NGS panels include checking gene content, technical sensitivity of sequencing and deletion/duplication analysis, quality of variant interpretation and reporting, turn-around time, and available familial follow-up testing. “If a family might consider future prenatal diagnosis, choose the lab that performs prenatal and diagnostic testing,” Dr. Richard said. “Equally important are client services such as ease of ordering, insurance coverage, and the ability to determine out-of-pocket cost to patients.”

Resources that enable consumers to compare panel content, methodology, turnaround time, and other parameters include the Genetic Testing Registry (GTR) operated by the National Center for Biotechnology Information, and Concert Genetics, a genetic testing company. The National Society of Genetic Counselors also offers a searchable database for finding a genetic counselor.

Exome sequencing includes the coding sequences of about 20,000 genes and has an average depth of 50 to about 150 reads. “It is a phenotype-driven test where only select variants are being reported fitting the phenotype,” Dr. Richard said. “The outcome of exome and genome sequencing much depends on optimization of bioinformatic pipelines and tools.” Besides small sequence variants, exome sequencing is able to identify a variety of different types of disease-causing variants, such as gene copy number variants seen in about 6% of positive cases, mosaicism, regions of homozygosity, uniparental disomy, and other unusual events and is cost effective.

Whole-genome sequencing, meanwhile, includes the entire genome, particularly noncoding regions, and has an average depth of more than 30 reads. “It’s based on single-molecule sequencing, has longer reads and more uniform coverage, compared to exome sequencing,” she said. “Higher cost, variant interpretation, and lack of coverage by payers are still presenting challenges for genome sequencing.” Genome sequencing can be done in a day or less.

According to diagnostic outcomes based on 280,000 individuals including 125,000 probands from GeneDx data, a definitive diagnosis was made in 26% of probands, of which 2.8% had more than one diagnostic finding and 1.8% had actionable secondary findings. In addition, 7% of the variants were found in candidate genes; 31% of probands had variants of uncertain significance, while 36% tested negative. “Nevertheless, the diagnostic yield of exome sequencing depends on the phenotype and cohort studied,” Dr. Richard continued.

At her company, she said, the highest positive rate is for multiple congenital anomalies (34%), skeletal system abnormalities (30%), and nervous system abnormalities (29%). Trio testing – the concurrent analysis of both biological parents and proband for all genes – “is a critical factor for success,” she added. “It not only improves the variant calling because we have three times the data and increases test sensitivity, it also provides more certain results, determines inheritance and allows for detection of parental mosaicism.”

According to Dr. Richard, trio testing has a one-third higher diagnostic rate than sequencing of the proband alone. Citing a published prospective study that compiled data from eight different exome- and genome-sequencing studies in critically ill neonates and children, trio testing made it possible to make a genetic diagnosis in up to 58% of children.

Whole-genome sequencing is estimated to have a 5%-10% higher diagnostic rate than exome sequencing. “However, we are still a ways away from using it as a routine diagnostic test for all test indications,” Dr. Richard said. “Automation, special bioinformatics algorithms and databases, and combination of genome sequencing with mRNA sequencing are being explored and built to further improve the diagnostic yield.”

Dr. Richard had no disclosures other than being an employee of GeneDx.

[email protected]

With more than 300 genetic skin disorders involving more than 1,000 genes and hundreds of genetic tests available on the market, it can be daunting for health care providers and families of pediatric patients to navigate the landscape.

“Testing options range from targeted variant testing and single-gene testing to exome and genome sequencing,” Gabriele Richard, MD, said at the annual meeting of the Society for Pediatric Dermatology. “It is not always easy to determine which testing is right.”

Increasingly, clinical genomic tests, including exome and genome sequencing, are used for patients with complex phenotypes, and possibly multiple disorders, who might have no diagnosis despite extensive prior testing, said Dr. Richard, medical director at Gaithersburg, Md.–based GeneDx., a molecular diagnostic laboratory that performs comprehensive testing for rare genetic disorders. These tests are also being used more for first-line testing in critically ill patients in the neonatal and pediatric intensive care units, and “have heralded a whole new era of gene and disease discovery,” she added.

Targeted variant testing is used for known familial variants, to test family members for carrier status and segregation, and to make a prenatal diagnosis, she said. Single-gene testing is available for most genes and has its place for conditions that can be clinically well-recognized, such as ichthyosis vulgaris, Darier disease, or Papillon-Lefèvre syndrome.

Specific tests for identifying gene deletions or duplications are exon-level microarrays, multiplex ligation-dependent probe amplification (MLPA), and chromosomal microarray analysis. “The latter has been successful in identifying diseases causing chromosomal abnormalities in over 10% of cases overall,” Dr. Richard said. An example of a skin disorder is X-linked ichthyosis caused by a deletion of the steroid sulfatase locus in more than 95% of affected males, she said.

“However, the current staple of molecular diagnostic testing is multigene next-generation sequencing (NGS) panels, which allow you to interrogate two to hundreds of genes concurrently, including sequencing and deletion duplication testing.” These tests are the most cost effective, she said, and are available for almost any genodermatosis or group of disorders with overlapping phenotypes, such as albinism or ichthyosis, epidermolysis bullosa and skin fragility, ectodermal dysplasia, or porphyria. According to Dr. Richard, the diagnostic outcomes of NGS panels mainly depend on test indication, panel size and gene curation, age of onset, and prevailing inheritance pattern of disorders.

Her recommended criteria for distinguishing the myriad of available NGS panels include checking gene content, technical sensitivity of sequencing and deletion/duplication analysis, quality of variant interpretation and reporting, turn-around time, and available familial follow-up testing. “If a family might consider future prenatal diagnosis, choose the lab that performs prenatal and diagnostic testing,” Dr. Richard said. “Equally important are client services such as ease of ordering, insurance coverage, and the ability to determine out-of-pocket cost to patients.”

Resources that enable consumers to compare panel content, methodology, turnaround time, and other parameters include the Genetic Testing Registry (GTR) operated by the National Center for Biotechnology Information, and Concert Genetics, a genetic testing company. The National Society of Genetic Counselors also offers a searchable database for finding a genetic counselor.

Exome sequencing includes the coding sequences of about 20,000 genes and has an average depth of 50 to about 150 reads. “It is a phenotype-driven test where only select variants are being reported fitting the phenotype,” Dr. Richard said. “The outcome of exome and genome sequencing much depends on optimization of bioinformatic pipelines and tools.” Besides small sequence variants, exome sequencing is able to identify a variety of different types of disease-causing variants, such as gene copy number variants seen in about 6% of positive cases, mosaicism, regions of homozygosity, uniparental disomy, and other unusual events and is cost effective.

Whole-genome sequencing, meanwhile, includes the entire genome, particularly noncoding regions, and has an average depth of more than 30 reads. “It’s based on single-molecule sequencing, has longer reads and more uniform coverage, compared to exome sequencing,” she said. “Higher cost, variant interpretation, and lack of coverage by payers are still presenting challenges for genome sequencing.” Genome sequencing can be done in a day or less.

According to diagnostic outcomes based on 280,000 individuals including 125,000 probands from GeneDx data, a definitive diagnosis was made in 26% of probands, of which 2.8% had more than one diagnostic finding and 1.8% had actionable secondary findings. In addition, 7% of the variants were found in candidate genes; 31% of probands had variants of uncertain significance, while 36% tested negative. “Nevertheless, the diagnostic yield of exome sequencing depends on the phenotype and cohort studied,” Dr. Richard continued.

At her company, she said, the highest positive rate is for multiple congenital anomalies (34%), skeletal system abnormalities (30%), and nervous system abnormalities (29%). Trio testing – the concurrent analysis of both biological parents and proband for all genes – “is a critical factor for success,” she added. “It not only improves the variant calling because we have three times the data and increases test sensitivity, it also provides more certain results, determines inheritance and allows for detection of parental mosaicism.”

According to Dr. Richard, trio testing has a one-third higher diagnostic rate than sequencing of the proband alone. Citing a published prospective study that compiled data from eight different exome- and genome-sequencing studies in critically ill neonates and children, trio testing made it possible to make a genetic diagnosis in up to 58% of children.

Whole-genome sequencing is estimated to have a 5%-10% higher diagnostic rate than exome sequencing. “However, we are still a ways away from using it as a routine diagnostic test for all test indications,” Dr. Richard said. “Automation, special bioinformatics algorithms and databases, and combination of genome sequencing with mRNA sequencing are being explored and built to further improve the diagnostic yield.”

Dr. Richard had no disclosures other than being an employee of GeneDx.

[email protected]

Clinical symptoms in a 19-year-old Vietnamese woman who experienced several life-threatening bleeding events, including ovarian hemorrhage, led to the discovery of a novel gene variant causing her bleeding disorder.

Blood analysis of the patients showed decreased fibrinogen level with “markedly elevated fibrinogen/fibrin degradation products and D-dimer levels.” Attempts to treat the patient with hemostatic surgery, administration of several medications, including nafamostat mesylate, tranexamic acid, and unfractionated heparin, produced no correction of her coagulation abnormalities, and the patient experienced repeated hemorrhagic events, according to researchers from the Tokyo Saiseikai Central Hospital, Japan, and colleagues.

However, the researchers found that treatment with recombinant human thrombomodulin (rhTM) remarkably improved the patient’s pathophysiology, according to the results of a case study reported in Blood Advances.
 

Genetic analysis

Upon screening and sequencing of the patient’s thrombomodulin gene, a previously unreported homozygous variation, c.793T>A (p.Cys265Ser) was discovered. Under normal circumstances, the Cys265 residue forms one of three disulfide bonds in the epidermal growth factor (EGF)-like domain 1 of thrombomoduliin (TM), according to the researchers.

However, transient expression analysis of the patient’s mutation using COS-1 cells demonstrated markedly reduced expression of TM-Cys265Ser on the plasma membrane relative to wild-type TM. The TM-Cys265Ser mutant was intracellularly degraded, probably due to EGF-like domain 1 misfolding, according to the researchers and the reduced expression of TM on the endothelial cell membrane may be responsible for the disseminated intravascular coagulation-like symptoms observed in the patient, the speculated.

“The clinical symptoms of the patient in this study were characterized by recurrent hemorrhage, indicating that TM-C265S mainly causes hyperfibrinolysis rather than hypercoagulation. The C265S mutation may disrupt the timely and delicate balance between coagulation and fibrinolysis,” the researchers suggested.

The authors reported that they had no conflicts of interest.

[email protected]

Clinical symptoms in a 19-year-old Vietnamese woman who experienced several life-threatening bleeding events, including ovarian hemorrhage, led to the discovery of a novel gene variant causing her bleeding disorder.

Blood analysis of the patients showed decreased fibrinogen level with “markedly elevated fibrinogen/fibrin degradation products and D-dimer levels.” Attempts to treat the patient with hemostatic surgery, administration of several medications, including nafamostat mesylate, tranexamic acid, and unfractionated heparin, produced no correction of her coagulation abnormalities, and the patient experienced repeated hemorrhagic events, according to researchers from the Tokyo Saiseikai Central Hospital, Japan, and colleagues.

However, the researchers found that treatment with recombinant human thrombomodulin (rhTM) remarkably improved the patient’s pathophysiology, according to the results of a case study reported in Blood Advances.
 

Genetic analysis

Upon screening and sequencing of the patient’s thrombomodulin gene, a previously unreported homozygous variation, c.793T>A (p.Cys265Ser) was discovered. Under normal circumstances, the Cys265 residue forms one of three disulfide bonds in the epidermal growth factor (EGF)-like domain 1 of thrombomoduliin (TM), according to the researchers.

However, transient expression analysis of the patient’s mutation using COS-1 cells demonstrated markedly reduced expression of TM-Cys265Ser on the plasma membrane relative to wild-type TM. The TM-Cys265Ser mutant was intracellularly degraded, probably due to EGF-like domain 1 misfolding, according to the researchers and the reduced expression of TM on the endothelial cell membrane may be responsible for the disseminated intravascular coagulation-like symptoms observed in the patient, the speculated.

“The clinical symptoms of the patient in this study were characterized by recurrent hemorrhage, indicating that TM-C265S mainly causes hyperfibrinolysis rather than hypercoagulation. The C265S mutation may disrupt the timely and delicate balance between coagulation and fibrinolysis,” the researchers suggested.

The authors reported that they had no conflicts of interest.

[email protected]

Clinical symptoms in a 19-year-old Vietnamese woman who experienced several life-threatening bleeding events, including ovarian hemorrhage, led to the discovery of a novel gene variant causing her bleeding disorder.

Blood analysis of the patients showed decreased fibrinogen level with “markedly elevated fibrinogen/fibrin degradation products and D-dimer levels.” Attempts to treat the patient with hemostatic surgery, administration of several medications, including nafamostat mesylate, tranexamic acid, and unfractionated heparin, produced no correction of her coagulation abnormalities, and the patient experienced repeated hemorrhagic events, according to researchers from the Tokyo Saiseikai Central Hospital, Japan, and colleagues.

However, the researchers found that treatment with recombinant human thrombomodulin (rhTM) remarkably improved the patient’s pathophysiology, according to the results of a case study reported in Blood Advances.
 

Genetic analysis

Upon screening and sequencing of the patient’s thrombomodulin gene, a previously unreported homozygous variation, c.793T>A (p.Cys265Ser) was discovered. Under normal circumstances, the Cys265 residue forms one of three disulfide bonds in the epidermal growth factor (EGF)-like domain 1 of thrombomoduliin (TM), according to the researchers.

However, transient expression analysis of the patient’s mutation using COS-1 cells demonstrated markedly reduced expression of TM-Cys265Ser on the plasma membrane relative to wild-type TM. The TM-Cys265Ser mutant was intracellularly degraded, probably due to EGF-like domain 1 misfolding, according to the researchers and the reduced expression of TM on the endothelial cell membrane may be responsible for the disseminated intravascular coagulation-like symptoms observed in the patient, the speculated.

“The clinical symptoms of the patient in this study were characterized by recurrent hemorrhage, indicating that TM-C265S mainly causes hyperfibrinolysis rather than hypercoagulation. The C265S mutation may disrupt the timely and delicate balance between coagulation and fibrinolysis,” the researchers suggested.

The authors reported that they had no conflicts of interest.

[email protected]

Autoeczematization (AE), or id reaction, is a disseminated eczematous reaction that occurs days or weeks after exposure to a primary stimulus, resulting from a release of antigen(s). Whitfield¹ first described AE in 1921, when he postulated that the id reaction was due to sensitization of the skin after a primary stimulus. He called it “a form of auto-intoxication derived from changes in the patient’s own tissues.”¹ The exact prevalence of id reactions is unknown; one study showed that 17% of patients with dermatophyte infections developed an id reaction, typically tinea pedis linked with vesicles on the palms.² Tinea capitis is one of the most common causes of AE in children, which is frequently misdiagnosed as a drug reaction. Approximately 37% of patients diagnosed with stasis dermatitis develop an id reaction (Figure 1). A history of contact dermatitis is common in patients presenting with AE.^2-6

Pathophysiology of Id Reactions

An abnormal immune response against autologous skin antigens may be responsible for the development of AE. Shelley⁵ postulated that hair follicles play an important role in id reactions, as Sharquie et al⁶ recently emphasized for many skin disorders. The pathogenesis of AE is uncertain, but circulating T lymphocytes play a role in this reaction. Normally, T cells are activated by a release of antigens after a primary exposure to a stimulus. However, overactivation of these T cells induces autoimmune reactions such as AE.⁷ Activated T lymphocytes express HLA-DR and IL-2 receptor, markers elevated in the peripheral blood of patients undergoing id reactions. After treatment, the levels of activated T lymphocytes decline. An increase in the number of CD25⁺ T cells and a decrease in the number of suppressor T cells in the blood may occur during an id reaction.^7-9 Keratinocytes produce proinflammatory cytokines, such as thymic stromal erythropoietin, IL-25, and IL-33, that activate T cells.^10-12 Therefore, the most likely pathogenesis of an id reaction is that T lymphocytes are activated at the primary reaction site due to proinflammatory cytokines released by keratinocytes. These activated T cells then travel systemically via hematogenous dissemination. The spread of activated T lymphocytes produces an eczematous reaction at secondary locations distant to the primary site.⁹

Clinical and Histopathological Features of Id Reactions

Clinically, AE is first evident as a vesicular dissemination that groups to form papules or nummular patches and usually is present on the legs, feet, arms, and/or trunk (Figure 2). The primary dermatitis is localized to the area that was the site of contact to the offending stimuli. This localized eczematous eruption begins with an acute or subacute onset. It has the appearance of small crusted vesicles with erythema (Figure 1). The first sign of AE is vesicles presenting near the primary site on flexural surfaces or on the hands and feet. A classic example is tinea pedis linked with vesicles on the palms and sides of the fingers, resembling dyshidrotic eczema. Sites of prior cutaneous trauma, such as dermatoses, scars, and burns, are common locations for early AE. In later stages, vesicles disseminate to the legs, arms, and trunk, where they group to form papules and nummular patches in a symmetrical pattern.^5,13-15 These lesions may be extremely pruritic. The pruritus may be so intense that it interrupts daily activities and disrupts the ability to fall or stay asleep.¹⁶

Histologically, biopsy specimens show psoriasiform spongiotic dermatitis with mononuclear cells contained in the vesicles. Interstitial edema and perivascular lymphohistiocytic infiltrates are evident. Eosinophils also may be present. This pattern is not unique toid reactions.^17-19 Although AE is a reaction pattern that may be due to a fungal or bacterial infection, the etiologic agent is not evident microscopically within the eczema itself.

Etiology of Id Reactions

Id reactions most commonly occur from either stasis dermatitis or tinea pedis, although a wide variety of other causes should be considered. Evaluation of the primary site rather than the id reaction may identify an infectious or parasitic agent. Sometimes the AE reaction is specifically named: dermatophytid with dermatophytosis, bacterid with a bacterial infectious process, and tuberculid with tuberculosis. Similarly, there may be reactions to underlying candidiasis, sporotrichosis, histoplasmosis, and other fungal infections that can cause a cutaneous id reaction.^18,20-22Mycobacterium species, Pseudomonas, Staphylococcus, and Streptococcus are bacterial causes of AE.^15,23-26 Viral infections that can cause an id reaction are herpes simplex virus and molluscum contagiosum.^27-29 Scabies, leishmaniasis, and pediculosis capitis are parasitic infections that may be etiologic.^14,30,31 In addition, noninfectious stimuli besides stasis dermatitis that can produce id reactions include medications, topical creams, tattoo ink, sutures, radiotherapy, and dyshidrotic eczema. The primary reaction to these agents is a localized dermatitis followed by the immunological response that induces a secondary reaction distant from the primary site.^17,18,32-38

Differential Diagnoses

Differential diagnoses include other types of eczema and some vesicular eruptions. Irritant contact dermatitis is another dermatosis that presents as a widespread vesicular eruption due to repetitive exposure to toxic irritants. The rash is erythematous with pustules, blisters, and crusts. It is only found in areas directly exposed to irritants, as opposed to AE, which spreads to areas distant to the primary reaction site. Irritant contact dermatitis presents with more of a burning sensation, whereas AE is more pruritic.^39,40 Allergic contact dermatitis presents with erythematous vesicles and papules and sometimes with bullae. There is edema and crust formation, which often can spread past the point of contact in later stages. Similar to AE, there is intense pruritus. However, allergic contact dermatitis most commonly is caused by exposure to metals, cosmetics, and fragrances, whereas infectious agents and stasis dermatitis are the most common causes of AE.^40,41 It may be challenging to distinguish AE from other causes of widespread eczematous dissemination. Vesicular eruptions sometimes require distinction from AE, including herpetic infections, insect bite reactions, and drug eruptions.^18,42

Treatment

The underlying condition should be treated to mitigate the inflammatory response causing the id reaction. If not skillfully orchestrated, the id reaction can reoccur. For infectious causes of AE, an antifungal, antibacterial, antiviral, or antiparasitic should be given. If stasis dermatitis is responsible for the id reaction, compression stockings and leg elevation are indicated. The id reaction itself is treated with systemic or topical corticosteroids and wet compresses if acute. The goal of these treatments is to reduce patient discomfort caused by the inflammation and pruritus.^18,43

Conclusion

Id reactions are an unusual phenomenon that commonly occurs after fungal skin infections and stasis dermatitis. T lymphocytes and keratinocytes may play a key role in this reaction, with newer research further delineating the process and possibly providing enhanced treatment options. Therapy focuses on treating the underlying condition, supplemented with corticosteroids for the autoeczema.

Autoeczematization (AE), or id reaction, is a disseminated eczematous reaction that occurs days or weeks after exposure to a primary stimulus, resulting from a release of antigen(s). Whitfield¹ first described AE in 1921, when he postulated that the id reaction was due to sensitization of the skin after a primary stimulus. He called it “a form of auto-intoxication derived from changes in the patient’s own tissues.”¹ The exact prevalence of id reactions is unknown; one study showed that 17% of patients with dermatophyte infections developed an id reaction, typically tinea pedis linked with vesicles on the palms.² Tinea capitis is one of the most common causes of AE in children, which is frequently misdiagnosed as a drug reaction. Approximately 37% of patients diagnosed with stasis dermatitis develop an id reaction (Figure 1). A history of contact dermatitis is common in patients presenting with AE.^2-6

Pathophysiology of Id Reactions

An abnormal immune response against autologous skin antigens may be responsible for the development of AE. Shelley⁵ postulated that hair follicles play an important role in id reactions, as Sharquie et al⁶ recently emphasized for many skin disorders. The pathogenesis of AE is uncertain, but circulating T lymphocytes play a role in this reaction. Normally, T cells are activated by a release of antigens after a primary exposure to a stimulus. However, overactivation of these T cells induces autoimmune reactions such as AE.⁷ Activated T lymphocytes express HLA-DR and IL-2 receptor, markers elevated in the peripheral blood of patients undergoing id reactions. After treatment, the levels of activated T lymphocytes decline. An increase in the number of CD25⁺ T cells and a decrease in the number of suppressor T cells in the blood may occur during an id reaction.^7-9 Keratinocytes produce proinflammatory cytokines, such as thymic stromal erythropoietin, IL-25, and IL-33, that activate T cells.^10-12 Therefore, the most likely pathogenesis of an id reaction is that T lymphocytes are activated at the primary reaction site due to proinflammatory cytokines released by keratinocytes. These activated T cells then travel systemically via hematogenous dissemination. The spread of activated T lymphocytes produces an eczematous reaction at secondary locations distant to the primary site.⁹

Clinical and Histopathological Features of Id Reactions

Clinically, AE is first evident as a vesicular dissemination that groups to form papules or nummular patches and usually is present on the legs, feet, arms, and/or trunk (Figure 2). The primary dermatitis is localized to the area that was the site of contact to the offending stimuli. This localized eczematous eruption begins with an acute or subacute onset. It has the appearance of small crusted vesicles with erythema (Figure 1). The first sign of AE is vesicles presenting near the primary site on flexural surfaces or on the hands and feet. A classic example is tinea pedis linked with vesicles on the palms and sides of the fingers, resembling dyshidrotic eczema. Sites of prior cutaneous trauma, such as dermatoses, scars, and burns, are common locations for early AE. In later stages, vesicles disseminate to the legs, arms, and trunk, where they group to form papules and nummular patches in a symmetrical pattern.^5,13-15 These lesions may be extremely pruritic. The pruritus may be so intense that it interrupts daily activities and disrupts the ability to fall or stay asleep.¹⁶

Histologically, biopsy specimens show psoriasiform spongiotic dermatitis with mononuclear cells contained in the vesicles. Interstitial edema and perivascular lymphohistiocytic infiltrates are evident. Eosinophils also may be present. This pattern is not unique toid reactions.^17-19 Although AE is a reaction pattern that may be due to a fungal or bacterial infection, the etiologic agent is not evident microscopically within the eczema itself.

Etiology of Id Reactions

Id reactions most commonly occur from either stasis dermatitis or tinea pedis, although a wide variety of other causes should be considered. Evaluation of the primary site rather than the id reaction may identify an infectious or parasitic agent. Sometimes the AE reaction is specifically named: dermatophytid with dermatophytosis, bacterid with a bacterial infectious process, and tuberculid with tuberculosis. Similarly, there may be reactions to underlying candidiasis, sporotrichosis, histoplasmosis, and other fungal infections that can cause a cutaneous id reaction.^18,20-22Mycobacterium species, Pseudomonas, Staphylococcus, and Streptococcus are bacterial causes of AE.^15,23-26 Viral infections that can cause an id reaction are herpes simplex virus and molluscum contagiosum.^27-29 Scabies, leishmaniasis, and pediculosis capitis are parasitic infections that may be etiologic.^14,30,31 In addition, noninfectious stimuli besides stasis dermatitis that can produce id reactions include medications, topical creams, tattoo ink, sutures, radiotherapy, and dyshidrotic eczema. The primary reaction to these agents is a localized dermatitis followed by the immunological response that induces a secondary reaction distant from the primary site.^17,18,32-38

Differential Diagnoses

Differential diagnoses include other types of eczema and some vesicular eruptions. Irritant contact dermatitis is another dermatosis that presents as a widespread vesicular eruption due to repetitive exposure to toxic irritants. The rash is erythematous with pustules, blisters, and crusts. It is only found in areas directly exposed to irritants, as opposed to AE, which spreads to areas distant to the primary reaction site. Irritant contact dermatitis presents with more of a burning sensation, whereas AE is more pruritic.^39,40 Allergic contact dermatitis presents with erythematous vesicles and papules and sometimes with bullae. There is edema and crust formation, which often can spread past the point of contact in later stages. Similar to AE, there is intense pruritus. However, allergic contact dermatitis most commonly is caused by exposure to metals, cosmetics, and fragrances, whereas infectious agents and stasis dermatitis are the most common causes of AE.^40,41 It may be challenging to distinguish AE from other causes of widespread eczematous dissemination. Vesicular eruptions sometimes require distinction from AE, including herpetic infections, insect bite reactions, and drug eruptions.^18,42

Treatment

The underlying condition should be treated to mitigate the inflammatory response causing the id reaction. If not skillfully orchestrated, the id reaction can reoccur. For infectious causes of AE, an antifungal, antibacterial, antiviral, or antiparasitic should be given. If stasis dermatitis is responsible for the id reaction, compression stockings and leg elevation are indicated. The id reaction itself is treated with systemic or topical corticosteroids and wet compresses if acute. The goal of these treatments is to reduce patient discomfort caused by the inflammation and pruritus.^18,43

Conclusion

Id reactions are an unusual phenomenon that commonly occurs after fungal skin infections and stasis dermatitis. T lymphocytes and keratinocytes may play a key role in this reaction, with newer research further delineating the process and possibly providing enhanced treatment options. Therapy focuses on treating the underlying condition, supplemented with corticosteroids for the autoeczema.

Autoeczematization (AE), or id reaction, is a disseminated eczematous reaction that occurs days or weeks after exposure to a primary stimulus, resulting from a release of antigen(s). Whitfield¹ first described AE in 1921, when he postulated that the id reaction was due to sensitization of the skin after a primary stimulus. He called it “a form of auto-intoxication derived from changes in the patient’s own tissues.”¹ The exact prevalence of id reactions is unknown; one study showed that 17% of patients with dermatophyte infections developed an id reaction, typically tinea pedis linked with vesicles on the palms.² Tinea capitis is one of the most common causes of AE in children, which is frequently misdiagnosed as a drug reaction. Approximately 37% of patients diagnosed with stasis dermatitis develop an id reaction (Figure 1). A history of contact dermatitis is common in patients presenting with AE.^2-6

Pathophysiology of Id Reactions

An abnormal immune response against autologous skin antigens may be responsible for the development of AE. Shelley⁵ postulated that hair follicles play an important role in id reactions, as Sharquie et al⁶ recently emphasized for many skin disorders. The pathogenesis of AE is uncertain, but circulating T lymphocytes play a role in this reaction. Normally, T cells are activated by a release of antigens after a primary exposure to a stimulus. However, overactivation of these T cells induces autoimmune reactions such as AE.⁷ Activated T lymphocytes express HLA-DR and IL-2 receptor, markers elevated in the peripheral blood of patients undergoing id reactions. After treatment, the levels of activated T lymphocytes decline. An increase in the number of CD25⁺ T cells and a decrease in the number of suppressor T cells in the blood may occur during an id reaction.^7-9 Keratinocytes produce proinflammatory cytokines, such as thymic stromal erythropoietin, IL-25, and IL-33, that activate T cells.^10-12 Therefore, the most likely pathogenesis of an id reaction is that T lymphocytes are activated at the primary reaction site due to proinflammatory cytokines released by keratinocytes. These activated T cells then travel systemically via hematogenous dissemination. The spread of activated T lymphocytes produces an eczematous reaction at secondary locations distant to the primary site.⁹

Clinical and Histopathological Features of Id Reactions

Clinically, AE is first evident as a vesicular dissemination that groups to form papules or nummular patches and usually is present on the legs, feet, arms, and/or trunk (Figure 2). The primary dermatitis is localized to the area that was the site of contact to the offending stimuli. This localized eczematous eruption begins with an acute or subacute onset. It has the appearance of small crusted vesicles with erythema (Figure 1). The first sign of AE is vesicles presenting near the primary site on flexural surfaces or on the hands and feet. A classic example is tinea pedis linked with vesicles on the palms and sides of the fingers, resembling dyshidrotic eczema. Sites of prior cutaneous trauma, such as dermatoses, scars, and burns, are common locations for early AE. In later stages, vesicles disseminate to the legs, arms, and trunk, where they group to form papules and nummular patches in a symmetrical pattern.^5,13-15 These lesions may be extremely pruritic. The pruritus may be so intense that it interrupts daily activities and disrupts the ability to fall or stay asleep.¹⁶

Histologically, biopsy specimens show psoriasiform spongiotic dermatitis with mononuclear cells contained in the vesicles. Interstitial edema and perivascular lymphohistiocytic infiltrates are evident. Eosinophils also may be present. This pattern is not unique toid reactions.^17-19 Although AE is a reaction pattern that may be due to a fungal or bacterial infection, the etiologic agent is not evident microscopically within the eczema itself.

Etiology of Id Reactions

Id reactions most commonly occur from either stasis dermatitis or tinea pedis, although a wide variety of other causes should be considered. Evaluation of the primary site rather than the id reaction may identify an infectious or parasitic agent. Sometimes the AE reaction is specifically named: dermatophytid with dermatophytosis, bacterid with a bacterial infectious process, and tuberculid with tuberculosis. Similarly, there may be reactions to underlying candidiasis, sporotrichosis, histoplasmosis, and other fungal infections that can cause a cutaneous id reaction.^18,20-22Mycobacterium species, Pseudomonas, Staphylococcus, and Streptococcus are bacterial causes of AE.^15,23-26 Viral infections that can cause an id reaction are herpes simplex virus and molluscum contagiosum.^27-29 Scabies, leishmaniasis, and pediculosis capitis are parasitic infections that may be etiologic.^14,30,31 In addition, noninfectious stimuli besides stasis dermatitis that can produce id reactions include medications, topical creams, tattoo ink, sutures, radiotherapy, and dyshidrotic eczema. The primary reaction to these agents is a localized dermatitis followed by the immunological response that induces a secondary reaction distant from the primary site.^17,18,32-38

Differential Diagnoses

Differential diagnoses include other types of eczema and some vesicular eruptions. Irritant contact dermatitis is another dermatosis that presents as a widespread vesicular eruption due to repetitive exposure to toxic irritants. The rash is erythematous with pustules, blisters, and crusts. It is only found in areas directly exposed to irritants, as opposed to AE, which spreads to areas distant to the primary reaction site. Irritant contact dermatitis presents with more of a burning sensation, whereas AE is more pruritic.^39,40 Allergic contact dermatitis presents with erythematous vesicles and papules and sometimes with bullae. There is edema and crust formation, which often can spread past the point of contact in later stages. Similar to AE, there is intense pruritus. However, allergic contact dermatitis most commonly is caused by exposure to metals, cosmetics, and fragrances, whereas infectious agents and stasis dermatitis are the most common causes of AE.^40,41 It may be challenging to distinguish AE from other causes of widespread eczematous dissemination. Vesicular eruptions sometimes require distinction from AE, including herpetic infections, insect bite reactions, and drug eruptions.^18,42

Treatment

The underlying condition should be treated to mitigate the inflammatory response causing the id reaction. If not skillfully orchestrated, the id reaction can reoccur. For infectious causes of AE, an antifungal, antibacterial, antiviral, or antiparasitic should be given. If stasis dermatitis is responsible for the id reaction, compression stockings and leg elevation are indicated. The id reaction itself is treated with systemic or topical corticosteroids and wet compresses if acute. The goal of these treatments is to reduce patient discomfort caused by the inflammation and pruritus.^18,43

Conclusion

Id reactions are an unusual phenomenon that commonly occurs after fungal skin infections and stasis dermatitis. T lymphocytes and keratinocytes may play a key role in this reaction, with newer research further delineating the process and possibly providing enhanced treatment options. Therapy focuses on treating the underlying condition, supplemented with corticosteroids for the autoeczema.

To the Editor:

Oral immunosuppressive therapies are prescribed for moderate to severe atopic dermatitis. Patients often consult YouTube to make informed decisions about these therapies. In the United States, most health-related online searches are initiated through a search engine, which frequently leads to social media sites such as YouTube. Recent studies have examined the reasons why users turn to the Internet for health-related information, indicating that users typically seek specific information regarding health concerns.^1,2 Furthermore, social media platforms such as YouTube are a popular means of sharing health information with the public.^3-5 Currently, YouTube has more than 1 billion registered users, and 30 million health-related videos are watched each day.⁶ Almost one-third of US consumers use YouTube, Facebook, and Twitter to obtain medical information.⁷ YouTube is a versatile tool because of its video-discovery mechanisms such as a keyword-based search engine, video-recommendation system, highlight feature for videos on home pages, and the capacity to embed YouTube videos on various web pages.⁸ Searchers use videos that are short, fast paced, emotion evoking, from credible sources, recently uploaded, and relevant to the searcher for aiding in health decisions.⁹ Furthermore, studies have demonstrated YouTube’s capacity to support a change in attitude and increase users’ knowledge. In fact, YouTube had higher impact on recall, attitudes, and behaviors when compared with written materials on other social media platforms, such as Facebook and Twitter.⁹ We conducted a cross-sectional study to examine the quality of YouTube videos on oral therapies for atopic dermatitis, such as cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil.

On April 23, 2020, we performed 8 searches using a private browser with default filters on YouTube (Figure). Injectables were not included in the analysis, as the YouTube experience on dupilumab previously has been investigated.¹⁰ The top 40 videos from each search were screened by 3 researchers. Duplicates, non–English-language videos, and videos that did not discuss atopic dermatitis or oral therapies were excluded, resulting in 73 videos included in this analysis. Testimonials generated by patients made up 39 of 73 (53.4%) videos. Health care professionals created 23 of 73 (31.5%) videos, and educators with financial interest created 11 of 73 (15.1%) videos. The dates of production for the videos spanned from 2008 to 2020.

Importantly, this analysis is limited by its lack of quality-assessment tools for video-based resources such as JAMA score and DISCERN score.^14,15 However, these metrics have limited ability to evaluate audiovisual elements, indicating the need for novel tools to score their validity.

To the Editor:

Oral immunosuppressive therapies are prescribed for moderate to severe atopic dermatitis. Patients often consult YouTube to make informed decisions about these therapies. In the United States, most health-related online searches are initiated through a search engine, which frequently leads to social media sites such as YouTube. Recent studies have examined the reasons why users turn to the Internet for health-related information, indicating that users typically seek specific information regarding health concerns.^1,2 Furthermore, social media platforms such as YouTube are a popular means of sharing health information with the public.^3-5 Currently, YouTube has more than 1 billion registered users, and 30 million health-related videos are watched each day.⁶ Almost one-third of US consumers use YouTube, Facebook, and Twitter to obtain medical information.⁷ YouTube is a versatile tool because of its video-discovery mechanisms such as a keyword-based search engine, video-recommendation system, highlight feature for videos on home pages, and the capacity to embed YouTube videos on various web pages.⁸ Searchers use videos that are short, fast paced, emotion evoking, from credible sources, recently uploaded, and relevant to the searcher for aiding in health decisions.⁹ Furthermore, studies have demonstrated YouTube’s capacity to support a change in attitude and increase users’ knowledge. In fact, YouTube had higher impact on recall, attitudes, and behaviors when compared with written materials on other social media platforms, such as Facebook and Twitter.⁹ We conducted a cross-sectional study to examine the quality of YouTube videos on oral therapies for atopic dermatitis, such as cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil.

On April 23, 2020, we performed 8 searches using a private browser with default filters on YouTube (Figure). Injectables were not included in the analysis, as the YouTube experience on dupilumab previously has been investigated.¹⁰ The top 40 videos from each search were screened by 3 researchers. Duplicates, non–English-language videos, and videos that did not discuss atopic dermatitis or oral therapies were excluded, resulting in 73 videos included in this analysis. Testimonials generated by patients made up 39 of 73 (53.4%) videos. Health care professionals created 23 of 73 (31.5%) videos, and educators with financial interest created 11 of 73 (15.1%) videos. The dates of production for the videos spanned from 2008 to 2020.

Importantly, this analysis is limited by its lack of quality-assessment tools for video-based resources such as JAMA score and DISCERN score.^14,15 However, these metrics have limited ability to evaluate audiovisual elements, indicating the need for novel tools to score their validity.

To the Editor:

Oral immunosuppressive therapies are prescribed for moderate to severe atopic dermatitis. Patients often consult YouTube to make informed decisions about these therapies. In the United States, most health-related online searches are initiated through a search engine, which frequently leads to social media sites such as YouTube. Recent studies have examined the reasons why users turn to the Internet for health-related information, indicating that users typically seek specific information regarding health concerns.^1,2 Furthermore, social media platforms such as YouTube are a popular means of sharing health information with the public.^3-5 Currently, YouTube has more than 1 billion registered users, and 30 million health-related videos are watched each day.⁶ Almost one-third of US consumers use YouTube, Facebook, and Twitter to obtain medical information.⁷ YouTube is a versatile tool because of its video-discovery mechanisms such as a keyword-based search engine, video-recommendation system, highlight feature for videos on home pages, and the capacity to embed YouTube videos on various web pages.⁸ Searchers use videos that are short, fast paced, emotion evoking, from credible sources, recently uploaded, and relevant to the searcher for aiding in health decisions.⁹ Furthermore, studies have demonstrated YouTube’s capacity to support a change in attitude and increase users’ knowledge. In fact, YouTube had higher impact on recall, attitudes, and behaviors when compared with written materials on other social media platforms, such as Facebook and Twitter.⁹ We conducted a cross-sectional study to examine the quality of YouTube videos on oral therapies for atopic dermatitis, such as cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil.

On April 23, 2020, we performed 8 searches using a private browser with default filters on YouTube (Figure). Injectables were not included in the analysis, as the YouTube experience on dupilumab previously has been investigated.¹⁰ The top 40 videos from each search were screened by 3 researchers. Duplicates, non–English-language videos, and videos that did not discuss atopic dermatitis or oral therapies were excluded, resulting in 73 videos included in this analysis. Testimonials generated by patients made up 39 of 73 (53.4%) videos. Health care professionals created 23 of 73 (31.5%) videos, and educators with financial interest created 11 of 73 (15.1%) videos. The dates of production for the videos spanned from 2008 to 2020.

Importantly, this analysis is limited by its lack of quality-assessment tools for video-based resources such as JAMA score and DISCERN score.^14,15 However, these metrics have limited ability to evaluate audiovisual elements, indicating the need for novel tools to score their validity.

To the Editor:

Atopic dermatitis (eczema) affects approximately 20% of children worldwide.¹ In atopic dermatitis management, patient education is crucial for optimal outcomes.² The COVID-19 pandemic has impacted patient-physician interactions. To ensure safety of patients and physicians, visits may have been canceled, postponed, or conducted virtually, leaving less time for discussion and questions.³ As a consequence, patients may seek information about atopic dermatitis from alternative sources, including YouTube videos. We performed a cross-sectional study to analyze YouTube videos about topical treatments for atopic dermatitis.

During the week of July 16, 2020, we performed 4 private browser YouTube searches with default filters using the following terms: eczema topicals, eczema topical treatments, atopic dermatitis topicals, and atopic dermatitis topical treatments. For video selection, we defined topical treatments as topical corticosteroids, topical calcineurin inhibitors, crisaborole, emollients, wet wraps, and any prospective treatment topically administered. For each of the 4 searches, 2 researchers (A.M. and A.T.) independently examined the top 75 videos, yielding a total of 300 videos. Of them, 98 videos were duplicates, 19 videos were not about atopic dermatitis, and 91 videos were not about topical treatments, leaving a total of 92 videos for analysis (Figure 1).

Although less popular, professional source videos had a significantly higher DISCERN overall quality rating score (question 16) compared to those categorized as nonprofessional source (3.92 vs 1.53; P<.001). In contrast, nonprofessional source videos scored significantly higher on the quality-of-life question (question 13) compared to professional source videos (3.90 vs 2.56; P<.001)(eTable). (Three professional source videos were removed from YouTube before DISCERN scores could be assigned.)

To the Editor:

Atopic dermatitis (eczema) affects approximately 20% of children worldwide.¹ In atopic dermatitis management, patient education is crucial for optimal outcomes.² The COVID-19 pandemic has impacted patient-physician interactions. To ensure safety of patients and physicians, visits may have been canceled, postponed, or conducted virtually, leaving less time for discussion and questions.³ As a consequence, patients may seek information about atopic dermatitis from alternative sources, including YouTube videos. We performed a cross-sectional study to analyze YouTube videos about topical treatments for atopic dermatitis.

During the week of July 16, 2020, we performed 4 private browser YouTube searches with default filters using the following terms: eczema topicals, eczema topical treatments, atopic dermatitis topicals, and atopic dermatitis topical treatments. For video selection, we defined topical treatments as topical corticosteroids, topical calcineurin inhibitors, crisaborole, emollients, wet wraps, and any prospective treatment topically administered. For each of the 4 searches, 2 researchers (A.M. and A.T.) independently examined the top 75 videos, yielding a total of 300 videos. Of them, 98 videos were duplicates, 19 videos were not about atopic dermatitis, and 91 videos were not about topical treatments, leaving a total of 92 videos for analysis (Figure 1).

Although less popular, professional source videos had a significantly higher DISCERN overall quality rating score (question 16) compared to those categorized as nonprofessional source (3.92 vs 1.53; P<.001). In contrast, nonprofessional source videos scored significantly higher on the quality-of-life question (question 13) compared to professional source videos (3.90 vs 2.56; P<.001)(eTable). (Three professional source videos were removed from YouTube before DISCERN scores could be assigned.)

To the Editor:

Atopic dermatitis (eczema) affects approximately 20% of children worldwide.¹ In atopic dermatitis management, patient education is crucial for optimal outcomes.² The COVID-19 pandemic has impacted patient-physician interactions. To ensure safety of patients and physicians, visits may have been canceled, postponed, or conducted virtually, leaving less time for discussion and questions.³ As a consequence, patients may seek information about atopic dermatitis from alternative sources, including YouTube videos. We performed a cross-sectional study to analyze YouTube videos about topical treatments for atopic dermatitis.

During the week of July 16, 2020, we performed 4 private browser YouTube searches with default filters using the following terms: eczema topicals, eczema topical treatments, atopic dermatitis topicals, and atopic dermatitis topical treatments. For video selection, we defined topical treatments as topical corticosteroids, topical calcineurin inhibitors, crisaborole, emollients, wet wraps, and any prospective treatment topically administered. For each of the 4 searches, 2 researchers (A.M. and A.T.) independently examined the top 75 videos, yielding a total of 300 videos. Of them, 98 videos were duplicates, 19 videos were not about atopic dermatitis, and 91 videos were not about topical treatments, leaving a total of 92 videos for analysis (Figure 1).

Although less popular, professional source videos had a significantly higher DISCERN overall quality rating score (question 16) compared to those categorized as nonprofessional source (3.92 vs 1.53; P<.001). In contrast, nonprofessional source videos scored significantly higher on the quality-of-life question (question 13) compared to professional source videos (3.90 vs 2.56; P<.001)(eTable). (Three professional source videos were removed from YouTube before DISCERN scores could be assigned.)

Plants can contribute to a variety of dermatoses. The Toxicodendron genus, which includes poison ivy, poison oak, and poison sumac, is a well-known and common cause of allergic contact dermatitis (ACD), but many other plants can cause direct or airborne contact dermatitis, especially in gardeners, florists, and farmers. This article provides an overview of different plant-related dermatoses and culprit plants as well as how these dermatoses should be diagnosed and treated.

Epidemiology

Plant dermatoses affect more than 50 million individuals each year.^1,2 In the United States, the Toxicodendron genus causes ACD in more than 70% of exposed individuals, leading to medical visits.³ An urgent care visit for a plant-related dermatitis is estimated to cost $168, while an emergency department visit can cost 3 times as much.⁴ Although less common, Compositae plants are another important culprit of plant dermatitis, particularly in gardeners, florists, and farmers. Data from the 2017-2018 North American Contact Dermatitis Group screening series (N=4947) showed sesquiterpene lactones and Compositae to be positive in 0.5% of patch-tested patients.⁵

Plant Dermatitis Classifications

Plant dermatitis can be classified into 5 main categories: ACD, mechanical irritant contact dermatitis, chemical irritant contact dermatitis, light-mediated dermatitis, and pseudophytodermatitis.⁶

Allergic contact dermatitis is an immune-mediated type IV delayed hypersensitivity reaction. The common molecular allergens in plants include phenols, α-methylene-γ-butyrolactones, quinones, terpenes, disulfides, isothiocyanates, and polyacetylenic derivatives.⁶

Plant contact dermatitis due to mechanical and chemical irritants is precipitated by multiple mechanisms, including disruption of the epidermal barrier and subsequent cytokine release from keratinocytes.⁷ Nonimmunologic contact urticaria from plants is thought to be a type of irritant reaction precipitated by mechanical or chemical trauma.⁸

Light-mediated dermatitis includes phytophotodermatitis and photoallergic contact dermatitis. Phytophotodermatitis is a phototoxic reaction triggered by exposure to both plant-derived furanocoumarin and UVA light.⁹ By contrast, photoallergic contact dermatitis is a delayed hypersensitivity reaction from prior sensitization to a light-activated antigen.¹⁰

Pseudophytodermatitis, as its name implies, is not truly mediated by an allergen or irritant intrinsic to the plant but rather by dyes, waxes, insecticides, or arthropods that inhabit the plant or are secondarily applied.⁶

Common Plant Allergens

Anacardiaceae Family
Most of the allergenic plants within the Anacardiaceae family belong to the Toxicodendron genus, which encompasses poison ivy (Toxicodendron radicans), poison oak (Toxicodendron pubescens,Toxicodendron quercifolium, Toxicodendron diversiloum), and poison sumac (Toxicodendron vernix). Poison ivy is the celebrity of the Anacardiaceae family and contributes to most cases of plant-related ACD. It is found in every state in the continental United States. Poison oak is another common culprit found in the western and southeastern United States.¹¹ Plants within the Anacardiaceae family contain an oleoresin called urushiol, which is the primary sensitizing substance. Although poison ivy and poison oak grow well in full sun to partial shade, poison sumac typically is found in damp swampy areas east of the Rocky Mountains. Most cases of ACD related to Anacardiaceae species are due to direct contact with urushiol from a Toxicodendron plant, but burning of brush containing Toxicodendron can cause airborne exposure when urushiol oil is carried by smoke particles.¹² Sensitization to Toxicodendron can cause ACD to other Anacardiaceae species such as the Japanese lacquer tree (Toxicodendron vernicifluum), mango tree (Mangifera indica), cashew tree (Anacardium occidentale), and Indian marking nut tree (Semecarpus anacardium).⁶ Cross-reactions to components of the ginkgo tree (Ginkgo biloba) also are possible.

Toxicodendron plants can be more easily identified and avoided with knowledge of their characteristic leaf patterns. The most dependable way to identify poison ivy and poison oak species is to look for plants with 3 leaves, giving rise to the common saying, “Leaves of three, leave them be.” Poison sumac plants have groups of 7 to 13 leaves arranged as pairs along a central rib. Another helpful finding is a black deposit that Toxicodendron species leave behind following trauma to the leaves. Urushiol oxidizes when exposed to air and turns into a black deposit that can be seen on damaged leaves themselves or can be demonstrated in a black spot test to verify if a plant is a Toxicodendron species. The test is performed by gathering (carefully, without direct contact) a few leaves in a paper towel and crushing them to release sap. Within minutes, the sap will turn black if the plant is indeed a Toxicodendron species.¹³Pruritic, edematous, erythematous papules, plaques, and eventual vesicles in a linear distribution are suspicious for Toxicodendron exposure. Although your pet will not develop Toxicodendron ACD, oleoresin-contaminated pets can transfer the oils to their owners after coming into contact with these plants. Toxicodendron dermatitis also can be acquired from oleoresin-contaminated fomites such as clothing and shoes worn in the garden or when hiking. Toxicodendron dermatitis can appear at different sites on the body at different times depending on the amount of oleoresin exposure as well as epidermal thickness. For example, the oleoresin can be transferred from the hands to body areas with a thinner stratum corneum (eg, genitalia) and cause subsequent dermatitis.¹

Compositae Family
The Compositae family (also known as Asteraceae) is a large plant family with more than 20,000 species, including numerous weeds, wildflowers, and vegetables. The flowers, leaves, stems, and pollens of the Compositae family are coated by cyclic esters called sesquiterpene lactones. Mitchell and Dupuis¹⁴ showed that sesquiterpene lactones are the allergens responsible for ACD to various Compositae plants, including ragweed (Ambrosia), sneezeweed (Helenium), and chrysanthemums (Chrysanthemum). Common Compositae vegetables such as lettuce (Lactuca sativa) have been reported to cause ACD in chefs, grocery store produce handlers, gardeners, and even owners of lettuce-eating pet guinea pigs and turtles.¹⁵ Similarly, artichokes (Cynara scolymus) can cause ACD in gardeners.¹⁶ Exposure to Compositae species also has been implicated in photoallergic reactions, and studies have demonstrated that some patients with chronic actinic dermatitis also have positive patch test reactions to Compositae species and/or sesquiterpene lactones.^17,18

In addition to direct contact with Compositae plants, airborne exposure to sesquiterpene lactones can cause ACD.¹⁴ The pattern of airborne contact dermatitis typically involves exposed areas such as the eyelids, central face, and/or neck. The beak sign also can be a clue to airborne contact dermatitis, which involves dermatitis of the face that spares the nasal tip and/or nasal ridge. It is thought that the beak sign may result from increased sebaceous gland concentration on the nose, which prevents penetration of allergens and irritants.¹⁹ Unlike photoallergic contact dermatitis, which also can involve the face, airborne ACD frequently involves photoprotected areas such as the submandibular chin and the upper lip. Davies and Kersey²⁰ reported the case of a groundsman who was cutting grass with dandelions (Taraxacum officinale) and was found to have associated airborne ACD of the face, neck, and forearms due to Compositae allergy. In a different setting, the aromas of chamomile (Matricaria chamomilla) have been reported to cause airborne ACD in a tea drinker.²¹ Paulsen²² found that ingestion of chamomile tea can induce systemic ACD in sensitized individuals.

Alstroemeriaceae, Liliaceae, and Primulaceae
Florists are exposed to many plant species and have a high prevalence of ACD. Thiboutot et al²³ found that 15 of 57 (26%) floral workers experienced hand dermatitis that cleared with time away from work. The Peruvian lily (Alstroemeria, Alstroemeriaceae family), which contains tuliposide A, was found to be the leading cause of sensitization.²³ Tulips (Tulipa, Liliaceae family), as the flower name suggests, also contain tuliposide A, which along with mechanical irritation from the course tecta fibers on the bulbs lead to a dermatitis known as tulip fingers.^24,25 Poison primrose (Primula obconica, Primulaceae family), cultivated for its highly colorful flowers, contains the contact allergen primin.⁶ A common clinical presentation of ACD for any of these culprit flowers is localized dermatitis of the thumb and index finger in a florist or gardener.

Plants That Cause Irritant Reactions

Cactuses
Although the long spines of the Cactaceae family of cactuses is a warning for passersby, it is the small and nearly invisible barbed hairs (glochids) that inflict a more dramatic cutaneous reaction. The prickly pear cactus (Opuntia species) is a good example of such a plant, as its glochids cause mechanical irritation but also can become embedded in the skin and result in subcutaneous granulomas known as sabra dermatitis.²⁶

Stinging Nettle
The dermatologic term urticaria owes its namesake to the stinging nettle plant, which comes from the family Urticaceae. The stinging nettle has small hairs on its leaves, referred to as stinging trichomes, which have needlelike tips that pierce the skin and inject a mix of histamine, formic acid, and acetylcholine, causing a pruritic dermatitis that may last up to 12 hours.²⁷ The plant is found worldwide and is a common weed in North America.

Phytophotodermatitis

Lemons and limes (Rutaceae family) are common culprits of phytophotodermatitis, often causing what is known as a margarita burn after outdoor consumption or preparation of this tasty citrus beverage.²⁸ An accidental spray of lime juice on the skin while adding it to a beer, guacamole, salsa, or any other food or beverage also can cause phytophotodermatitis.^29-31 Although the juice of lemons and limes contains psoralens, the rind can contain a 6- to 186-fold increased concentration.³² Psoralen is the photoactive agent in Rutaceae plants that intercalates in double-stranded DNA and promotes intrastrand cross-links when exposed to UVA light, which ultimately leads to dermatitis.⁹ Phytophotodermatitis commonly causes erythema, edema, and painful bullae on sun-exposed areas and classically heals with hyperpigmentation.

Pseudophytodermatitis can occur in grain farmers and harvesters who handle wheat and/or barley and incidentally come in contact with insects and chemicals on the plant material. Pseudophytodermatitis from mites in the wheat and/or barley plant can occur at harvest time when contact with the plant material is high. Insects such as the North American itch mite (Pediculoides ventricosus) can cause petechiae, wheals, and pustules. In addition, insecticides such as malathion and arsenical sprays that are applied to plant leaves can cause pseudophytodermatitis, which may be initially diagnosed as dermatitis to the plant itself.⁶

Patch Testing to Plants

When a patient presents with recurrent or persistent dermatitis and a plant contact allergen is suspected, patch testing is indicated. Most comprehensive patch test series contain various plant allergens, such as sesquiterpene lactones, Compositae mix, and limonene hydroperoxides, and patch testing to a specialized plant series may be necessary. Poison ivy/oak/sumac allergens typically are not included in patch test series because of the high prevalence of allergic reactions to these chemicals and the likelihood of sensitization when patch testing with urushiol. Compositae contact sensitization can be difficult to diagnose because neither sesquiterpene lactone mix 0.1% nor parthenolide 0.1% are sensitive enough to pick up all Compositae allergies.^33,34 Paulsen and Andersen³⁴ proposed that if Compositae sensitization is suspected, testing should include sesquiterpene lactone, parthenolide, and Compositae mix II 2.5%, as well as other potential Compositae allergens based on the patient’s history.³⁴

Because plants can have geographic variability and contain potentially unknown allergens,³⁵ testing to plant components may increase the diagnostic yield of patch testing. Dividing the plant into component parts (ie, stem, bulb, leaf, flower) is helpful, as different components have different allergen concentrations. It is important to consult expert resources before proceeding with plant component patch testing because irritant reactions are frequent and may confound the testing.³⁶

Prevention and Treatment

For all plant dermatoses, the mainstay of prevention is to avoid contact with the offending plant material. Gloves can be an important protective tool for plant dermatitis prevention; the correct material depends on the plant species being handled. Rubber gloves should not be worn to protect against Toxicodendron plants since the catechols in urushiol are soluble in rubber; vinyl gloves should be worn instead.⁶ Marks³⁷ found that tuliposide A, the allergen in the Peruvian lily (Alstroemeria), penetrates both vinyl and latex gloves; it does not penetrate nitrile gloves. If exposed, the risk of dermatitis can be decreased if the allergen is washed away with soap and water as soon as possible. Some allergens such as Toxicodendron are absorbed quickly and need to be washed off within 10 minutes of exposure.⁶ Importantly, exposed gardening gloves may continue to perpetuate ACD if the allergen is not also washed off the gloves themselves.

For light-mediated dermatoses, sun avoidance or use of an effective sunscreen can reduce symptoms in an individual who has already been exposed.¹⁰ UVA light activates psoralen-mediated dermatitis but not until 30 to 120 minutes after absorption into the skin.³⁸

Barrier creams are thought to be protective against plant ACD through a variety of mechanisms. The cream itself is meant to reduce skin contact to an allergen or irritant. Additionally, barrier creams contain active ingredients such as silicone, hydrocarbons, and aluminum chlorohydrate, which are thought to trap or transform offending agents before contacting the skin. When contact with a Toxicodendron species is anticipated, Marks et al³⁹ found that dermatitis was absent or significantly reduced when 144 patients were pretreated with quaternium-18 bentonite lotion 5% (P<.0001).

Although allergen avoidance and use of gloves and barrier creams are the mainstays of preventing plant dermatoses, treatment often is required to control postexposure symptoms. For all plant dermatoses, topical corticosteroids can be used to reduce inflammation and pruritus. In some cases, systemic steroids may be necessary. To prevent rebound of dermatitis, patients often require a 3-week or longer course of oral steroids to quell the reaction, particularly if the dermatitis is vigorous or an id reaction is present.⁴⁰ Antihistamines and cold compresses also can provide symptomatic relief.

Final Interpretation

Plants can cause a variety of dermatoses. Although Toxicodendron plants are the most frequent cause of ACD, it is important to keep in mind that florists, gardeners, and farmers are exposed to a large variety of allergens, irritants, and phototoxic agents that cause dermatoses as well. Confirmation of plant-induced ACD involves patch testing against suspected species. Prevention involves use of appropriate barriers and avoidance of implicated plants. Treatment includes topical steroids, antihistamines, and prednisone.

Plants can contribute to a variety of dermatoses. The Toxicodendron genus, which includes poison ivy, poison oak, and poison sumac, is a well-known and common cause of allergic contact dermatitis (ACD), but many other plants can cause direct or airborne contact dermatitis, especially in gardeners, florists, and farmers. This article provides an overview of different plant-related dermatoses and culprit plants as well as how these dermatoses should be diagnosed and treated.

Epidemiology

Plant dermatoses affect more than 50 million individuals each year.^1,2 In the United States, the Toxicodendron genus causes ACD in more than 70% of exposed individuals, leading to medical visits.³ An urgent care visit for a plant-related dermatitis is estimated to cost $168, while an emergency department visit can cost 3 times as much.⁴ Although less common, Compositae plants are another important culprit of plant dermatitis, particularly in gardeners, florists, and farmers. Data from the 2017-2018 North American Contact Dermatitis Group screening series (N=4947) showed sesquiterpene lactones and Compositae to be positive in 0.5% of patch-tested patients.⁵

Plant Dermatitis Classifications

Plant dermatitis can be classified into 5 main categories: ACD, mechanical irritant contact dermatitis, chemical irritant contact dermatitis, light-mediated dermatitis, and pseudophytodermatitis.⁶

Allergic contact dermatitis is an immune-mediated type IV delayed hypersensitivity reaction. The common molecular allergens in plants include phenols, α-methylene-γ-butyrolactones, quinones, terpenes, disulfides, isothiocyanates, and polyacetylenic derivatives.⁶

Plant contact dermatitis due to mechanical and chemical irritants is precipitated by multiple mechanisms, including disruption of the epidermal barrier and subsequent cytokine release from keratinocytes.⁷ Nonimmunologic contact urticaria from plants is thought to be a type of irritant reaction precipitated by mechanical or chemical trauma.⁸

Light-mediated dermatitis includes phytophotodermatitis and photoallergic contact dermatitis. Phytophotodermatitis is a phototoxic reaction triggered by exposure to both plant-derived furanocoumarin and UVA light.⁹ By contrast, photoallergic contact dermatitis is a delayed hypersensitivity reaction from prior sensitization to a light-activated antigen.¹⁰

Pseudophytodermatitis, as its name implies, is not truly mediated by an allergen or irritant intrinsic to the plant but rather by dyes, waxes, insecticides, or arthropods that inhabit the plant or are secondarily applied.⁶

Common Plant Allergens

Anacardiaceae Family
Most of the allergenic plants within the Anacardiaceae family belong to the Toxicodendron genus, which encompasses poison ivy (Toxicodendron radicans), poison oak (Toxicodendron pubescens,Toxicodendron quercifolium, Toxicodendron diversiloum), and poison sumac (Toxicodendron vernix). Poison ivy is the celebrity of the Anacardiaceae family and contributes to most cases of plant-related ACD. It is found in every state in the continental United States. Poison oak is another common culprit found in the western and southeastern United States.¹¹ Plants within the Anacardiaceae family contain an oleoresin called urushiol, which is the primary sensitizing substance. Although poison ivy and poison oak grow well in full sun to partial shade, poison sumac typically is found in damp swampy areas east of the Rocky Mountains. Most cases of ACD related to Anacardiaceae species are due to direct contact with urushiol from a Toxicodendron plant, but burning of brush containing Toxicodendron can cause airborne exposure when urushiol oil is carried by smoke particles.¹² Sensitization to Toxicodendron can cause ACD to other Anacardiaceae species such as the Japanese lacquer tree (Toxicodendron vernicifluum), mango tree (Mangifera indica), cashew tree (Anacardium occidentale), and Indian marking nut tree (Semecarpus anacardium).⁶ Cross-reactions to components of the ginkgo tree (Ginkgo biloba) also are possible.

Toxicodendron plants can be more easily identified and avoided with knowledge of their characteristic leaf patterns. The most dependable way to identify poison ivy and poison oak species is to look for plants with 3 leaves, giving rise to the common saying, “Leaves of three, leave them be.” Poison sumac plants have groups of 7 to 13 leaves arranged as pairs along a central rib. Another helpful finding is a black deposit that Toxicodendron species leave behind following trauma to the leaves. Urushiol oxidizes when exposed to air and turns into a black deposit that can be seen on damaged leaves themselves or can be demonstrated in a black spot test to verify if a plant is a Toxicodendron species. The test is performed by gathering (carefully, without direct contact) a few leaves in a paper towel and crushing them to release sap. Within minutes, the sap will turn black if the plant is indeed a Toxicodendron species.¹³Pruritic, edematous, erythematous papules, plaques, and eventual vesicles in a linear distribution are suspicious for Toxicodendron exposure. Although your pet will not develop Toxicodendron ACD, oleoresin-contaminated pets can transfer the oils to their owners after coming into contact with these plants. Toxicodendron dermatitis also can be acquired from oleoresin-contaminated fomites such as clothing and shoes worn in the garden or when hiking. Toxicodendron dermatitis can appear at different sites on the body at different times depending on the amount of oleoresin exposure as well as epidermal thickness. For example, the oleoresin can be transferred from the hands to body areas with a thinner stratum corneum (eg, genitalia) and cause subsequent dermatitis.¹

Compositae Family
The Compositae family (also known as Asteraceae) is a large plant family with more than 20,000 species, including numerous weeds, wildflowers, and vegetables. The flowers, leaves, stems, and pollens of the Compositae family are coated by cyclic esters called sesquiterpene lactones. Mitchell and Dupuis¹⁴ showed that sesquiterpene lactones are the allergens responsible for ACD to various Compositae plants, including ragweed (Ambrosia), sneezeweed (Helenium), and chrysanthemums (Chrysanthemum). Common Compositae vegetables such as lettuce (Lactuca sativa) have been reported to cause ACD in chefs, grocery store produce handlers, gardeners, and even owners of lettuce-eating pet guinea pigs and turtles.¹⁵ Similarly, artichokes (Cynara scolymus) can cause ACD in gardeners.¹⁶ Exposure to Compositae species also has been implicated in photoallergic reactions, and studies have demonstrated that some patients with chronic actinic dermatitis also have positive patch test reactions to Compositae species and/or sesquiterpene lactones.^17,18

In addition to direct contact with Compositae plants, airborne exposure to sesquiterpene lactones can cause ACD.¹⁴ The pattern of airborne contact dermatitis typically involves exposed areas such as the eyelids, central face, and/or neck. The beak sign also can be a clue to airborne contact dermatitis, which involves dermatitis of the face that spares the nasal tip and/or nasal ridge. It is thought that the beak sign may result from increased sebaceous gland concentration on the nose, which prevents penetration of allergens and irritants.¹⁹ Unlike photoallergic contact dermatitis, which also can involve the face, airborne ACD frequently involves photoprotected areas such as the submandibular chin and the upper lip. Davies and Kersey²⁰ reported the case of a groundsman who was cutting grass with dandelions (Taraxacum officinale) and was found to have associated airborne ACD of the face, neck, and forearms due to Compositae allergy. In a different setting, the aromas of chamomile (Matricaria chamomilla) have been reported to cause airborne ACD in a tea drinker.²¹ Paulsen²² found that ingestion of chamomile tea can induce systemic ACD in sensitized individuals.

Alstroemeriaceae, Liliaceae, and Primulaceae
Florists are exposed to many plant species and have a high prevalence of ACD. Thiboutot et al²³ found that 15 of 57 (26%) floral workers experienced hand dermatitis that cleared with time away from work. The Peruvian lily (Alstroemeria, Alstroemeriaceae family), which contains tuliposide A, was found to be the leading cause of sensitization.²³ Tulips (Tulipa, Liliaceae family), as the flower name suggests, also contain tuliposide A, which along with mechanical irritation from the course tecta fibers on the bulbs lead to a dermatitis known as tulip fingers.^24,25 Poison primrose (Primula obconica, Primulaceae family), cultivated for its highly colorful flowers, contains the contact allergen primin.⁶ A common clinical presentation of ACD for any of these culprit flowers is localized dermatitis of the thumb and index finger in a florist or gardener.

Plants That Cause Irritant Reactions

Cactuses
Although the long spines of the Cactaceae family of cactuses is a warning for passersby, it is the small and nearly invisible barbed hairs (glochids) that inflict a more dramatic cutaneous reaction. The prickly pear cactus (Opuntia species) is a good example of such a plant, as its glochids cause mechanical irritation but also can become embedded in the skin and result in subcutaneous granulomas known as sabra dermatitis.²⁶

Stinging Nettle
The dermatologic term urticaria owes its namesake to the stinging nettle plant, which comes from the family Urticaceae. The stinging nettle has small hairs on its leaves, referred to as stinging trichomes, which have needlelike tips that pierce the skin and inject a mix of histamine, formic acid, and acetylcholine, causing a pruritic dermatitis that may last up to 12 hours.²⁷ The plant is found worldwide and is a common weed in North America.

Phytophotodermatitis

Lemons and limes (Rutaceae family) are common culprits of phytophotodermatitis, often causing what is known as a margarita burn after outdoor consumption or preparation of this tasty citrus beverage.²⁸ An accidental spray of lime juice on the skin while adding it to a beer, guacamole, salsa, or any other food or beverage also can cause phytophotodermatitis.^29-31 Although the juice of lemons and limes contains psoralens, the rind can contain a 6- to 186-fold increased concentration.³² Psoralen is the photoactive agent in Rutaceae plants that intercalates in double-stranded DNA and promotes intrastrand cross-links when exposed to UVA light, which ultimately leads to dermatitis.⁹ Phytophotodermatitis commonly causes erythema, edema, and painful bullae on sun-exposed areas and classically heals with hyperpigmentation.

Pseudophytodermatitis can occur in grain farmers and harvesters who handle wheat and/or barley and incidentally come in contact with insects and chemicals on the plant material. Pseudophytodermatitis from mites in the wheat and/or barley plant can occur at harvest time when contact with the plant material is high. Insects such as the North American itch mite (Pediculoides ventricosus) can cause petechiae, wheals, and pustules. In addition, insecticides such as malathion and arsenical sprays that are applied to plant leaves can cause pseudophytodermatitis, which may be initially diagnosed as dermatitis to the plant itself.⁶

Patch Testing to Plants

When a patient presents with recurrent or persistent dermatitis and a plant contact allergen is suspected, patch testing is indicated. Most comprehensive patch test series contain various plant allergens, such as sesquiterpene lactones, Compositae mix, and limonene hydroperoxides, and patch testing to a specialized plant series may be necessary. Poison ivy/oak/sumac allergens typically are not included in patch test series because of the high prevalence of allergic reactions to these chemicals and the likelihood of sensitization when patch testing with urushiol. Compositae contact sensitization can be difficult to diagnose because neither sesquiterpene lactone mix 0.1% nor parthenolide 0.1% are sensitive enough to pick up all Compositae allergies.^33,34 Paulsen and Andersen³⁴ proposed that if Compositae sensitization is suspected, testing should include sesquiterpene lactone, parthenolide, and Compositae mix II 2.5%, as well as other potential Compositae allergens based on the patient’s history.³⁴

Because plants can have geographic variability and contain potentially unknown allergens,³⁵ testing to plant components may increase the diagnostic yield of patch testing. Dividing the plant into component parts (ie, stem, bulb, leaf, flower) is helpful, as different components have different allergen concentrations. It is important to consult expert resources before proceeding with plant component patch testing because irritant reactions are frequent and may confound the testing.³⁶

Prevention and Treatment

For all plant dermatoses, the mainstay of prevention is to avoid contact with the offending plant material. Gloves can be an important protective tool for plant dermatitis prevention; the correct material depends on the plant species being handled. Rubber gloves should not be worn to protect against Toxicodendron plants since the catechols in urushiol are soluble in rubber; vinyl gloves should be worn instead.⁶ Marks³⁷ found that tuliposide A, the allergen in the Peruvian lily (Alstroemeria), penetrates both vinyl and latex gloves; it does not penetrate nitrile gloves. If exposed, the risk of dermatitis can be decreased if the allergen is washed away with soap and water as soon as possible. Some allergens such as Toxicodendron are absorbed quickly and need to be washed off within 10 minutes of exposure.⁶ Importantly, exposed gardening gloves may continue to perpetuate ACD if the allergen is not also washed off the gloves themselves.

For light-mediated dermatoses, sun avoidance or use of an effective sunscreen can reduce symptoms in an individual who has already been exposed.¹⁰ UVA light activates psoralen-mediated dermatitis but not until 30 to 120 minutes after absorption into the skin.³⁸

Barrier creams are thought to be protective against plant ACD through a variety of mechanisms. The cream itself is meant to reduce skin contact to an allergen or irritant. Additionally, barrier creams contain active ingredients such as silicone, hydrocarbons, and aluminum chlorohydrate, which are thought to trap or transform offending agents before contacting the skin. When contact with a Toxicodendron species is anticipated, Marks et al³⁹ found that dermatitis was absent or significantly reduced when 144 patients were pretreated with quaternium-18 bentonite lotion 5% (P<.0001).

Although allergen avoidance and use of gloves and barrier creams are the mainstays of preventing plant dermatoses, treatment often is required to control postexposure symptoms. For all plant dermatoses, topical corticosteroids can be used to reduce inflammation and pruritus. In some cases, systemic steroids may be necessary. To prevent rebound of dermatitis, patients often require a 3-week or longer course of oral steroids to quell the reaction, particularly if the dermatitis is vigorous or an id reaction is present.⁴⁰ Antihistamines and cold compresses also can provide symptomatic relief.

Final Interpretation

Plants can cause a variety of dermatoses. Although Toxicodendron plants are the most frequent cause of ACD, it is important to keep in mind that florists, gardeners, and farmers are exposed to a large variety of allergens, irritants, and phototoxic agents that cause dermatoses as well. Confirmation of plant-induced ACD involves patch testing against suspected species. Prevention involves use of appropriate barriers and avoidance of implicated plants. Treatment includes topical steroids, antihistamines, and prednisone.

Plants can contribute to a variety of dermatoses. The Toxicodendron genus, which includes poison ivy, poison oak, and poison sumac, is a well-known and common cause of allergic contact dermatitis (ACD), but many other plants can cause direct or airborne contact dermatitis, especially in gardeners, florists, and farmers. This article provides an overview of different plant-related dermatoses and culprit plants as well as how these dermatoses should be diagnosed and treated.

Epidemiology

Plant dermatoses affect more than 50 million individuals each year.^1,2 In the United States, the Toxicodendron genus causes ACD in more than 70% of exposed individuals, leading to medical visits.³ An urgent care visit for a plant-related dermatitis is estimated to cost $168, while an emergency department visit can cost 3 times as much.⁴ Although less common, Compositae plants are another important culprit of plant dermatitis, particularly in gardeners, florists, and farmers. Data from the 2017-2018 North American Contact Dermatitis Group screening series (N=4947) showed sesquiterpene lactones and Compositae to be positive in 0.5% of patch-tested patients.⁵

Plant Dermatitis Classifications

Plant dermatitis can be classified into 5 main categories: ACD, mechanical irritant contact dermatitis, chemical irritant contact dermatitis, light-mediated dermatitis, and pseudophytodermatitis.⁶

Allergic contact dermatitis is an immune-mediated type IV delayed hypersensitivity reaction. The common molecular allergens in plants include phenols, α-methylene-γ-butyrolactones, quinones, terpenes, disulfides, isothiocyanates, and polyacetylenic derivatives.⁶

Plant contact dermatitis due to mechanical and chemical irritants is precipitated by multiple mechanisms, including disruption of the epidermal barrier and subsequent cytokine release from keratinocytes.⁷ Nonimmunologic contact urticaria from plants is thought to be a type of irritant reaction precipitated by mechanical or chemical trauma.⁸

Light-mediated dermatitis includes phytophotodermatitis and photoallergic contact dermatitis. Phytophotodermatitis is a phototoxic reaction triggered by exposure to both plant-derived furanocoumarin and UVA light.⁹ By contrast, photoallergic contact dermatitis is a delayed hypersensitivity reaction from prior sensitization to a light-activated antigen.¹⁰

Pseudophytodermatitis, as its name implies, is not truly mediated by an allergen or irritant intrinsic to the plant but rather by dyes, waxes, insecticides, or arthropods that inhabit the plant or are secondarily applied.⁶

Common Plant Allergens

Anacardiaceae Family
Most of the allergenic plants within the Anacardiaceae family belong to the Toxicodendron genus, which encompasses poison ivy (Toxicodendron radicans), poison oak (Toxicodendron pubescens,Toxicodendron quercifolium, Toxicodendron diversiloum), and poison sumac (Toxicodendron vernix). Poison ivy is the celebrity of the Anacardiaceae family and contributes to most cases of plant-related ACD. It is found in every state in the continental United States. Poison oak is another common culprit found in the western and southeastern United States.¹¹ Plants within the Anacardiaceae family contain an oleoresin called urushiol, which is the primary sensitizing substance. Although poison ivy and poison oak grow well in full sun to partial shade, poison sumac typically is found in damp swampy areas east of the Rocky Mountains. Most cases of ACD related to Anacardiaceae species are due to direct contact with urushiol from a Toxicodendron plant, but burning of brush containing Toxicodendron can cause airborne exposure when urushiol oil is carried by smoke particles.¹² Sensitization to Toxicodendron can cause ACD to other Anacardiaceae species such as the Japanese lacquer tree (Toxicodendron vernicifluum), mango tree (Mangifera indica), cashew tree (Anacardium occidentale), and Indian marking nut tree (Semecarpus anacardium).⁶ Cross-reactions to components of the ginkgo tree (Ginkgo biloba) also are possible.

Toxicodendron plants can be more easily identified and avoided with knowledge of their characteristic leaf patterns. The most dependable way to identify poison ivy and poison oak species is to look for plants with 3 leaves, giving rise to the common saying, “Leaves of three, leave them be.” Poison sumac plants have groups of 7 to 13 leaves arranged as pairs along a central rib. Another helpful finding is a black deposit that Toxicodendron species leave behind following trauma to the leaves. Urushiol oxidizes when exposed to air and turns into a black deposit that can be seen on damaged leaves themselves or can be demonstrated in a black spot test to verify if a plant is a Toxicodendron species. The test is performed by gathering (carefully, without direct contact) a few leaves in a paper towel and crushing them to release sap. Within minutes, the sap will turn black if the plant is indeed a Toxicodendron species.¹³Pruritic, edematous, erythematous papules, plaques, and eventual vesicles in a linear distribution are suspicious for Toxicodendron exposure. Although your pet will not develop Toxicodendron ACD, oleoresin-contaminated pets can transfer the oils to their owners after coming into contact with these plants. Toxicodendron dermatitis also can be acquired from oleoresin-contaminated fomites such as clothing and shoes worn in the garden or when hiking. Toxicodendron dermatitis can appear at different sites on the body at different times depending on the amount of oleoresin exposure as well as epidermal thickness. For example, the oleoresin can be transferred from the hands to body areas with a thinner stratum corneum (eg, genitalia) and cause subsequent dermatitis.¹

Compositae Family
The Compositae family (also known as Asteraceae) is a large plant family with more than 20,000 species, including numerous weeds, wildflowers, and vegetables. The flowers, leaves, stems, and pollens of the Compositae family are coated by cyclic esters called sesquiterpene lactones. Mitchell and Dupuis¹⁴ showed that sesquiterpene lactones are the allergens responsible for ACD to various Compositae plants, including ragweed (Ambrosia), sneezeweed (Helenium), and chrysanthemums (Chrysanthemum). Common Compositae vegetables such as lettuce (Lactuca sativa) have been reported to cause ACD in chefs, grocery store produce handlers, gardeners, and even owners of lettuce-eating pet guinea pigs and turtles.¹⁵ Similarly, artichokes (Cynara scolymus) can cause ACD in gardeners.¹⁶ Exposure to Compositae species also has been implicated in photoallergic reactions, and studies have demonstrated that some patients with chronic actinic dermatitis also have positive patch test reactions to Compositae species and/or sesquiterpene lactones.^17,18

In addition to direct contact with Compositae plants, airborne exposure to sesquiterpene lactones can cause ACD.¹⁴ The pattern of airborne contact dermatitis typically involves exposed areas such as the eyelids, central face, and/or neck. The beak sign also can be a clue to airborne contact dermatitis, which involves dermatitis of the face that spares the nasal tip and/or nasal ridge. It is thought that the beak sign may result from increased sebaceous gland concentration on the nose, which prevents penetration of allergens and irritants.¹⁹ Unlike photoallergic contact dermatitis, which also can involve the face, airborne ACD frequently involves photoprotected areas such as the submandibular chin and the upper lip. Davies and Kersey²⁰ reported the case of a groundsman who was cutting grass with dandelions (Taraxacum officinale) and was found to have associated airborne ACD of the face, neck, and forearms due to Compositae allergy. In a different setting, the aromas of chamomile (Matricaria chamomilla) have been reported to cause airborne ACD in a tea drinker.²¹ Paulsen²² found that ingestion of chamomile tea can induce systemic ACD in sensitized individuals.

Alstroemeriaceae, Liliaceae, and Primulaceae
Florists are exposed to many plant species and have a high prevalence of ACD. Thiboutot et al²³ found that 15 of 57 (26%) floral workers experienced hand dermatitis that cleared with time away from work. The Peruvian lily (Alstroemeria, Alstroemeriaceae family), which contains tuliposide A, was found to be the leading cause of sensitization.²³ Tulips (Tulipa, Liliaceae family), as the flower name suggests, also contain tuliposide A, which along with mechanical irritation from the course tecta fibers on the bulbs lead to a dermatitis known as tulip fingers.^24,25 Poison primrose (Primula obconica, Primulaceae family), cultivated for its highly colorful flowers, contains the contact allergen primin.⁶ A common clinical presentation of ACD for any of these culprit flowers is localized dermatitis of the thumb and index finger in a florist or gardener.

Plants That Cause Irritant Reactions

Cactuses
Although the long spines of the Cactaceae family of cactuses is a warning for passersby, it is the small and nearly invisible barbed hairs (glochids) that inflict a more dramatic cutaneous reaction. The prickly pear cactus (Opuntia species) is a good example of such a plant, as its glochids cause mechanical irritation but also can become embedded in the skin and result in subcutaneous granulomas known as sabra dermatitis.²⁶

Stinging Nettle
The dermatologic term urticaria owes its namesake to the stinging nettle plant, which comes from the family Urticaceae. The stinging nettle has small hairs on its leaves, referred to as stinging trichomes, which have needlelike tips that pierce the skin and inject a mix of histamine, formic acid, and acetylcholine, causing a pruritic dermatitis that may last up to 12 hours.²⁷ The plant is found worldwide and is a common weed in North America.

Phytophotodermatitis

Lemons and limes (Rutaceae family) are common culprits of phytophotodermatitis, often causing what is known as a margarita burn after outdoor consumption or preparation of this tasty citrus beverage.²⁸ An accidental spray of lime juice on the skin while adding it to a beer, guacamole, salsa, or any other food or beverage also can cause phytophotodermatitis.^29-31 Although the juice of lemons and limes contains psoralens, the rind can contain a 6- to 186-fold increased concentration.³² Psoralen is the photoactive agent in Rutaceae plants that intercalates in double-stranded DNA and promotes intrastrand cross-links when exposed to UVA light, which ultimately leads to dermatitis.⁹ Phytophotodermatitis commonly causes erythema, edema, and painful bullae on sun-exposed areas and classically heals with hyperpigmentation.

Pseudophytodermatitis can occur in grain farmers and harvesters who handle wheat and/or barley and incidentally come in contact with insects and chemicals on the plant material. Pseudophytodermatitis from mites in the wheat and/or barley plant can occur at harvest time when contact with the plant material is high. Insects such as the North American itch mite (Pediculoides ventricosus) can cause petechiae, wheals, and pustules. In addition, insecticides such as malathion and arsenical sprays that are applied to plant leaves can cause pseudophytodermatitis, which may be initially diagnosed as dermatitis to the plant itself.⁶

Patch Testing to Plants

When a patient presents with recurrent or persistent dermatitis and a plant contact allergen is suspected, patch testing is indicated. Most comprehensive patch test series contain various plant allergens, such as sesquiterpene lactones, Compositae mix, and limonene hydroperoxides, and patch testing to a specialized plant series may be necessary. Poison ivy/oak/sumac allergens typically are not included in patch test series because of the high prevalence of allergic reactions to these chemicals and the likelihood of sensitization when patch testing with urushiol. Compositae contact sensitization can be difficult to diagnose because neither sesquiterpene lactone mix 0.1% nor parthenolide 0.1% are sensitive enough to pick up all Compositae allergies.^33,34 Paulsen and Andersen³⁴ proposed that if Compositae sensitization is suspected, testing should include sesquiterpene lactone, parthenolide, and Compositae mix II 2.5%, as well as other potential Compositae allergens based on the patient’s history.³⁴

Because plants can have geographic variability and contain potentially unknown allergens,³⁵ testing to plant components may increase the diagnostic yield of patch testing. Dividing the plant into component parts (ie, stem, bulb, leaf, flower) is helpful, as different components have different allergen concentrations. It is important to consult expert resources before proceeding with plant component patch testing because irritant reactions are frequent and may confound the testing.³⁶

Prevention and Treatment

For all plant dermatoses, the mainstay of prevention is to avoid contact with the offending plant material. Gloves can be an important protective tool for plant dermatitis prevention; the correct material depends on the plant species being handled. Rubber gloves should not be worn to protect against Toxicodendron plants since the catechols in urushiol are soluble in rubber; vinyl gloves should be worn instead.⁶ Marks³⁷ found that tuliposide A, the allergen in the Peruvian lily (Alstroemeria), penetrates both vinyl and latex gloves; it does not penetrate nitrile gloves. If exposed, the risk of dermatitis can be decreased if the allergen is washed away with soap and water as soon as possible. Some allergens such as Toxicodendron are absorbed quickly and need to be washed off within 10 minutes of exposure.⁶ Importantly, exposed gardening gloves may continue to perpetuate ACD if the allergen is not also washed off the gloves themselves.

For light-mediated dermatoses, sun avoidance or use of an effective sunscreen can reduce symptoms in an individual who has already been exposed.¹⁰ UVA light activates psoralen-mediated dermatitis but not until 30 to 120 minutes after absorption into the skin.³⁸

Barrier creams are thought to be protective against plant ACD through a variety of mechanisms. The cream itself is meant to reduce skin contact to an allergen or irritant. Additionally, barrier creams contain active ingredients such as silicone, hydrocarbons, and aluminum chlorohydrate, which are thought to trap or transform offending agents before contacting the skin. When contact with a Toxicodendron species is anticipated, Marks et al³⁹ found that dermatitis was absent or significantly reduced when 144 patients were pretreated with quaternium-18 bentonite lotion 5% (P<.0001).

Although allergen avoidance and use of gloves and barrier creams are the mainstays of preventing plant dermatoses, treatment often is required to control postexposure symptoms. For all plant dermatoses, topical corticosteroids can be used to reduce inflammation and pruritus. In some cases, systemic steroids may be necessary. To prevent rebound of dermatitis, patients often require a 3-week or longer course of oral steroids to quell the reaction, particularly if the dermatitis is vigorous or an id reaction is present.⁴⁰ Antihistamines and cold compresses also can provide symptomatic relief.

Final Interpretation

Plants can cause a variety of dermatoses. Although Toxicodendron plants are the most frequent cause of ACD, it is important to keep in mind that florists, gardeners, and farmers are exposed to a large variety of allergens, irritants, and phototoxic agents that cause dermatoses as well. Confirmation of plant-induced ACD involves patch testing against suspected species. Prevention involves use of appropriate barriers and avoidance of implicated plants. Treatment includes topical steroids, antihistamines, and prednisone.

A new study rebuts the conventional rheumatology wisdom about ankylosing spondylitis (AS) by reporting that actually there’s no gender gap in the prevalence of the disease. Researchers found no statistically significant difference in rates between men and women based on an analysis of military medical records.

feellife/Thinkstock

“Our findings challenge the widely held belief that AS in the U.S. occurs substantially more frequently in males than females,” the study authors, led by data scientist D. Alan Nelson, PhD, of Stanford (Calif.) University, wrote in a study published Aug. 30 in Arthritis Care & Research.

The researchers launched the study to fill a gap in knowledge regarding case rates by gender. “The incidence of AS in the U.S. has been understudied and incompletely characterized,” they wrote.

Even though AS is fairly common, affecting an estimated 1% of the American adult population (2.5 million people), only one published population study has examined rates by gender in the United States. That study tracked cases in Minnesota’s Olmsted County during 1980-2009 and found that the ratio of cases in men vs. women was 3.8:1, which was “consistent with more recent estimates” at the time.

However, the population in that study in 1980 was 100% White, the authors of the new study note. A Canadian study that tracked an Ontario population from 1995 to 2010, meanwhile, suggested that AS rates among women were rising and the gender gap was shrinking. AS rates as a whole also nearly tripled, possibly because of more awareness.

For the new study, researchers retrospectively tracked 728,556 members of the U.S. military who underwent guideline-directed screening for back pain during 2014-2017. The study population was about 68% White, 22% Black, 5% Asian or Pacific Islander, and the remainder were other races or unknown. About 85% were male.

The subjects were monitored for a mean of 2.21 years, and 438 (0.06%) were diagnosed with AS at least once over that period.

The researchers found that the AS rates among males vs. females were similar (incidence rate ratio, 1.16; P = .23; adjusted odds ratio, 0.79; 95% confidence interval, 0.61-1.02; P = .072).

The researchers also found that Whites were more likely to develop AS than Blacks (aOR, 1.39; 95% CI, 1.01-1.66; P = .04).

The risk of AS increased with age, the researchers reported, with the odds growing sevenfold in the 45-and-older population vs. the under-24 population (aOR, 7.3; 95% CI, 5.7-10.3; P < .001).

The researchers noted that their study examined a more diverse population than the earlier Minnesota study. It’s also possible that the results of the two studies differed because of differences in definitions of AS diagnosis or imprecision in diagnosis codes, they wrote.

The researchers added that “the finding of a 1.21 male-female prevalence ratio of AS in the Canadian Ontario study was also generally consistent with our findings. Similar to our study population, the Canadian population was racially more diverse than the Olmsted study population at the times of both studies.”

Some limitations of the study include the fact that the military population is not a random sample and may have low rates of AS. “It is highly likely that most clinically evident cases of AS would have been screened out prior to enrollment in the military service,” they wrote. “Differences between military service members and the general population may explain why we observed a different association between AS incidence and age in comparison to that reported by prior studies. The increasing risk of AS with adult age that we observed could reflect selective discharge patterns related to very early symptoms of AS in this population.”

The study was funded in part by a grant from the Spondylitis Association of America. No information about potential conflicts of interest was provided in the manuscript.

A new study rebuts the conventional rheumatology wisdom about ankylosing spondylitis (AS) by reporting that actually there’s no gender gap in the prevalence of the disease. Researchers found no statistically significant difference in rates between men and women based on an analysis of military medical records.

feellife/Thinkstock

“Our findings challenge the widely held belief that AS in the U.S. occurs substantially more frequently in males than females,” the study authors, led by data scientist D. Alan Nelson, PhD, of Stanford (Calif.) University, wrote in a study published Aug. 30 in Arthritis Care & Research.

The researchers launched the study to fill a gap in knowledge regarding case rates by gender. “The incidence of AS in the U.S. has been understudied and incompletely characterized,” they wrote.

Even though AS is fairly common, affecting an estimated 1% of the American adult population (2.5 million people), only one published population study has examined rates by gender in the United States. That study tracked cases in Minnesota’s Olmsted County during 1980-2009 and found that the ratio of cases in men vs. women was 3.8:1, which was “consistent with more recent estimates” at the time.

However, the population in that study in 1980 was 100% White, the authors of the new study note. A Canadian study that tracked an Ontario population from 1995 to 2010, meanwhile, suggested that AS rates among women were rising and the gender gap was shrinking. AS rates as a whole also nearly tripled, possibly because of more awareness.

For the new study, researchers retrospectively tracked 728,556 members of the U.S. military who underwent guideline-directed screening for back pain during 2014-2017. The study population was about 68% White, 22% Black, 5% Asian or Pacific Islander, and the remainder were other races or unknown. About 85% were male.

The subjects were monitored for a mean of 2.21 years, and 438 (0.06%) were diagnosed with AS at least once over that period.

The researchers found that the AS rates among males vs. females were similar (incidence rate ratio, 1.16; P = .23; adjusted odds ratio, 0.79; 95% confidence interval, 0.61-1.02; P = .072).

The researchers also found that Whites were more likely to develop AS than Blacks (aOR, 1.39; 95% CI, 1.01-1.66; P = .04).

The risk of AS increased with age, the researchers reported, with the odds growing sevenfold in the 45-and-older population vs. the under-24 population (aOR, 7.3; 95% CI, 5.7-10.3; P < .001).

The researchers noted that their study examined a more diverse population than the earlier Minnesota study. It’s also possible that the results of the two studies differed because of differences in definitions of AS diagnosis or imprecision in diagnosis codes, they wrote.

The researchers added that “the finding of a 1.21 male-female prevalence ratio of AS in the Canadian Ontario study was also generally consistent with our findings. Similar to our study population, the Canadian population was racially more diverse than the Olmsted study population at the times of both studies.”

Some limitations of the study include the fact that the military population is not a random sample and may have low rates of AS. “It is highly likely that most clinically evident cases of AS would have been screened out prior to enrollment in the military service,” they wrote. “Differences between military service members and the general population may explain why we observed a different association between AS incidence and age in comparison to that reported by prior studies. The increasing risk of AS with adult age that we observed could reflect selective discharge patterns related to very early symptoms of AS in this population.”

The study was funded in part by a grant from the Spondylitis Association of America. No information about potential conflicts of interest was provided in the manuscript.

A new study rebuts the conventional rheumatology wisdom about ankylosing spondylitis (AS) by reporting that actually there’s no gender gap in the prevalence of the disease. Researchers found no statistically significant difference in rates between men and women based on an analysis of military medical records.

feellife/Thinkstock

“Our findings challenge the widely held belief that AS in the U.S. occurs substantially more frequently in males than females,” the study authors, led by data scientist D. Alan Nelson, PhD, of Stanford (Calif.) University, wrote in a study published Aug. 30 in Arthritis Care & Research.

The researchers launched the study to fill a gap in knowledge regarding case rates by gender. “The incidence of AS in the U.S. has been understudied and incompletely characterized,” they wrote.

Even though AS is fairly common, affecting an estimated 1% of the American adult population (2.5 million people), only one published population study has examined rates by gender in the United States. That study tracked cases in Minnesota’s Olmsted County during 1980-2009 and found that the ratio of cases in men vs. women was 3.8:1, which was “consistent with more recent estimates” at the time.

However, the population in that study in 1980 was 100% White, the authors of the new study note. A Canadian study that tracked an Ontario population from 1995 to 2010, meanwhile, suggested that AS rates among women were rising and the gender gap was shrinking. AS rates as a whole also nearly tripled, possibly because of more awareness.

For the new study, researchers retrospectively tracked 728,556 members of the U.S. military who underwent guideline-directed screening for back pain during 2014-2017. The study population was about 68% White, 22% Black, 5% Asian or Pacific Islander, and the remainder were other races or unknown. About 85% were male.

The subjects were monitored for a mean of 2.21 years, and 438 (0.06%) were diagnosed with AS at least once over that period.

The researchers found that the AS rates among males vs. females were similar (incidence rate ratio, 1.16; P = .23; adjusted odds ratio, 0.79; 95% confidence interval, 0.61-1.02; P = .072).

The researchers also found that Whites were more likely to develop AS than Blacks (aOR, 1.39; 95% CI, 1.01-1.66; P = .04).

The risk of AS increased with age, the researchers reported, with the odds growing sevenfold in the 45-and-older population vs. the under-24 population (aOR, 7.3; 95% CI, 5.7-10.3; P < .001).

The researchers noted that their study examined a more diverse population than the earlier Minnesota study. It’s also possible that the results of the two studies differed because of differences in definitions of AS diagnosis or imprecision in diagnosis codes, they wrote.

The researchers added that “the finding of a 1.21 male-female prevalence ratio of AS in the Canadian Ontario study was also generally consistent with our findings. Similar to our study population, the Canadian population was racially more diverse than the Olmsted study population at the times of both studies.”

Some limitations of the study include the fact that the military population is not a random sample and may have low rates of AS. “It is highly likely that most clinically evident cases of AS would have been screened out prior to enrollment in the military service,” they wrote. “Differences between military service members and the general population may explain why we observed a different association between AS incidence and age in comparison to that reported by prior studies. The increasing risk of AS with adult age that we observed could reflect selective discharge patterns related to very early symptoms of AS in this population.”

The study was funded in part by a grant from the Spondylitis Association of America. No information about potential conflicts of interest was provided in the manuscript.