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Community Outreach Benefits Dermatology Residents and Their Patients

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The sun often is rising in the rearview mirror as I travel with the University of New Mexico dermatology team from Albuquerque to our satellite clinic in Gallup, New Mexico. This twice-monthly trip—with a group usually comprising an attending physician, residents, and medical students—provides an invaluable opportunity for me to take part in delivering care to a majority Native American population and connects our institution and its trainees to the state’s rural and indigenous cultures and communities.

Community outreach is an important initiative for many dermatology residency training programs. Engaging with the community outside the clinic setting allows residents to hone their clinical skills, interact with and meet new people, and help to improve access to health care, especially for members of underserved populations.

Limited access to health care remains a pressing issue in the United States, especially for underserved and rural communities. There currently is no standardized way to measure access to care, but multiple contributing factors have been identified, including but not limited to patient wait times and throughput, provider turnover, ratio of dermatologists to patient population, insurance type, and patient outcomes.1 Fortunately, there are many ways for dermatology residents to get involved and improve access to dermatologic services in their communities, including skin cancer screenings, free clinics, and teledermatology.

Skin Cancer Screenings

More than 40% of community outreach initiatives offered by dermatology residency programs are related to skin cancer screening and prevention.2 The American Academy of Dermatology’s free skin cancer check program (https://www.aad.org/member/career/volunteer/spot) offers a way to participate in or even host a skin cancer screening in your community. Since 1985, this program has identified nearly 300,000 suspicious lesions and more than 30,000 suspected melanomas. Resources for setting up a skin cancer screening in your community are available on the program’s website. Residents may take this opportunity to teach medical students how to perform full-body skin examinations and/or practice making independent decisions as the supervisor for medical trainees. Skin cancer screening events not only expand access to care in underserved communities but also help residents feel more connected to the local community, especially if they have moved to a new location for their residency training.

Free Clinics

Engaging in educational opportunities offered through residency programs is another way to participate in community outreach. In particular, many programs are affiliated with a School of Medicine within their institution that allows residents to spearhead volunteer opportunities such as working at a free clinic. In fact, more than 30% of initiatives offered at dermatology residency programs are free general dermatology clinics.2 Residents are in the unique position of being both learners themselves as well as educators to trainees.3 As part of our role, we can provide crucial specialty care to the community by working in concert with medical students and while also familiarizing ourselves with treating populations that we may not reach in our daily clinical work. For example, by participating in free clinics, we can provide care to vulnerable populations who typically may have financial or time barriers that prevent them from seeking care at the institution-associated clinic, including individuals experiencing homelessness, patients who are uninsured, and individuals who cannot take time off work to pursue medical care. Our presence in the community helps to reduce barriers to specialty care, particularly in the field of dermatology where the access shortage in the context of rising skin cancer rates prompts public health concerns.4

Teledermatology

Teledermatology became a way to extend our reach in the community more than ever before during the COVID-19 pandemic. Advances in audio, visual, and data telecommunication have been particularly helpful in dermatology, a specialty that relies heavily on visual cues for diagnosis. Synchronous, asynchronous, and hybrid teledermatology services implemented during the pandemic have gained favor among patients and dermatologists and are still applied in current practice.5,6

For example, in the state of New Mexico (where there is a severe shortage of board-certified dermatologists to care for the state’s population), teledermatology has allowed rural providers of all specialties to consult University of New Mexico dermatologists by sending clinical photographs along with patient information and history via secure messaging. Instead of having the patient travel hundreds of miles to see the nearest dermatologist for their skin condition or endure long wait times to get in to see a specialist, primary providers now can initiate treatment or work-up for their patient’s skin issue in a timely manner with the use of teledermatology to consult specialists.

Teledermatology has demonstrated cost-effectiveness, accuracy, and efficiency in conveniently expanding access to care. It offers patients and dermatologists flexibility in receiving and delivering health care, respectively.7 As residents, learning how to navigate this technologic frontier in health care delivery is imperative, as it will remain a prevalent tool in the future care of our communities, particularly in underserved areas.

Final Thoughts

Through community outreach initiatives, dermatology residents have an opportunity not only to enrich our education but also to connect with and become closer to our patients. Skin cancer screenings, free clinics, and teledermatology have provided ways to reach more communities and remain important aspects of dermatology residency.

References
  1. Patel B, Blalock TW. Defining “access to care” for dermatology at academic medical institutions. J Am Acad Dermatol. 2023;89:627-628. doi:10.1016/j.jaad.2023.03.014
  2. Fritsche M, Maglakelidze N, Zaenglein A, et al. Community outreach initiatives in dermatology: cross-sectional study. Arch Dermatol Res. 2023;315:2693-2695. doi:10.1007/s00403-023-02629-y
  3. Chiu LW. Teaching tips for dermatology residents. Cutis. 2024;113:E17-E19. doi:10.12788/cutis.1046
  4. Duniphin DD. Limited access to dermatology specialty care: barriers and teledermatology. Dermatol Pract Concept. 2023;13:E2023031. doi:10.5826/dpc.1301a31
  5. Ibrahim AE, Magdy M, Khalaf EM, et al. Teledermatology in the time of COVID-19. Int J Clin Pract. 2021;75:e15000. doi:10.1111/ijcp.15000
  6. Farr MA, Duvic M, Joshi TP. Teledermatology during COVID-19: an updated review. Am J Clin Dermatol. 2021;22:467-475. doi:10.1007/s40257-021-00601-y
  7. Lipner SR. Optimizing patient care with teledermatology: improving access, efficiency, and satisfaction. Cutis. 2024;114:63-64. doi:10.12788/cutis.1073
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Correspondence: Le Wen Chiu, MD, UNMH Dermatology Clinic, 1021 Medical Arts NE, Albuquerque, NM 87102 (LChiu@salud.unm.edu).

Cutis. 2024 October;114(4):E24-E25. doi:10.12788/cutis.1127

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Cutis. 2024 October;114(4):E24-E25. doi:10.12788/cutis.1127

Author and Disclosure Information

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The author has no relevant financial disclosures to report.

Correspondence: Le Wen Chiu, MD, UNMH Dermatology Clinic, 1021 Medical Arts NE, Albuquerque, NM 87102 (LChiu@salud.unm.edu).

Cutis. 2024 October;114(4):E24-E25. doi:10.12788/cutis.1127

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The sun often is rising in the rearview mirror as I travel with the University of New Mexico dermatology team from Albuquerque to our satellite clinic in Gallup, New Mexico. This twice-monthly trip—with a group usually comprising an attending physician, residents, and medical students—provides an invaluable opportunity for me to take part in delivering care to a majority Native American population and connects our institution and its trainees to the state’s rural and indigenous cultures and communities.

Community outreach is an important initiative for many dermatology residency training programs. Engaging with the community outside the clinic setting allows residents to hone their clinical skills, interact with and meet new people, and help to improve access to health care, especially for members of underserved populations.

Limited access to health care remains a pressing issue in the United States, especially for underserved and rural communities. There currently is no standardized way to measure access to care, but multiple contributing factors have been identified, including but not limited to patient wait times and throughput, provider turnover, ratio of dermatologists to patient population, insurance type, and patient outcomes.1 Fortunately, there are many ways for dermatology residents to get involved and improve access to dermatologic services in their communities, including skin cancer screenings, free clinics, and teledermatology.

Skin Cancer Screenings

More than 40% of community outreach initiatives offered by dermatology residency programs are related to skin cancer screening and prevention.2 The American Academy of Dermatology’s free skin cancer check program (https://www.aad.org/member/career/volunteer/spot) offers a way to participate in or even host a skin cancer screening in your community. Since 1985, this program has identified nearly 300,000 suspicious lesions and more than 30,000 suspected melanomas. Resources for setting up a skin cancer screening in your community are available on the program’s website. Residents may take this opportunity to teach medical students how to perform full-body skin examinations and/or practice making independent decisions as the supervisor for medical trainees. Skin cancer screening events not only expand access to care in underserved communities but also help residents feel more connected to the local community, especially if they have moved to a new location for their residency training.

Free Clinics

Engaging in educational opportunities offered through residency programs is another way to participate in community outreach. In particular, many programs are affiliated with a School of Medicine within their institution that allows residents to spearhead volunteer opportunities such as working at a free clinic. In fact, more than 30% of initiatives offered at dermatology residency programs are free general dermatology clinics.2 Residents are in the unique position of being both learners themselves as well as educators to trainees.3 As part of our role, we can provide crucial specialty care to the community by working in concert with medical students and while also familiarizing ourselves with treating populations that we may not reach in our daily clinical work. For example, by participating in free clinics, we can provide care to vulnerable populations who typically may have financial or time barriers that prevent them from seeking care at the institution-associated clinic, including individuals experiencing homelessness, patients who are uninsured, and individuals who cannot take time off work to pursue medical care. Our presence in the community helps to reduce barriers to specialty care, particularly in the field of dermatology where the access shortage in the context of rising skin cancer rates prompts public health concerns.4

Teledermatology

Teledermatology became a way to extend our reach in the community more than ever before during the COVID-19 pandemic. Advances in audio, visual, and data telecommunication have been particularly helpful in dermatology, a specialty that relies heavily on visual cues for diagnosis. Synchronous, asynchronous, and hybrid teledermatology services implemented during the pandemic have gained favor among patients and dermatologists and are still applied in current practice.5,6

For example, in the state of New Mexico (where there is a severe shortage of board-certified dermatologists to care for the state’s population), teledermatology has allowed rural providers of all specialties to consult University of New Mexico dermatologists by sending clinical photographs along with patient information and history via secure messaging. Instead of having the patient travel hundreds of miles to see the nearest dermatologist for their skin condition or endure long wait times to get in to see a specialist, primary providers now can initiate treatment or work-up for their patient’s skin issue in a timely manner with the use of teledermatology to consult specialists.

Teledermatology has demonstrated cost-effectiveness, accuracy, and efficiency in conveniently expanding access to care. It offers patients and dermatologists flexibility in receiving and delivering health care, respectively.7 As residents, learning how to navigate this technologic frontier in health care delivery is imperative, as it will remain a prevalent tool in the future care of our communities, particularly in underserved areas.

Final Thoughts

Through community outreach initiatives, dermatology residents have an opportunity not only to enrich our education but also to connect with and become closer to our patients. Skin cancer screenings, free clinics, and teledermatology have provided ways to reach more communities and remain important aspects of dermatology residency.

The sun often is rising in the rearview mirror as I travel with the University of New Mexico dermatology team from Albuquerque to our satellite clinic in Gallup, New Mexico. This twice-monthly trip—with a group usually comprising an attending physician, residents, and medical students—provides an invaluable opportunity for me to take part in delivering care to a majority Native American population and connects our institution and its trainees to the state’s rural and indigenous cultures and communities.

Community outreach is an important initiative for many dermatology residency training programs. Engaging with the community outside the clinic setting allows residents to hone their clinical skills, interact with and meet new people, and help to improve access to health care, especially for members of underserved populations.

Limited access to health care remains a pressing issue in the United States, especially for underserved and rural communities. There currently is no standardized way to measure access to care, but multiple contributing factors have been identified, including but not limited to patient wait times and throughput, provider turnover, ratio of dermatologists to patient population, insurance type, and patient outcomes.1 Fortunately, there are many ways for dermatology residents to get involved and improve access to dermatologic services in their communities, including skin cancer screenings, free clinics, and teledermatology.

Skin Cancer Screenings

More than 40% of community outreach initiatives offered by dermatology residency programs are related to skin cancer screening and prevention.2 The American Academy of Dermatology’s free skin cancer check program (https://www.aad.org/member/career/volunteer/spot) offers a way to participate in or even host a skin cancer screening in your community. Since 1985, this program has identified nearly 300,000 suspicious lesions and more than 30,000 suspected melanomas. Resources for setting up a skin cancer screening in your community are available on the program’s website. Residents may take this opportunity to teach medical students how to perform full-body skin examinations and/or practice making independent decisions as the supervisor for medical trainees. Skin cancer screening events not only expand access to care in underserved communities but also help residents feel more connected to the local community, especially if they have moved to a new location for their residency training.

Free Clinics

Engaging in educational opportunities offered through residency programs is another way to participate in community outreach. In particular, many programs are affiliated with a School of Medicine within their institution that allows residents to spearhead volunteer opportunities such as working at a free clinic. In fact, more than 30% of initiatives offered at dermatology residency programs are free general dermatology clinics.2 Residents are in the unique position of being both learners themselves as well as educators to trainees.3 As part of our role, we can provide crucial specialty care to the community by working in concert with medical students and while also familiarizing ourselves with treating populations that we may not reach in our daily clinical work. For example, by participating in free clinics, we can provide care to vulnerable populations who typically may have financial or time barriers that prevent them from seeking care at the institution-associated clinic, including individuals experiencing homelessness, patients who are uninsured, and individuals who cannot take time off work to pursue medical care. Our presence in the community helps to reduce barriers to specialty care, particularly in the field of dermatology where the access shortage in the context of rising skin cancer rates prompts public health concerns.4

Teledermatology

Teledermatology became a way to extend our reach in the community more than ever before during the COVID-19 pandemic. Advances in audio, visual, and data telecommunication have been particularly helpful in dermatology, a specialty that relies heavily on visual cues for diagnosis. Synchronous, asynchronous, and hybrid teledermatology services implemented during the pandemic have gained favor among patients and dermatologists and are still applied in current practice.5,6

For example, in the state of New Mexico (where there is a severe shortage of board-certified dermatologists to care for the state’s population), teledermatology has allowed rural providers of all specialties to consult University of New Mexico dermatologists by sending clinical photographs along with patient information and history via secure messaging. Instead of having the patient travel hundreds of miles to see the nearest dermatologist for their skin condition or endure long wait times to get in to see a specialist, primary providers now can initiate treatment or work-up for their patient’s skin issue in a timely manner with the use of teledermatology to consult specialists.

Teledermatology has demonstrated cost-effectiveness, accuracy, and efficiency in conveniently expanding access to care. It offers patients and dermatologists flexibility in receiving and delivering health care, respectively.7 As residents, learning how to navigate this technologic frontier in health care delivery is imperative, as it will remain a prevalent tool in the future care of our communities, particularly in underserved areas.

Final Thoughts

Through community outreach initiatives, dermatology residents have an opportunity not only to enrich our education but also to connect with and become closer to our patients. Skin cancer screenings, free clinics, and teledermatology have provided ways to reach more communities and remain important aspects of dermatology residency.

References
  1. Patel B, Blalock TW. Defining “access to care” for dermatology at academic medical institutions. J Am Acad Dermatol. 2023;89:627-628. doi:10.1016/j.jaad.2023.03.014
  2. Fritsche M, Maglakelidze N, Zaenglein A, et al. Community outreach initiatives in dermatology: cross-sectional study. Arch Dermatol Res. 2023;315:2693-2695. doi:10.1007/s00403-023-02629-y
  3. Chiu LW. Teaching tips for dermatology residents. Cutis. 2024;113:E17-E19. doi:10.12788/cutis.1046
  4. Duniphin DD. Limited access to dermatology specialty care: barriers and teledermatology. Dermatol Pract Concept. 2023;13:E2023031. doi:10.5826/dpc.1301a31
  5. Ibrahim AE, Magdy M, Khalaf EM, et al. Teledermatology in the time of COVID-19. Int J Clin Pract. 2021;75:e15000. doi:10.1111/ijcp.15000
  6. Farr MA, Duvic M, Joshi TP. Teledermatology during COVID-19: an updated review. Am J Clin Dermatol. 2021;22:467-475. doi:10.1007/s40257-021-00601-y
  7. Lipner SR. Optimizing patient care with teledermatology: improving access, efficiency, and satisfaction. Cutis. 2024;114:63-64. doi:10.12788/cutis.1073
References
  1. Patel B, Blalock TW. Defining “access to care” for dermatology at academic medical institutions. J Am Acad Dermatol. 2023;89:627-628. doi:10.1016/j.jaad.2023.03.014
  2. Fritsche M, Maglakelidze N, Zaenglein A, et al. Community outreach initiatives in dermatology: cross-sectional study. Arch Dermatol Res. 2023;315:2693-2695. doi:10.1007/s00403-023-02629-y
  3. Chiu LW. Teaching tips for dermatology residents. Cutis. 2024;113:E17-E19. doi:10.12788/cutis.1046
  4. Duniphin DD. Limited access to dermatology specialty care: barriers and teledermatology. Dermatol Pract Concept. 2023;13:E2023031. doi:10.5826/dpc.1301a31
  5. Ibrahim AE, Magdy M, Khalaf EM, et al. Teledermatology in the time of COVID-19. Int J Clin Pract. 2021;75:e15000. doi:10.1111/ijcp.15000
  6. Farr MA, Duvic M, Joshi TP. Teledermatology during COVID-19: an updated review. Am J Clin Dermatol. 2021;22:467-475. doi:10.1007/s40257-021-00601-y
  7. Lipner SR. Optimizing patient care with teledermatology: improving access, efficiency, and satisfaction. Cutis. 2024;114:63-64. doi:10.12788/cutis.1073
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  • Outreach initiatives can help residents feel more connected to their community and expand access to care.
  • Skin cancer screenings, free clinics, and teledermatology are a few ways residents may get involved in their local communities.
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Eruption of Multiple Linear Hyperpigmented Plaques

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Eruption of Multiple Linear Hyperpigmented Plaques

THE DIAGNOSIS: Chemotherapy-Induced Flagellate Dermatitis

Based on the clinical presentation and temporal relation with chemotherapy, a diagnosis of bleomycininduced flagellate dermatitis (FD) was made, as bleomycin is the only chemotherapeutic agent from this regimen that has been linked with FD.1,2 Laboratory findings revealed eosinophilia, further supporting a druginduced dermatitis. The patient was treated with oral steroids and diphenhydramine to alleviate itching and discomfort. The chemotherapy was temporarily discontinued until symptomatic improvement was observed within 2 to 3 days.

Flagellate dermatitis is characterized by unique erythematous, linear, intermingled streaks of adjoining firm papules—often preceded by a prodrome of global pruritus—that eventually become hyperpigmented as the erythema subsides. The clinical manifestation of FD can be idiopathic; true/mechanical (dermatitis artefacta, abuse, sadomasochism); chemotherapy induced (peplomycin, trastuzumab, cisplatin, docetaxel, bendamustine); toxin induced (shiitake mushroom, cnidarian stings, Paederus insects); related to rheumatologic diseases (dermatomyositis, adult-onset Still disease), dermatographism, phytophotodermatitis, or poison ivy dermatitis; or induced by chikungunya fever.1

The term flagellate originates from the Latin word flagellum, which pertains to the distinctive whiplike pattern. It was first described by Moulin et al3 in 1970 in reference to bleomycin-induced linear hyperpigmentation. Bleomycin, a glycopeptide antibiotic derived from Streptomyces verticillus, is used to treat Hodgkin lymphoma, squamous cell carcinoma, and germ cell tumors. The worldwide incidence of bleomycin-induced FD is 8% to 22% and commonly is associated with a cumulative dose greater than 100 U.2 Clinical presentation is variable in terms of onset, distribution, and morphology of the eruption and could be independent of dose, route of administration, or type of malignancy being treated. The flagellate rash commonly involves the trunk, arms, and legs; can develop within hours to 6 months of starting bleomycin therapy; often is preceded by generalized itching; and eventually heals with hyperpigmentation.

Possible mechanisms of bleomycin-induced FD include localized melanogenesis, inflammatory pigmentary incontinence, alterations to normal pigmentation patterns, cytotoxic effects of the drug itself, minor trauma/ scratching leading to increased blood flow and causing local accumulation of bleomycin, heat recall, and reduced epidermal turnover leading to extended interaction between keratinocytes and melanocytes.2 Heat exposure can act as a trigger for bleomycin-induced skin rash recall even months after the treatment is stopped.

Apart from discontinuing the drug, there is no specific treatment available for bleomycin-induced FD. The primary objective of treatment is to alleviate pruritus, which often involves the use of topical or systemic corticosteroids and oral antihistamines. The duration of treatment depends on the patient’s clinical response. Once treatment is discontinued, FD typically resolves within 6 to 8 months. However, there can be a permanent postinflammatory hyperpigmentation in the affected area.4 Although there is a concern for increased mortality after postponement of chemotherapy,5 the decision to proceed with or discontinue the chemotherapy regimen necessitates a comprehensive interdisciplinary discussion and a meticulous assessment of the risks and benefits that is customized to each individual patient. Flagellate dermatitis can reoccur with bleomycin re-exposure; a combined approach of proactive topical and systemic steroid treatment seems to diminish the likelihood of FD recurrence.5

Our case underscores the importance of recognizing, detecting, and managing FD promptly in individuals undergoing bleomycin-based chemotherapy. Medical professionals should familiarize themselves with this distinct adverse effect linked to bleomycin, enabling prompt discontinuation if necessary, and educate patients about the condition’s typically temporary nature, thereby alleviating their concerns.

References
  1. Bhushan P, Manjul P, Baliyan V. Flagellate dermatoses. Indian J Dermatol Venereol Leprol. 2014;80:149-152.
  2. Ziemer M, Goetze S, Juhasz K, et al. Flagellate dermatitis as a bleomycinspecific adverse effect of cytostatic therapy: a clinical-histopathologic correlation. Am J Clin Dermatol. 2011;12:68-76. doi:10.2165/11537080-000000000-00000
  3. Moulin G, Fière B, Beyvin A. Cutaneous pigmentation caused by bleomycin. Article in French. Bull Soc Fr Dermatol Syphiligr. 1970;77:293-296.
  4. Biswas A, Chaudhari PB, Sharma P, et al. Bleomycin induced flagellate erythema: revisiting a unique complication. J Cancer Res Ther. 2013;9:500-503. doi:10.4103/0973-1482.119358
  5. Hanna TP, King WD, Thibodeau S, et al. Mortality due to cancer treatment delay: systematic review and meta-analysis. BMJ. 2020;371:m4087. doi:10.1136/bmj.m4087
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Drs. Satasia and Hamadani are from the Department of Internal Medicine, Saint Peter’s University Hospital, New Brunswick, New Jersey. Dr. Fein is from the Department of Oncology, Robert Wood Johnson University Hospital, New Brunswick.

The authors have no relevant financial disclosures to report.

Correspondence: Mansi R. Satasia, MD, Saint Peters University Hospital, 254 Easton Ave, New Brunswick, NJ 08901 (msatasia93@gmail.com).

Cutis. 2024 October;114(4):E22-E23. doi:10.12788/cutis.1128

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Drs. Satasia and Hamadani are from the Department of Internal Medicine, Saint Peter’s University Hospital, New Brunswick, New Jersey. Dr. Fein is from the Department of Oncology, Robert Wood Johnson University Hospital, New Brunswick.

The authors have no relevant financial disclosures to report.

Correspondence: Mansi R. Satasia, MD, Saint Peters University Hospital, 254 Easton Ave, New Brunswick, NJ 08901 (msatasia93@gmail.com).

Cutis. 2024 October;114(4):E22-E23. doi:10.12788/cutis.1128

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Drs. Satasia and Hamadani are from the Department of Internal Medicine, Saint Peter’s University Hospital, New Brunswick, New Jersey. Dr. Fein is from the Department of Oncology, Robert Wood Johnson University Hospital, New Brunswick.

The authors have no relevant financial disclosures to report.

Correspondence: Mansi R. Satasia, MD, Saint Peters University Hospital, 254 Easton Ave, New Brunswick, NJ 08901 (msatasia93@gmail.com).

Cutis. 2024 October;114(4):E22-E23. doi:10.12788/cutis.1128

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THE DIAGNOSIS: Chemotherapy-Induced Flagellate Dermatitis

Based on the clinical presentation and temporal relation with chemotherapy, a diagnosis of bleomycininduced flagellate dermatitis (FD) was made, as bleomycin is the only chemotherapeutic agent from this regimen that has been linked with FD.1,2 Laboratory findings revealed eosinophilia, further supporting a druginduced dermatitis. The patient was treated with oral steroids and diphenhydramine to alleviate itching and discomfort. The chemotherapy was temporarily discontinued until symptomatic improvement was observed within 2 to 3 days.

Flagellate dermatitis is characterized by unique erythematous, linear, intermingled streaks of adjoining firm papules—often preceded by a prodrome of global pruritus—that eventually become hyperpigmented as the erythema subsides. The clinical manifestation of FD can be idiopathic; true/mechanical (dermatitis artefacta, abuse, sadomasochism); chemotherapy induced (peplomycin, trastuzumab, cisplatin, docetaxel, bendamustine); toxin induced (shiitake mushroom, cnidarian stings, Paederus insects); related to rheumatologic diseases (dermatomyositis, adult-onset Still disease), dermatographism, phytophotodermatitis, or poison ivy dermatitis; or induced by chikungunya fever.1

The term flagellate originates from the Latin word flagellum, which pertains to the distinctive whiplike pattern. It was first described by Moulin et al3 in 1970 in reference to bleomycin-induced linear hyperpigmentation. Bleomycin, a glycopeptide antibiotic derived from Streptomyces verticillus, is used to treat Hodgkin lymphoma, squamous cell carcinoma, and germ cell tumors. The worldwide incidence of bleomycin-induced FD is 8% to 22% and commonly is associated with a cumulative dose greater than 100 U.2 Clinical presentation is variable in terms of onset, distribution, and morphology of the eruption and could be independent of dose, route of administration, or type of malignancy being treated. The flagellate rash commonly involves the trunk, arms, and legs; can develop within hours to 6 months of starting bleomycin therapy; often is preceded by generalized itching; and eventually heals with hyperpigmentation.

Possible mechanisms of bleomycin-induced FD include localized melanogenesis, inflammatory pigmentary incontinence, alterations to normal pigmentation patterns, cytotoxic effects of the drug itself, minor trauma/ scratching leading to increased blood flow and causing local accumulation of bleomycin, heat recall, and reduced epidermal turnover leading to extended interaction between keratinocytes and melanocytes.2 Heat exposure can act as a trigger for bleomycin-induced skin rash recall even months after the treatment is stopped.

Apart from discontinuing the drug, there is no specific treatment available for bleomycin-induced FD. The primary objective of treatment is to alleviate pruritus, which often involves the use of topical or systemic corticosteroids and oral antihistamines. The duration of treatment depends on the patient’s clinical response. Once treatment is discontinued, FD typically resolves within 6 to 8 months. However, there can be a permanent postinflammatory hyperpigmentation in the affected area.4 Although there is a concern for increased mortality after postponement of chemotherapy,5 the decision to proceed with or discontinue the chemotherapy regimen necessitates a comprehensive interdisciplinary discussion and a meticulous assessment of the risks and benefits that is customized to each individual patient. Flagellate dermatitis can reoccur with bleomycin re-exposure; a combined approach of proactive topical and systemic steroid treatment seems to diminish the likelihood of FD recurrence.5

Our case underscores the importance of recognizing, detecting, and managing FD promptly in individuals undergoing bleomycin-based chemotherapy. Medical professionals should familiarize themselves with this distinct adverse effect linked to bleomycin, enabling prompt discontinuation if necessary, and educate patients about the condition’s typically temporary nature, thereby alleviating their concerns.

THE DIAGNOSIS: Chemotherapy-Induced Flagellate Dermatitis

Based on the clinical presentation and temporal relation with chemotherapy, a diagnosis of bleomycininduced flagellate dermatitis (FD) was made, as bleomycin is the only chemotherapeutic agent from this regimen that has been linked with FD.1,2 Laboratory findings revealed eosinophilia, further supporting a druginduced dermatitis. The patient was treated with oral steroids and diphenhydramine to alleviate itching and discomfort. The chemotherapy was temporarily discontinued until symptomatic improvement was observed within 2 to 3 days.

Flagellate dermatitis is characterized by unique erythematous, linear, intermingled streaks of adjoining firm papules—often preceded by a prodrome of global pruritus—that eventually become hyperpigmented as the erythema subsides. The clinical manifestation of FD can be idiopathic; true/mechanical (dermatitis artefacta, abuse, sadomasochism); chemotherapy induced (peplomycin, trastuzumab, cisplatin, docetaxel, bendamustine); toxin induced (shiitake mushroom, cnidarian stings, Paederus insects); related to rheumatologic diseases (dermatomyositis, adult-onset Still disease), dermatographism, phytophotodermatitis, or poison ivy dermatitis; or induced by chikungunya fever.1

The term flagellate originates from the Latin word flagellum, which pertains to the distinctive whiplike pattern. It was first described by Moulin et al3 in 1970 in reference to bleomycin-induced linear hyperpigmentation. Bleomycin, a glycopeptide antibiotic derived from Streptomyces verticillus, is used to treat Hodgkin lymphoma, squamous cell carcinoma, and germ cell tumors. The worldwide incidence of bleomycin-induced FD is 8% to 22% and commonly is associated with a cumulative dose greater than 100 U.2 Clinical presentation is variable in terms of onset, distribution, and morphology of the eruption and could be independent of dose, route of administration, or type of malignancy being treated. The flagellate rash commonly involves the trunk, arms, and legs; can develop within hours to 6 months of starting bleomycin therapy; often is preceded by generalized itching; and eventually heals with hyperpigmentation.

Possible mechanisms of bleomycin-induced FD include localized melanogenesis, inflammatory pigmentary incontinence, alterations to normal pigmentation patterns, cytotoxic effects of the drug itself, minor trauma/ scratching leading to increased blood flow and causing local accumulation of bleomycin, heat recall, and reduced epidermal turnover leading to extended interaction between keratinocytes and melanocytes.2 Heat exposure can act as a trigger for bleomycin-induced skin rash recall even months after the treatment is stopped.

Apart from discontinuing the drug, there is no specific treatment available for bleomycin-induced FD. The primary objective of treatment is to alleviate pruritus, which often involves the use of topical or systemic corticosteroids and oral antihistamines. The duration of treatment depends on the patient’s clinical response. Once treatment is discontinued, FD typically resolves within 6 to 8 months. However, there can be a permanent postinflammatory hyperpigmentation in the affected area.4 Although there is a concern for increased mortality after postponement of chemotherapy,5 the decision to proceed with or discontinue the chemotherapy regimen necessitates a comprehensive interdisciplinary discussion and a meticulous assessment of the risks and benefits that is customized to each individual patient. Flagellate dermatitis can reoccur with bleomycin re-exposure; a combined approach of proactive topical and systemic steroid treatment seems to diminish the likelihood of FD recurrence.5

Our case underscores the importance of recognizing, detecting, and managing FD promptly in individuals undergoing bleomycin-based chemotherapy. Medical professionals should familiarize themselves with this distinct adverse effect linked to bleomycin, enabling prompt discontinuation if necessary, and educate patients about the condition’s typically temporary nature, thereby alleviating their concerns.

References
  1. Bhushan P, Manjul P, Baliyan V. Flagellate dermatoses. Indian J Dermatol Venereol Leprol. 2014;80:149-152.
  2. Ziemer M, Goetze S, Juhasz K, et al. Flagellate dermatitis as a bleomycinspecific adverse effect of cytostatic therapy: a clinical-histopathologic correlation. Am J Clin Dermatol. 2011;12:68-76. doi:10.2165/11537080-000000000-00000
  3. Moulin G, Fière B, Beyvin A. Cutaneous pigmentation caused by bleomycin. Article in French. Bull Soc Fr Dermatol Syphiligr. 1970;77:293-296.
  4. Biswas A, Chaudhari PB, Sharma P, et al. Bleomycin induced flagellate erythema: revisiting a unique complication. J Cancer Res Ther. 2013;9:500-503. doi:10.4103/0973-1482.119358
  5. Hanna TP, King WD, Thibodeau S, et al. Mortality due to cancer treatment delay: systematic review and meta-analysis. BMJ. 2020;371:m4087. doi:10.1136/bmj.m4087
References
  1. Bhushan P, Manjul P, Baliyan V. Flagellate dermatoses. Indian J Dermatol Venereol Leprol. 2014;80:149-152.
  2. Ziemer M, Goetze S, Juhasz K, et al. Flagellate dermatitis as a bleomycinspecific adverse effect of cytostatic therapy: a clinical-histopathologic correlation. Am J Clin Dermatol. 2011;12:68-76. doi:10.2165/11537080-000000000-00000
  3. Moulin G, Fière B, Beyvin A. Cutaneous pigmentation caused by bleomycin. Article in French. Bull Soc Fr Dermatol Syphiligr. 1970;77:293-296.
  4. Biswas A, Chaudhari PB, Sharma P, et al. Bleomycin induced flagellate erythema: revisiting a unique complication. J Cancer Res Ther. 2013;9:500-503. doi:10.4103/0973-1482.119358
  5. Hanna TP, King WD, Thibodeau S, et al. Mortality due to cancer treatment delay: systematic review and meta-analysis. BMJ. 2020;371:m4087. doi:10.1136/bmj.m4087
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A 28-year-old man presented for evaluation of an intensely itchy rash of 5 days’ duration involving the face, trunk, arms, and legs. The patient recently had been diagnosed with classical Hodgkin lymphoma and was started on a biweekly chemotherapy regimen of adriamycin, bleomycin, vinblastine, and dacarbazine 3 weeks prior. He reported that a red, itchy, papular rash had developed on the hands 1 week after starting chemotherapy and improved with antihistamines. Symptoms of the current rash included night sweats, occasional fever, substantial unintentional weight loss, and fatigue. He had no history of urticaria, angioedema, anaphylaxis, or nail changes.

Physical examination revealed widespread, itchy, linear and curvilinear hyperpigmented plaques on the upper arms, shoulders, back (top), face, and thighs, as well as erythematous grouped papules on the bilateral palms (bottom). There was no mucosal or systemic involvement.

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Six Tips for Media Interviews

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As a physician, you might be contacted by the media to provide your professional opinion and advice. Or you might be looking for media interview opportunities to market your practice or side project. And if you do research, media interviews can be an effective way to spread the word. It’s important to prepare for a media interview so that you achieve the outcome you are looking for. Here are six tips I learned from writing health articles, interviewing experts, and being interviewed myself. 

Keep your message simple. When you are a subject expert, you might think that the basics are obvious or even boring, and that the nuances are more important. However, most of the audience is looking for big-picture information that they can apply to their lives. Consider a few key takeaways, keeping in mind that your interview is likely to be edited to short sound bites or a few quotes. It may help to jot down notes so that you cover the fundamentals clearly. You could even write and rehearse a script beforehand. If there is something complicated or subtle that you want to convey, you can preface it by saying, “This is confusing but very important …” to let the audience know to give extra consideration to what you are about to say.

Avoid extremes and hyperbole. Sometimes, exaggerated statements make their way into medical discussions. Statements such as “it doesn’t matter how many calories you consume — it’s all about the quality” are common oversimplifications. But you might be upset to see your name next to a comment like this because it is not actually correct. Check the phrasing of your key takeaways to avoid being stuck defending or explaining an inaccurate statement when your patients ask you about it later. 

Ask the interviewers what they are looking for. Many medical topics have some controversial element, so it is good to know what you’re getting into. Find out the purpose of the article or interview before you decide whether it is right for you. It could be about another doctor in town who is being sued; if you don’t want to be associated with that story, it might be best to decline the interview. 

Explain your goals. You might accept or pursue an interview to raise awareness about an underrecognized condition. You might want the public to identify and get help for early symptoms, or you might want to create empathy for people coping with a disease you treat. Consider why you are participating in an interview, and communicate that to the interviewer to ensure that your objective can be part of the final product. 

Know whom you’re dealing with. It is good to learn about the publication/media channel before you agree to participate. It may have a political bias, or perhaps the interview is intended to promote a specific product. If you agree with and support their purposes, then you may be happy to lend your opinion. But learning about the “voice” of the publication in advance allows you to make an informed decision about whether you want to be identified with a particular political ideology or product endorsement.

Ask to see your quotes before publication. It’s good to have the opportunity to make corrections in case you are accidentally misquoted or misunderstood. It is best to ask to see quotes before you agree to the interview. Some reporters may agree to (or even prefer) a written question-and-answer format so that they can directly quote your responses without rephrasing your words. You could suggest this, especially if you are too busy for a call or live meeting.

As a physician, your insights and advice can be highly beneficial to others. You can also use media interviews to propel your career forward. Doing your homework can ensure that you will be pleased with the final product and how your words were used. 
 

Dr. Moawad, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

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As a physician, you might be contacted by the media to provide your professional opinion and advice. Or you might be looking for media interview opportunities to market your practice or side project. And if you do research, media interviews can be an effective way to spread the word. It’s important to prepare for a media interview so that you achieve the outcome you are looking for. Here are six tips I learned from writing health articles, interviewing experts, and being interviewed myself. 

Keep your message simple. When you are a subject expert, you might think that the basics are obvious or even boring, and that the nuances are more important. However, most of the audience is looking for big-picture information that they can apply to their lives. Consider a few key takeaways, keeping in mind that your interview is likely to be edited to short sound bites or a few quotes. It may help to jot down notes so that you cover the fundamentals clearly. You could even write and rehearse a script beforehand. If there is something complicated or subtle that you want to convey, you can preface it by saying, “This is confusing but very important …” to let the audience know to give extra consideration to what you are about to say.

Avoid extremes and hyperbole. Sometimes, exaggerated statements make their way into medical discussions. Statements such as “it doesn’t matter how many calories you consume — it’s all about the quality” are common oversimplifications. But you might be upset to see your name next to a comment like this because it is not actually correct. Check the phrasing of your key takeaways to avoid being stuck defending or explaining an inaccurate statement when your patients ask you about it later. 

Ask the interviewers what they are looking for. Many medical topics have some controversial element, so it is good to know what you’re getting into. Find out the purpose of the article or interview before you decide whether it is right for you. It could be about another doctor in town who is being sued; if you don’t want to be associated with that story, it might be best to decline the interview. 

Explain your goals. You might accept or pursue an interview to raise awareness about an underrecognized condition. You might want the public to identify and get help for early symptoms, or you might want to create empathy for people coping with a disease you treat. Consider why you are participating in an interview, and communicate that to the interviewer to ensure that your objective can be part of the final product. 

Know whom you’re dealing with. It is good to learn about the publication/media channel before you agree to participate. It may have a political bias, or perhaps the interview is intended to promote a specific product. If you agree with and support their purposes, then you may be happy to lend your opinion. But learning about the “voice” of the publication in advance allows you to make an informed decision about whether you want to be identified with a particular political ideology or product endorsement.

Ask to see your quotes before publication. It’s good to have the opportunity to make corrections in case you are accidentally misquoted or misunderstood. It is best to ask to see quotes before you agree to the interview. Some reporters may agree to (or even prefer) a written question-and-answer format so that they can directly quote your responses without rephrasing your words. You could suggest this, especially if you are too busy for a call or live meeting.

As a physician, your insights and advice can be highly beneficial to others. You can also use media interviews to propel your career forward. Doing your homework can ensure that you will be pleased with the final product and how your words were used. 
 

Dr. Moawad, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

As a physician, you might be contacted by the media to provide your professional opinion and advice. Or you might be looking for media interview opportunities to market your practice or side project. And if you do research, media interviews can be an effective way to spread the word. It’s important to prepare for a media interview so that you achieve the outcome you are looking for. Here are six tips I learned from writing health articles, interviewing experts, and being interviewed myself. 

Keep your message simple. When you are a subject expert, you might think that the basics are obvious or even boring, and that the nuances are more important. However, most of the audience is looking for big-picture information that they can apply to their lives. Consider a few key takeaways, keeping in mind that your interview is likely to be edited to short sound bites or a few quotes. It may help to jot down notes so that you cover the fundamentals clearly. You could even write and rehearse a script beforehand. If there is something complicated or subtle that you want to convey, you can preface it by saying, “This is confusing but very important …” to let the audience know to give extra consideration to what you are about to say.

Avoid extremes and hyperbole. Sometimes, exaggerated statements make their way into medical discussions. Statements such as “it doesn’t matter how many calories you consume — it’s all about the quality” are common oversimplifications. But you might be upset to see your name next to a comment like this because it is not actually correct. Check the phrasing of your key takeaways to avoid being stuck defending or explaining an inaccurate statement when your patients ask you about it later. 

Ask the interviewers what they are looking for. Many medical topics have some controversial element, so it is good to know what you’re getting into. Find out the purpose of the article or interview before you decide whether it is right for you. It could be about another doctor in town who is being sued; if you don’t want to be associated with that story, it might be best to decline the interview. 

Explain your goals. You might accept or pursue an interview to raise awareness about an underrecognized condition. You might want the public to identify and get help for early symptoms, or you might want to create empathy for people coping with a disease you treat. Consider why you are participating in an interview, and communicate that to the interviewer to ensure that your objective can be part of the final product. 

Know whom you’re dealing with. It is good to learn about the publication/media channel before you agree to participate. It may have a political bias, or perhaps the interview is intended to promote a specific product. If you agree with and support their purposes, then you may be happy to lend your opinion. But learning about the “voice” of the publication in advance allows you to make an informed decision about whether you want to be identified with a particular political ideology or product endorsement.

Ask to see your quotes before publication. It’s good to have the opportunity to make corrections in case you are accidentally misquoted or misunderstood. It is best to ask to see quotes before you agree to the interview. Some reporters may agree to (or even prefer) a written question-and-answer format so that they can directly quote your responses without rephrasing your words. You could suggest this, especially if you are too busy for a call or live meeting.

As a physician, your insights and advice can be highly beneficial to others. You can also use media interviews to propel your career forward. Doing your homework can ensure that you will be pleased with the final product and how your words were used. 
 

Dr. Moawad, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

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Study Finds Elevated Skin Cancer Risk Among US Veterans

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US veterans were nearly three times more likely to develop skin cancer than the general population, according to a large cross-sectional analysis of recent national data.

“US veterans are known to have increased risk of cancers and cancer morbidity compared to the general US population,” one of the study authors, Sepideh Ashrafzadeh, MD, a third-year dermatology resident at Massachusetts General Hospital, Boston, told this news organization following the annual meeting of the American Society for Dermatologic Surgery, where the results were presented. “There have been several studies that have shown that US veterans have an increased prevalence of melanoma compared to nonveterans,” she said, noting, however, that no study has investigated the prevalence of nonmelanoma skin cancers (NMSCs), which include basal cell carcinomas and squamous cell carcinomas, compared with the general population.

Dr. Ashrafzadeh
Dr. Sepideh Ashrafzadeh

To address this knowledge gap, the researchers performed a national cross-sectional study of adults aged 18 years or older from the 2019-2023 National Health Interview Surveys to examine the prevalence of melanoma and NMSCs among veterans compared with the general US population. They aggregated and tabulated the data by veteran status, defined as having served at any point in the US armed forces, reserves, or national guard, and by demographic and socioeconomic status variables. Next, they performed multivariate logistic regression for skin cancer risk adjusted for age, sex, race, ethnicity, urbanicity, and disability status.

The study population consisted of 14,301 veterans and 209,936 nonveterans. Compared with nonveterans, veterans were more likely to have been diagnosed with skin cancer at some point in their lives (7% vs 2.4%; P < .001); had a higher mean age of skin cancer diagnosis (61.1 vs 55.8 years; P < .001); were more likely to have been diagnosed with melanoma (2.8% vs 0.9%; P < .001), and were more likely to have been diagnosed with NMSC (4.4% vs 1.6%; P < .001).

The researchers found that older age, White race, non-Hispanic ethnicity, and veteran status were all associated with higher odds of developing NMSCs, even after adjusting for relevant covariates. Specifically, veterans had 1.23 higher odds of developing NMSC than the general population, while two factors were protective for developing NMSCs: Living in a rural setting (adjusted odds ratio [aOR], 0.78) and receiving supplemental security income or disability income (aOR, 0.69).

In another part of the study, the researchers evaluated demographic and socioeconomic variables associated with developing melanoma among veterans. These included the following: Male (aOR, 1.16), older age (50-64 years: aOR, 6.82; 65-74 years: aOR, 12.55; and 75 years or older: aOR, 16.16), White race (aOR, 9.24), and non-Hispanic ethnicity (aOR, 7.15).

“Veterans may have occupational risks such as sun and chemical exposure, as well as behavioral habits for sun protection, that may contribute to their elevated risk of melanoma and NMSCs,” Ashrafzadeh said. “Therefore, US veterans would benefit from targeted and regular skin cancer screenings, sun protective preventative resources such as hats and sunscreen, and access to medical and surgical care for diagnosis and treatment of skin cancers.”

Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Connecticut, who was asked to comment on the findings, said that a key strength of the study is that it drew from a nationally representative sample. “A limitation is that skin cancer was self-reported rather than based on documented medical histories,” Ko said. “The study confirms that skin cancer risk is higher in older individuals (> 75 as compared to < 50) and in individuals of self-reported white race and non-Hispanic ethnicity,” she added.

Neither the researchers nor Ko reported having relevant disclosures.
 

A version of this article first appeared on Medscape.com.

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US veterans were nearly three times more likely to develop skin cancer than the general population, according to a large cross-sectional analysis of recent national data.

“US veterans are known to have increased risk of cancers and cancer morbidity compared to the general US population,” one of the study authors, Sepideh Ashrafzadeh, MD, a third-year dermatology resident at Massachusetts General Hospital, Boston, told this news organization following the annual meeting of the American Society for Dermatologic Surgery, where the results were presented. “There have been several studies that have shown that US veterans have an increased prevalence of melanoma compared to nonveterans,” she said, noting, however, that no study has investigated the prevalence of nonmelanoma skin cancers (NMSCs), which include basal cell carcinomas and squamous cell carcinomas, compared with the general population.

Dr. Ashrafzadeh
Dr. Sepideh Ashrafzadeh

To address this knowledge gap, the researchers performed a national cross-sectional study of adults aged 18 years or older from the 2019-2023 National Health Interview Surveys to examine the prevalence of melanoma and NMSCs among veterans compared with the general US population. They aggregated and tabulated the data by veteran status, defined as having served at any point in the US armed forces, reserves, or national guard, and by demographic and socioeconomic status variables. Next, they performed multivariate logistic regression for skin cancer risk adjusted for age, sex, race, ethnicity, urbanicity, and disability status.

The study population consisted of 14,301 veterans and 209,936 nonveterans. Compared with nonveterans, veterans were more likely to have been diagnosed with skin cancer at some point in their lives (7% vs 2.4%; P < .001); had a higher mean age of skin cancer diagnosis (61.1 vs 55.8 years; P < .001); were more likely to have been diagnosed with melanoma (2.8% vs 0.9%; P < .001), and were more likely to have been diagnosed with NMSC (4.4% vs 1.6%; P < .001).

The researchers found that older age, White race, non-Hispanic ethnicity, and veteran status were all associated with higher odds of developing NMSCs, even after adjusting for relevant covariates. Specifically, veterans had 1.23 higher odds of developing NMSC than the general population, while two factors were protective for developing NMSCs: Living in a rural setting (adjusted odds ratio [aOR], 0.78) and receiving supplemental security income or disability income (aOR, 0.69).

In another part of the study, the researchers evaluated demographic and socioeconomic variables associated with developing melanoma among veterans. These included the following: Male (aOR, 1.16), older age (50-64 years: aOR, 6.82; 65-74 years: aOR, 12.55; and 75 years or older: aOR, 16.16), White race (aOR, 9.24), and non-Hispanic ethnicity (aOR, 7.15).

“Veterans may have occupational risks such as sun and chemical exposure, as well as behavioral habits for sun protection, that may contribute to their elevated risk of melanoma and NMSCs,” Ashrafzadeh said. “Therefore, US veterans would benefit from targeted and regular skin cancer screenings, sun protective preventative resources such as hats and sunscreen, and access to medical and surgical care for diagnosis and treatment of skin cancers.”

Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Connecticut, who was asked to comment on the findings, said that a key strength of the study is that it drew from a nationally representative sample. “A limitation is that skin cancer was self-reported rather than based on documented medical histories,” Ko said. “The study confirms that skin cancer risk is higher in older individuals (> 75 as compared to < 50) and in individuals of self-reported white race and non-Hispanic ethnicity,” she added.

Neither the researchers nor Ko reported having relevant disclosures.
 

A version of this article first appeared on Medscape.com.

US veterans were nearly three times more likely to develop skin cancer than the general population, according to a large cross-sectional analysis of recent national data.

“US veterans are known to have increased risk of cancers and cancer morbidity compared to the general US population,” one of the study authors, Sepideh Ashrafzadeh, MD, a third-year dermatology resident at Massachusetts General Hospital, Boston, told this news organization following the annual meeting of the American Society for Dermatologic Surgery, where the results were presented. “There have been several studies that have shown that US veterans have an increased prevalence of melanoma compared to nonveterans,” she said, noting, however, that no study has investigated the prevalence of nonmelanoma skin cancers (NMSCs), which include basal cell carcinomas and squamous cell carcinomas, compared with the general population.

Dr. Ashrafzadeh
Dr. Sepideh Ashrafzadeh

To address this knowledge gap, the researchers performed a national cross-sectional study of adults aged 18 years or older from the 2019-2023 National Health Interview Surveys to examine the prevalence of melanoma and NMSCs among veterans compared with the general US population. They aggregated and tabulated the data by veteran status, defined as having served at any point in the US armed forces, reserves, or national guard, and by demographic and socioeconomic status variables. Next, they performed multivariate logistic regression for skin cancer risk adjusted for age, sex, race, ethnicity, urbanicity, and disability status.

The study population consisted of 14,301 veterans and 209,936 nonveterans. Compared with nonveterans, veterans were more likely to have been diagnosed with skin cancer at some point in their lives (7% vs 2.4%; P < .001); had a higher mean age of skin cancer diagnosis (61.1 vs 55.8 years; P < .001); were more likely to have been diagnosed with melanoma (2.8% vs 0.9%; P < .001), and were more likely to have been diagnosed with NMSC (4.4% vs 1.6%; P < .001).

The researchers found that older age, White race, non-Hispanic ethnicity, and veteran status were all associated with higher odds of developing NMSCs, even after adjusting for relevant covariates. Specifically, veterans had 1.23 higher odds of developing NMSC than the general population, while two factors were protective for developing NMSCs: Living in a rural setting (adjusted odds ratio [aOR], 0.78) and receiving supplemental security income or disability income (aOR, 0.69).

In another part of the study, the researchers evaluated demographic and socioeconomic variables associated with developing melanoma among veterans. These included the following: Male (aOR, 1.16), older age (50-64 years: aOR, 6.82; 65-74 years: aOR, 12.55; and 75 years or older: aOR, 16.16), White race (aOR, 9.24), and non-Hispanic ethnicity (aOR, 7.15).

“Veterans may have occupational risks such as sun and chemical exposure, as well as behavioral habits for sun protection, that may contribute to their elevated risk of melanoma and NMSCs,” Ashrafzadeh said. “Therefore, US veterans would benefit from targeted and regular skin cancer screenings, sun protective preventative resources such as hats and sunscreen, and access to medical and surgical care for diagnosis and treatment of skin cancers.”

Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Connecticut, who was asked to comment on the findings, said that a key strength of the study is that it drew from a nationally representative sample. “A limitation is that skin cancer was self-reported rather than based on documented medical histories,” Ko said. “The study confirms that skin cancer risk is higher in older individuals (> 75 as compared to < 50) and in individuals of self-reported white race and non-Hispanic ethnicity,” she added.

Neither the researchers nor Ko reported having relevant disclosures.
 

A version of this article first appeared on Medscape.com.

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Cancer’s Other Toll: Long-Term Financial Fallout for Survivors

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— While the physical toll of cancer is well documented, the financial toll can also be severe and lasting.

Overall, patients with cancer tend to face higher rates of debt collection, medical collections, and bankruptcies, as well as lower credit scores, according to two new studies presented at the American College of Surgeons Clinical Congress 2024.

“These are the first studies to provide numerical evidence of financial toxicity among cancer survivors,” Benjamin C. James, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, both in Boston, Massachusetts, who worked on both studies, said in a statement. “Previous data on this topic largely relies on subjective survey reviews.”

In one study, researchers used the Massachusetts Cancer Registry to identify 99,175 patients diagnosed with cancer between 2010 and 2019 and matched them with 188,875 control individuals without cancer. Researchers then assessed financial toxicity using Experian credit bureau data for participants.

Overall, patients with cancer faced a range of financial challenges that often lasted years following their diagnosis.

Patients were nearly five times more likely to experience bankruptcy and had average credit scores nearly 80 points lower than control individuals without cancer. The drop in credit scores was more pronounced for survivors of bladder, liver, lung, and colorectal cancer (CRC) and persisted for up to 9.5 years.

For certain cancer types, in particular, “we are looking years after a diagnosis, and we see that the credit score goes down and it never comes back up,” James said.

The other study, which used a sample of 7227 patients with CRC from Massachusetts, identified several factors that correlated with lower credit scores.

Compared with patients who only had surgery, peers who underwent radiation only experienced a 62-point drop in their credit score after their diagnosis, while those who had chemotherapy alone had just over a 14-point drop in their credit score. Among patients who had combination treatments, those who underwent both surgery and radiation experienced a nearly 16-point drop in their credit score and those who had surgery and chemoradiation actually experienced a 2.59 bump, compared with those who had surgery alone.

Financial toxicity was worse for patients younger than 62 years, those identifying as Black or Hispanic individuals, unmarried individuals, those with an annual income below $52,000, and those living in deprived areas.

The studies add to findings from the 2015 North American Thyroid Cancer Survivorship Study, which reported that 50% of thyroid cancer survivors encountered financial toxicity because of their diagnosis.

James said the persistent financial strain of cancer care, even in a state like Massachusetts, which mandates universal healthcare, underscores the need for “broader policy changes and reforms, including reconsidering debt collection practices.”

“Financial security should be a priority in cancer care,” he added.

The studies had no specific funding. The authors have disclosed no relevant conflict of interest.

A version of this article first appeared on Medscape.com.

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— While the physical toll of cancer is well documented, the financial toll can also be severe and lasting.

Overall, patients with cancer tend to face higher rates of debt collection, medical collections, and bankruptcies, as well as lower credit scores, according to two new studies presented at the American College of Surgeons Clinical Congress 2024.

“These are the first studies to provide numerical evidence of financial toxicity among cancer survivors,” Benjamin C. James, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, both in Boston, Massachusetts, who worked on both studies, said in a statement. “Previous data on this topic largely relies on subjective survey reviews.”

In one study, researchers used the Massachusetts Cancer Registry to identify 99,175 patients diagnosed with cancer between 2010 and 2019 and matched them with 188,875 control individuals without cancer. Researchers then assessed financial toxicity using Experian credit bureau data for participants.

Overall, patients with cancer faced a range of financial challenges that often lasted years following their diagnosis.

Patients were nearly five times more likely to experience bankruptcy and had average credit scores nearly 80 points lower than control individuals without cancer. The drop in credit scores was more pronounced for survivors of bladder, liver, lung, and colorectal cancer (CRC) and persisted for up to 9.5 years.

For certain cancer types, in particular, “we are looking years after a diagnosis, and we see that the credit score goes down and it never comes back up,” James said.

The other study, which used a sample of 7227 patients with CRC from Massachusetts, identified several factors that correlated with lower credit scores.

Compared with patients who only had surgery, peers who underwent radiation only experienced a 62-point drop in their credit score after their diagnosis, while those who had chemotherapy alone had just over a 14-point drop in their credit score. Among patients who had combination treatments, those who underwent both surgery and radiation experienced a nearly 16-point drop in their credit score and those who had surgery and chemoradiation actually experienced a 2.59 bump, compared with those who had surgery alone.

Financial toxicity was worse for patients younger than 62 years, those identifying as Black or Hispanic individuals, unmarried individuals, those with an annual income below $52,000, and those living in deprived areas.

The studies add to findings from the 2015 North American Thyroid Cancer Survivorship Study, which reported that 50% of thyroid cancer survivors encountered financial toxicity because of their diagnosis.

James said the persistent financial strain of cancer care, even in a state like Massachusetts, which mandates universal healthcare, underscores the need for “broader policy changes and reforms, including reconsidering debt collection practices.”

“Financial security should be a priority in cancer care,” he added.

The studies had no specific funding. The authors have disclosed no relevant conflict of interest.

A version of this article first appeared on Medscape.com.

— While the physical toll of cancer is well documented, the financial toll can also be severe and lasting.

Overall, patients with cancer tend to face higher rates of debt collection, medical collections, and bankruptcies, as well as lower credit scores, according to two new studies presented at the American College of Surgeons Clinical Congress 2024.

“These are the first studies to provide numerical evidence of financial toxicity among cancer survivors,” Benjamin C. James, MD, with Beth Israel Deaconess Medical Center and Harvard Medical School, both in Boston, Massachusetts, who worked on both studies, said in a statement. “Previous data on this topic largely relies on subjective survey reviews.”

In one study, researchers used the Massachusetts Cancer Registry to identify 99,175 patients diagnosed with cancer between 2010 and 2019 and matched them with 188,875 control individuals without cancer. Researchers then assessed financial toxicity using Experian credit bureau data for participants.

Overall, patients with cancer faced a range of financial challenges that often lasted years following their diagnosis.

Patients were nearly five times more likely to experience bankruptcy and had average credit scores nearly 80 points lower than control individuals without cancer. The drop in credit scores was more pronounced for survivors of bladder, liver, lung, and colorectal cancer (CRC) and persisted for up to 9.5 years.

For certain cancer types, in particular, “we are looking years after a diagnosis, and we see that the credit score goes down and it never comes back up,” James said.

The other study, which used a sample of 7227 patients with CRC from Massachusetts, identified several factors that correlated with lower credit scores.

Compared with patients who only had surgery, peers who underwent radiation only experienced a 62-point drop in their credit score after their diagnosis, while those who had chemotherapy alone had just over a 14-point drop in their credit score. Among patients who had combination treatments, those who underwent both surgery and radiation experienced a nearly 16-point drop in their credit score and those who had surgery and chemoradiation actually experienced a 2.59 bump, compared with those who had surgery alone.

Financial toxicity was worse for patients younger than 62 years, those identifying as Black or Hispanic individuals, unmarried individuals, those with an annual income below $52,000, and those living in deprived areas.

The studies add to findings from the 2015 North American Thyroid Cancer Survivorship Study, which reported that 50% of thyroid cancer survivors encountered financial toxicity because of their diagnosis.

James said the persistent financial strain of cancer care, even in a state like Massachusetts, which mandates universal healthcare, underscores the need for “broader policy changes and reforms, including reconsidering debt collection practices.”

“Financial security should be a priority in cancer care,” he added.

The studies had no specific funding. The authors have disclosed no relevant conflict of interest.

A version of this article first appeared on Medscape.com.

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Asteraceae Dermatitis: Everyday Plants With Allergenic Potential

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Asteraceae Dermatitis: Everyday Plants With Allergenic Potential

The Asteraceae (formerly Compositae) family of plants is derived from the ancient Greek word aster, meaning “star,” referring to the starlike arrangement of flower petals around a central disc known as a capitulum. What initially appears as a single flower is actually a composite of several smaller flowers, hence the former name Compositae.1 Well-known members of the Asteraceae family include ornamental annuals (eg, sunflowers, marigolds, cosmos), herbaceous ­perennials (eg, chrysanthemums, dandelions), vegetables (eg, lettuce, chicory, artichokes), herbs (eg, chamomile, tarragon), and weeds (eg, ragweed, horseweed, capeweed)(Figure 1).2

FIGURE 1. Members of the Asteraceae family. A, Black-eyed Susan (Rudbeckia hirta). B, Purple coneflower (Echinacea purpurea). C, Indian blanket (Gaillardia pulchella). D, Oxeye daisy (Leucanthemum vulgare).

There are more than 25,000 species of Asteraceae plants that thrive in a wide range of climates worldwide. Cases of Asteraceae-induced skin reactions have been reported in North America, Europe, Asia, and Australia.3 Members of the Asteraceae family are ubiquitous in gardens, along roadsides, and in the wilderness. Occupational exposure commonly affects gardeners, florists, farmers, and forestry workers through either direct contact with plants or via airborne pollen. Furthermore, plants of the Asteraceae family are used in various products, including pediculicides (eg, insect repellents), cosmetics (eg, eye creams, body washes), and food products (eg, cooking oils, sweetening agents, coffee substitutes, herbal teas).4-6 These plants have substantial allergic potential, resulting in numerous cutaneous reactions.

Allergic Potential

Asteraceae plants can elicit both immediate and delayed hypersensitivity reactions (HSRs); for instance, exposure to ragweed pollen may cause an IgE-mediated type 1 HSR manifesting as allergic rhinitis or a type IV HSR manifesting as airborne allergic contact dermatitis.7,8 The main contact allergens present in Asteraceae plants are sesquiterpene lactones, which are found in the leaves, stems, flowers, and pollen.9-11 Sesquiterpene lactones consist of an α-methyl group attached to a lactone ring combined with a sesquiterpene.12 Patch testing can be used to diagnose Asteraceae allergy; however, the results are not consistently reliable because there is no perfect screening allergen. Patch test preparations commonly used to detect Asteraceae allergy include Compositae mix (consisting of Anthemis nobilis extract, Chamomilla recutita extract, Achillea millefolium extract, Tanacetum vulgare extract, Arnica montana extract, and parthenolide) and sesquiterpene lactone mix (consisting of alantolactone, dehydrocostus lactone, and costunolide). In North America, the prevalence of positive patch tests to Compositae mix and sesquiterpene lactone mix is approximately 2% and 0.5%, respectively.13 When patch testing is performed, both Compositae mix and sesquiterpene lactone mix should be utilized to minimize the risk of missing Asteraceae allergy, as sesquiterpene lactone mix alone does not detect all Compositae-sensitized patients. Additionally, it may be necessary to test supplemental Asteraceae allergens, including preparations from specific plants to which the patient has been exposed. Exposure to Asteraceae-containing cosmetic products may lead to dermatitis, though this is highly dependent on the particular plant species involved. For instance, the prevalence of sensitization is high in arnica (tincture) and elecampane but low with more commonly used species such as German chamomile.14

Cutaneous Manifestations

Asteraceae dermatitis, which also is known as Australian bush dermatitis, weed dermatitis, and chrysanthemum dermatitis,2 can manifest on any area of the body that directly contacts the plant or is exposed to the pollen. Asteraceae dermatitis historically was reported in older adults with a recent history of plant exposure.6,15 However, recent data have shown a female preponderance and a younger mean age of onset (46–49 years).16

There are multiple distinct clinical manifestations of Asteraceae dermatitis. The most common cutaneous finding is localized vesicular or eczematous patches on the hands or wrists. Other variations include eczematous rashes on the exposed skin of the hands, arms, face, and neck; generalized eczema; and isolated facial eczema.16,17 These variations can be attributed to contact dermatitis caused by airborne pollen, which may mimic photodermatitis. However, airborne Asteraceae dermatitis can be distinguished clinically from photodermatitis by the involvement of sun-protected areas such as the skinfolds of the eyelids, retroauricular sulci, and nasolabial folds (Figure 2).2,9 In rare cases, systemic allergic contact dermatitis can occur if the Asteraceae allergen is ingested.2,18

FIGURE 2. Characteristic sparing of the shaded areas of the face in airborne Asteraceae dermatitis.


Other diagnostic clues include dermatitis that flares during the summer, at the peak of the growing season, with remission in the cooler months. Potential risk factors include a childhood history of atopic dermatitis and allergic rhinitis.16 With prolonged exposure, patients may develop chronic actinic dermatitis, an immunologically mediated photodermatosis characterized by lichenified and pruritic eczematous plaques located predominantly on sun-exposed areas with notable sparing of the skin folds.19 The association between Asteraceae dermatitis and chronic actinic dermatitis is highly variable, with some studies reporting a 25% correlation and others finding a stronger association of up to 80%.2,15,20 Asteraceae allergy appears to be a relatively uncommon cause of photoallergy in North America. In one recent study, 16% (3/19) of patients with chronic actinic dermatitis had positive patch or photopatch tests to sesquiterpene lactone mix, but in another large study of photopatch testing it was reported to be a rare photoallergen.21,22

Parthenium dermatitis is an allergic contact dermatitis caused by exposure to Parthenium hysterophorus, a weed of the Asteraceae family that is responsible for 30% of cases of contact dermatitis in India.23,24 Unlike the more classic manifestation of Asteraceae dermatitis, which primarily affects the upper extremities in cases from North America and Europe, Parthenium dermatitis typically occurs in an airborne pattern distribution.24

Management

While complete avoidance of Asteraceae plants is ideal, it often is unrealistic due to their abundance in nature. Therefore, minimizing exposure to the causative plants is recommended. Primary preventive measures such as wearing protective gloves and clothing and applying bentonite clay prior to exposure should be taken when working outdoors. Promptly showering after contact with plants also can reduce the risk for Asteraceae dermatitis.

Symptomatic treatment is appropriate for mild cases and includes topical corticosteroids and calcineurin inhibitors. For severe cases, systemic corticosteroids may be needed for acute flares, with azathioprine, mycophenolate, cyclosporine, or methotrexate available for recalcitrant disease. Verma et al25 found that treatment with azathioprine for 6 months resulted in greater than 60% clearance in all 12 patients, with a majority achieving 80% to 100% clearance. Methotrexate has been used at doses of 15 mg once weekly.26 Narrowband UVB and psoralen plus UVA have been effective in extensive cases; however, care should be exercised in patients with photosensitive dermatitis, who instead should practice strict photoprotection.27-29 Lakshmi et al30 reported the use of cyclosporine during the acute phase of Asteraceae dermatitis at a dose of 2.5 mg/kg daily for 4 to 8 weeks. There have been several case reports of dupilumab treating allergic contact dermatitis; however, there have been 3 cases of patients with atopic dermatitis developing Asteraceae dermatitis while taking dupilumab.31,32 Recently, oral Janus kinase inhibitors have shown success in treating refractory cases of airborne Asteraceae dermatitis.33,34 Further research is needed to determine the safety and efficacy of dupilumab and Janus kinase inhibitors for treatment of Asteraceae dermatitis.

Final Thoughts

The Asteraceae plant family is vast and diverse, with more than 200 species reported to cause allergic contact dermatitis.12 Common modes of contact include gardening, occupational exposure, airborne pollen, and use of pediculicides and cosmetics that contain components of Asteraceae plants. Educating patients on how to minimize contact with Asteraceae plants is the most effective management strategy; topical agents and oral immunosuppressives can be used for symptomatic treatment.

References
  1. Morhardt S, Morhardt E. California Desert Flowers: An Introduction to Families, Genera, and Species. University of California Press; 2004.
  2. Gordon LA. Compositae dermatitis. Australas J Dermatol. 1999;40:123-130. doi:10.1046/j.1440-0960.1999.00341.x
  3. Denisow-Pietrzyk M, Pietrzyk Ł, Denisow B. Asteraceae species as potential environmental factors of allergy. Environ Sci Pollut Res Int. 2019;26:6290-6300. doi:10.1007/s11356-019-04146-w
  4. Paulsen E, Chistensen LP, Andersen KE. Cosmetics and herbal remedies with Compositae plant extracts—are they tolerated by Compositae-allergic patients? Contact Dermatitis. 2008;58:15-23. doi:10.1111/j.1600-0536.2007.01250.x
  5. Burry JN, Reid JG, Kirk J. Australian bush dermatitis. Contact Dermatitis. 1975;1:263-264. doi:10.1111/j.1600-0536.1975.tb05422.x
  6. Punchihewa N, Palmer A, Nixon R. Allergic contact dermatitis to Compositae: an Australian case series. Contact Dermatitis. 2022;87:356-362. doi:10.1111/cod.14162
  7. Chen KW, Marusciac L, Tamas PT, et al. Ragweed pollen allergy: burden, characteristics, and management of an imported allergen source in Europe. Int Arch Allergy Immunol. 2018;176:163-180. doi:10.1159/000487997
  8. Schloemer JA, Zirwas MJ, Burkhart CG. Airborne contact dermatitis: common causes in the USA. Int J Dermatol. 2015;54:271-274. doi:10.1111/ijd.12692
  9. Arlette J, Mitchell JC. Compositae dermatitis. current aspects. Contact Dermatitis. 1981;7:129-136. doi:10.1111/j.1600-0536.1981.tb04584.x
  10. Mitchell JC, Dupuis G. Allergic contact dermatitis from sesquiterpenoids of the Compositae family of plants. Br J Dermatol. 1971;84:139-150. doi:10.1111/j.1365-2133.1971.tb06857.x
  11. Salapovic H, Geier J, Reznicek G. Quantification of Sesquiterpene lactones in Asteraceae plant extracts: evaluation of their allergenic potential. Sci Pharm. 2013;81:807-818. doi:10.3797/scipharm.1306-17
  12. Paulsen E. Compositae dermatitis: a survey. Contact Dermatitis. 1992;26:76-86. doi:10.1111/j.1600-0536.1992.tb00888.x. Published correction appears in Contact Dermatitis. 1992;27:208.
  13. DeKoven JG, Silverberg JI, Warshaw EM, et al. North American Contact Dermatitis Group patch test results: 2017-2018. Dermatitis. 2021;32:111-123. doi:10.1097/DER.0000000000000729
  14. Paulsen E. Contact sensitization from Compositae-containing herbal remedies and cosmetics. Contact Dermatitis. 2002;47:189-198. doi:10.1034/j.1600-0536.2002.470401.x
  15. Frain-Bell W, Johnson BE. Contact allergic sensitivity to plants and the photosensitivity dermatitis and actinic reticuloid syndrome. Br J Dermatol. 1979;101:503-512.
  16. Paulsen E, Andersen KE. Clinical patterns of Compositae dermatitis in Danish monosensitized patients. Contact Dermatitis. 2018;78:185-193. doi:10.1111/cod.12916
  17. Jovanovic´ M, Poljacki M. Compositae dermatitis. Med Pregl. 2003;56:43-49. doi:10.2298/mpns0302043j
  18. Krook G. Occupational dermatitis from Lactuca sativa (lettuce) and Cichorium (endive). simultaneous occurrence of immediate and delayed allergy as a cause of contact dermatitis. Contact Dermatitis. 1977;3:27-36. doi:10.1111/j.1600-0536.1977.tb03583.x
  19. Paek SY, Lim HW. Chronic actinic dermatitis. Dermatol Clin. 2014;32:355-361, viii-ix. doi:10.1016/j.det.2014.03.007
  20. du P Menagé H, Hawk JL, White IR. Sesquiterpene lactone mix contact sensitivity and its relationship to chronic actinic dermatitis: a follow-up study. Contact Dermatitis. 1998;39:119-122. doi:10.1111/j.1600-0536.1998.tb05859.x
  21. Wang CX, Belsito DV. Chronic actinic dermatitis revisited. Dermatitis. 2020;31:68-74. doi:10.1097/DER.0000000000000531
  22. DeLeo VA, Adler BL, Warshaw EM, et al. Photopatch test results of the North American contact dermatitis group, 1999-2009. Photodermatol Photoimmunol Photomed. 2022;38:288-291. doi:10.1111/phpp.12742
  23. McGovern TW, LaWarre S. Botanical briefs: the scourge of India—Parthenium hysterophorus L. Cutis. 2001;67:27-34. Published correction appears in Cutis. 2001;67:154.
  24. Sharma VK, Verma P, Maharaja K. Parthenium dermatitis. Photochem Photobiol Sci. 2013;12:85-94. doi:10.1039/c2pp25186h
  25. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulse doses. Indian J Dermatol Venereol Leprol. 2006;72:24-27. doi:10.4103/0378-6323.19713
  26. Sharma VK, Bhat R, Sethuraman G, et al. Treatment of Parthenium dermatitis with methotrexate. Contact Dermatitis. 2007;57:118-119. doi:10.1111/j.1600-0536.2006.00950.x
  27. Burke DA, Corey G, Storrs FJ. Psoralen plus UVA protocol for Compositae photosensitivity. Am J Contact Dermat. 1996;7:171-176.
  28. Lovell CR. Allergic contact dermatitis due to plants. In: Plants and the Skin. Blackwell Scientific Publications; 1993:96-254.
  29. Dogra S, Parsad D, Handa S. Narrowband ultraviolet B in airborne contact dermatitis: a ray of hope! Br J Dermatol. 2004;150:373-374. doi:10.1111/j.1365-2133.2004.05724.x
  30. Lakshmi C, Srinivas CR, Jayaraman A. Ciclosporin in Parthenium dermatitis—a report of 2 cases. Contact Dermatitis. 2008;59:245-248. doi:10.1111/j.1600-0536.2007.01208.x
  31. Hendricks AJ, Yosipovitch G, Shi VY. Dupilumab use in dermatologic conditions beyond atopic dermatitis—a systematic review. J Dermatolog Treat. 2021;32:19-28. doi:10.1080/09546634.2019.1689227
  32. Napolitano M, Fabbrocini G, Patruno C. Allergic contact dermatitis to Compositae: a possible cause of dupilumab-associated facial and neck dermatitis in atopic dermatitis patients? Contact Dermatitis. 2021;85:473-474. doi:10.1111/cod.13898
  33. Muddebihal A, Sardana K, Sinha S, et al. Tofacitinib in refractory Parthenium-induced airborne allergic contact dermatitis. Contact Dermatitis. 2023;88:150-152. doi:10.1111/cod.14234
  34. Baltazar D, Shinamoto SR, Hamann CP, et al. Occupational airborne allergic contact dermatitis to invasive Compositae species treated with abrocitinib: a case report. Contact Dermatitis. 2022;87:542-544. doi:10.1111/cod.14204
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Dr. Wallace is from the Medical College of Georgia, Augusta. Dr. Elston is from the Department of Dermatology & Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors have no relevant financial disclosures to report.

Correspondence: Carly E. Wallace, DO, Medical College of Georgia, 1120 15th St, BI 5070, Augusta, GA 30912 (cwallace55295@med.lecom.edu).

Cutis. 2024 October;114(4):E18-E21. doi:10.12788/cutis.1125

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Dr. Wallace is from the Medical College of Georgia, Augusta. Dr. Elston is from the Department of Dermatology & Dermatologic Surgery, Medical University of South Carolina, Charleston.

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Correspondence: Carly E. Wallace, DO, Medical College of Georgia, 1120 15th St, BI 5070, Augusta, GA 30912 (cwallace55295@med.lecom.edu).

Cutis. 2024 October;114(4):E18-E21. doi:10.12788/cutis.1125

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Correspondence: Carly E. Wallace, DO, Medical College of Georgia, 1120 15th St, BI 5070, Augusta, GA 30912 (cwallace55295@med.lecom.edu).

Cutis. 2024 October;114(4):E18-E21. doi:10.12788/cutis.1125

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The Asteraceae (formerly Compositae) family of plants is derived from the ancient Greek word aster, meaning “star,” referring to the starlike arrangement of flower petals around a central disc known as a capitulum. What initially appears as a single flower is actually a composite of several smaller flowers, hence the former name Compositae.1 Well-known members of the Asteraceae family include ornamental annuals (eg, sunflowers, marigolds, cosmos), herbaceous ­perennials (eg, chrysanthemums, dandelions), vegetables (eg, lettuce, chicory, artichokes), herbs (eg, chamomile, tarragon), and weeds (eg, ragweed, horseweed, capeweed)(Figure 1).2

FIGURE 1. Members of the Asteraceae family. A, Black-eyed Susan (Rudbeckia hirta). B, Purple coneflower (Echinacea purpurea). C, Indian blanket (Gaillardia pulchella). D, Oxeye daisy (Leucanthemum vulgare).

There are more than 25,000 species of Asteraceae plants that thrive in a wide range of climates worldwide. Cases of Asteraceae-induced skin reactions have been reported in North America, Europe, Asia, and Australia.3 Members of the Asteraceae family are ubiquitous in gardens, along roadsides, and in the wilderness. Occupational exposure commonly affects gardeners, florists, farmers, and forestry workers through either direct contact with plants or via airborne pollen. Furthermore, plants of the Asteraceae family are used in various products, including pediculicides (eg, insect repellents), cosmetics (eg, eye creams, body washes), and food products (eg, cooking oils, sweetening agents, coffee substitutes, herbal teas).4-6 These plants have substantial allergic potential, resulting in numerous cutaneous reactions.

Allergic Potential

Asteraceae plants can elicit both immediate and delayed hypersensitivity reactions (HSRs); for instance, exposure to ragweed pollen may cause an IgE-mediated type 1 HSR manifesting as allergic rhinitis or a type IV HSR manifesting as airborne allergic contact dermatitis.7,8 The main contact allergens present in Asteraceae plants are sesquiterpene lactones, which are found in the leaves, stems, flowers, and pollen.9-11 Sesquiterpene lactones consist of an α-methyl group attached to a lactone ring combined with a sesquiterpene.12 Patch testing can be used to diagnose Asteraceae allergy; however, the results are not consistently reliable because there is no perfect screening allergen. Patch test preparations commonly used to detect Asteraceae allergy include Compositae mix (consisting of Anthemis nobilis extract, Chamomilla recutita extract, Achillea millefolium extract, Tanacetum vulgare extract, Arnica montana extract, and parthenolide) and sesquiterpene lactone mix (consisting of alantolactone, dehydrocostus lactone, and costunolide). In North America, the prevalence of positive patch tests to Compositae mix and sesquiterpene lactone mix is approximately 2% and 0.5%, respectively.13 When patch testing is performed, both Compositae mix and sesquiterpene lactone mix should be utilized to minimize the risk of missing Asteraceae allergy, as sesquiterpene lactone mix alone does not detect all Compositae-sensitized patients. Additionally, it may be necessary to test supplemental Asteraceae allergens, including preparations from specific plants to which the patient has been exposed. Exposure to Asteraceae-containing cosmetic products may lead to dermatitis, though this is highly dependent on the particular plant species involved. For instance, the prevalence of sensitization is high in arnica (tincture) and elecampane but low with more commonly used species such as German chamomile.14

Cutaneous Manifestations

Asteraceae dermatitis, which also is known as Australian bush dermatitis, weed dermatitis, and chrysanthemum dermatitis,2 can manifest on any area of the body that directly contacts the plant or is exposed to the pollen. Asteraceae dermatitis historically was reported in older adults with a recent history of plant exposure.6,15 However, recent data have shown a female preponderance and a younger mean age of onset (46–49 years).16

There are multiple distinct clinical manifestations of Asteraceae dermatitis. The most common cutaneous finding is localized vesicular or eczematous patches on the hands or wrists. Other variations include eczematous rashes on the exposed skin of the hands, arms, face, and neck; generalized eczema; and isolated facial eczema.16,17 These variations can be attributed to contact dermatitis caused by airborne pollen, which may mimic photodermatitis. However, airborne Asteraceae dermatitis can be distinguished clinically from photodermatitis by the involvement of sun-protected areas such as the skinfolds of the eyelids, retroauricular sulci, and nasolabial folds (Figure 2).2,9 In rare cases, systemic allergic contact dermatitis can occur if the Asteraceae allergen is ingested.2,18

FIGURE 2. Characteristic sparing of the shaded areas of the face in airborne Asteraceae dermatitis.


Other diagnostic clues include dermatitis that flares during the summer, at the peak of the growing season, with remission in the cooler months. Potential risk factors include a childhood history of atopic dermatitis and allergic rhinitis.16 With prolonged exposure, patients may develop chronic actinic dermatitis, an immunologically mediated photodermatosis characterized by lichenified and pruritic eczematous plaques located predominantly on sun-exposed areas with notable sparing of the skin folds.19 The association between Asteraceae dermatitis and chronic actinic dermatitis is highly variable, with some studies reporting a 25% correlation and others finding a stronger association of up to 80%.2,15,20 Asteraceae allergy appears to be a relatively uncommon cause of photoallergy in North America. In one recent study, 16% (3/19) of patients with chronic actinic dermatitis had positive patch or photopatch tests to sesquiterpene lactone mix, but in another large study of photopatch testing it was reported to be a rare photoallergen.21,22

Parthenium dermatitis is an allergic contact dermatitis caused by exposure to Parthenium hysterophorus, a weed of the Asteraceae family that is responsible for 30% of cases of contact dermatitis in India.23,24 Unlike the more classic manifestation of Asteraceae dermatitis, which primarily affects the upper extremities in cases from North America and Europe, Parthenium dermatitis typically occurs in an airborne pattern distribution.24

Management

While complete avoidance of Asteraceae plants is ideal, it often is unrealistic due to their abundance in nature. Therefore, minimizing exposure to the causative plants is recommended. Primary preventive measures such as wearing protective gloves and clothing and applying bentonite clay prior to exposure should be taken when working outdoors. Promptly showering after contact with plants also can reduce the risk for Asteraceae dermatitis.

Symptomatic treatment is appropriate for mild cases and includes topical corticosteroids and calcineurin inhibitors. For severe cases, systemic corticosteroids may be needed for acute flares, with azathioprine, mycophenolate, cyclosporine, or methotrexate available for recalcitrant disease. Verma et al25 found that treatment with azathioprine for 6 months resulted in greater than 60% clearance in all 12 patients, with a majority achieving 80% to 100% clearance. Methotrexate has been used at doses of 15 mg once weekly.26 Narrowband UVB and psoralen plus UVA have been effective in extensive cases; however, care should be exercised in patients with photosensitive dermatitis, who instead should practice strict photoprotection.27-29 Lakshmi et al30 reported the use of cyclosporine during the acute phase of Asteraceae dermatitis at a dose of 2.5 mg/kg daily for 4 to 8 weeks. There have been several case reports of dupilumab treating allergic contact dermatitis; however, there have been 3 cases of patients with atopic dermatitis developing Asteraceae dermatitis while taking dupilumab.31,32 Recently, oral Janus kinase inhibitors have shown success in treating refractory cases of airborne Asteraceae dermatitis.33,34 Further research is needed to determine the safety and efficacy of dupilumab and Janus kinase inhibitors for treatment of Asteraceae dermatitis.

Final Thoughts

The Asteraceae plant family is vast and diverse, with more than 200 species reported to cause allergic contact dermatitis.12 Common modes of contact include gardening, occupational exposure, airborne pollen, and use of pediculicides and cosmetics that contain components of Asteraceae plants. Educating patients on how to minimize contact with Asteraceae plants is the most effective management strategy; topical agents and oral immunosuppressives can be used for symptomatic treatment.

The Asteraceae (formerly Compositae) family of plants is derived from the ancient Greek word aster, meaning “star,” referring to the starlike arrangement of flower petals around a central disc known as a capitulum. What initially appears as a single flower is actually a composite of several smaller flowers, hence the former name Compositae.1 Well-known members of the Asteraceae family include ornamental annuals (eg, sunflowers, marigolds, cosmos), herbaceous ­perennials (eg, chrysanthemums, dandelions), vegetables (eg, lettuce, chicory, artichokes), herbs (eg, chamomile, tarragon), and weeds (eg, ragweed, horseweed, capeweed)(Figure 1).2

FIGURE 1. Members of the Asteraceae family. A, Black-eyed Susan (Rudbeckia hirta). B, Purple coneflower (Echinacea purpurea). C, Indian blanket (Gaillardia pulchella). D, Oxeye daisy (Leucanthemum vulgare).

There are more than 25,000 species of Asteraceae plants that thrive in a wide range of climates worldwide. Cases of Asteraceae-induced skin reactions have been reported in North America, Europe, Asia, and Australia.3 Members of the Asteraceae family are ubiquitous in gardens, along roadsides, and in the wilderness. Occupational exposure commonly affects gardeners, florists, farmers, and forestry workers through either direct contact with plants or via airborne pollen. Furthermore, plants of the Asteraceae family are used in various products, including pediculicides (eg, insect repellents), cosmetics (eg, eye creams, body washes), and food products (eg, cooking oils, sweetening agents, coffee substitutes, herbal teas).4-6 These plants have substantial allergic potential, resulting in numerous cutaneous reactions.

Allergic Potential

Asteraceae plants can elicit both immediate and delayed hypersensitivity reactions (HSRs); for instance, exposure to ragweed pollen may cause an IgE-mediated type 1 HSR manifesting as allergic rhinitis or a type IV HSR manifesting as airborne allergic contact dermatitis.7,8 The main contact allergens present in Asteraceae plants are sesquiterpene lactones, which are found in the leaves, stems, flowers, and pollen.9-11 Sesquiterpene lactones consist of an α-methyl group attached to a lactone ring combined with a sesquiterpene.12 Patch testing can be used to diagnose Asteraceae allergy; however, the results are not consistently reliable because there is no perfect screening allergen. Patch test preparations commonly used to detect Asteraceae allergy include Compositae mix (consisting of Anthemis nobilis extract, Chamomilla recutita extract, Achillea millefolium extract, Tanacetum vulgare extract, Arnica montana extract, and parthenolide) and sesquiterpene lactone mix (consisting of alantolactone, dehydrocostus lactone, and costunolide). In North America, the prevalence of positive patch tests to Compositae mix and sesquiterpene lactone mix is approximately 2% and 0.5%, respectively.13 When patch testing is performed, both Compositae mix and sesquiterpene lactone mix should be utilized to minimize the risk of missing Asteraceae allergy, as sesquiterpene lactone mix alone does not detect all Compositae-sensitized patients. Additionally, it may be necessary to test supplemental Asteraceae allergens, including preparations from specific plants to which the patient has been exposed. Exposure to Asteraceae-containing cosmetic products may lead to dermatitis, though this is highly dependent on the particular plant species involved. For instance, the prevalence of sensitization is high in arnica (tincture) and elecampane but low with more commonly used species such as German chamomile.14

Cutaneous Manifestations

Asteraceae dermatitis, which also is known as Australian bush dermatitis, weed dermatitis, and chrysanthemum dermatitis,2 can manifest on any area of the body that directly contacts the plant or is exposed to the pollen. Asteraceae dermatitis historically was reported in older adults with a recent history of plant exposure.6,15 However, recent data have shown a female preponderance and a younger mean age of onset (46–49 years).16

There are multiple distinct clinical manifestations of Asteraceae dermatitis. The most common cutaneous finding is localized vesicular or eczematous patches on the hands or wrists. Other variations include eczematous rashes on the exposed skin of the hands, arms, face, and neck; generalized eczema; and isolated facial eczema.16,17 These variations can be attributed to contact dermatitis caused by airborne pollen, which may mimic photodermatitis. However, airborne Asteraceae dermatitis can be distinguished clinically from photodermatitis by the involvement of sun-protected areas such as the skinfolds of the eyelids, retroauricular sulci, and nasolabial folds (Figure 2).2,9 In rare cases, systemic allergic contact dermatitis can occur if the Asteraceae allergen is ingested.2,18

FIGURE 2. Characteristic sparing of the shaded areas of the face in airborne Asteraceae dermatitis.


Other diagnostic clues include dermatitis that flares during the summer, at the peak of the growing season, with remission in the cooler months. Potential risk factors include a childhood history of atopic dermatitis and allergic rhinitis.16 With prolonged exposure, patients may develop chronic actinic dermatitis, an immunologically mediated photodermatosis characterized by lichenified and pruritic eczematous plaques located predominantly on sun-exposed areas with notable sparing of the skin folds.19 The association between Asteraceae dermatitis and chronic actinic dermatitis is highly variable, with some studies reporting a 25% correlation and others finding a stronger association of up to 80%.2,15,20 Asteraceae allergy appears to be a relatively uncommon cause of photoallergy in North America. In one recent study, 16% (3/19) of patients with chronic actinic dermatitis had positive patch or photopatch tests to sesquiterpene lactone mix, but in another large study of photopatch testing it was reported to be a rare photoallergen.21,22

Parthenium dermatitis is an allergic contact dermatitis caused by exposure to Parthenium hysterophorus, a weed of the Asteraceae family that is responsible for 30% of cases of contact dermatitis in India.23,24 Unlike the more classic manifestation of Asteraceae dermatitis, which primarily affects the upper extremities in cases from North America and Europe, Parthenium dermatitis typically occurs in an airborne pattern distribution.24

Management

While complete avoidance of Asteraceae plants is ideal, it often is unrealistic due to their abundance in nature. Therefore, minimizing exposure to the causative plants is recommended. Primary preventive measures such as wearing protective gloves and clothing and applying bentonite clay prior to exposure should be taken when working outdoors. Promptly showering after contact with plants also can reduce the risk for Asteraceae dermatitis.

Symptomatic treatment is appropriate for mild cases and includes topical corticosteroids and calcineurin inhibitors. For severe cases, systemic corticosteroids may be needed for acute flares, with azathioprine, mycophenolate, cyclosporine, or methotrexate available for recalcitrant disease. Verma et al25 found that treatment with azathioprine for 6 months resulted in greater than 60% clearance in all 12 patients, with a majority achieving 80% to 100% clearance. Methotrexate has been used at doses of 15 mg once weekly.26 Narrowband UVB and psoralen plus UVA have been effective in extensive cases; however, care should be exercised in patients with photosensitive dermatitis, who instead should practice strict photoprotection.27-29 Lakshmi et al30 reported the use of cyclosporine during the acute phase of Asteraceae dermatitis at a dose of 2.5 mg/kg daily for 4 to 8 weeks. There have been several case reports of dupilumab treating allergic contact dermatitis; however, there have been 3 cases of patients with atopic dermatitis developing Asteraceae dermatitis while taking dupilumab.31,32 Recently, oral Janus kinase inhibitors have shown success in treating refractory cases of airborne Asteraceae dermatitis.33,34 Further research is needed to determine the safety and efficacy of dupilumab and Janus kinase inhibitors for treatment of Asteraceae dermatitis.

Final Thoughts

The Asteraceae plant family is vast and diverse, with more than 200 species reported to cause allergic contact dermatitis.12 Common modes of contact include gardening, occupational exposure, airborne pollen, and use of pediculicides and cosmetics that contain components of Asteraceae plants. Educating patients on how to minimize contact with Asteraceae plants is the most effective management strategy; topical agents and oral immunosuppressives can be used for symptomatic treatment.

References
  1. Morhardt S, Morhardt E. California Desert Flowers: An Introduction to Families, Genera, and Species. University of California Press; 2004.
  2. Gordon LA. Compositae dermatitis. Australas J Dermatol. 1999;40:123-130. doi:10.1046/j.1440-0960.1999.00341.x
  3. Denisow-Pietrzyk M, Pietrzyk Ł, Denisow B. Asteraceae species as potential environmental factors of allergy. Environ Sci Pollut Res Int. 2019;26:6290-6300. doi:10.1007/s11356-019-04146-w
  4. Paulsen E, Chistensen LP, Andersen KE. Cosmetics and herbal remedies with Compositae plant extracts—are they tolerated by Compositae-allergic patients? Contact Dermatitis. 2008;58:15-23. doi:10.1111/j.1600-0536.2007.01250.x
  5. Burry JN, Reid JG, Kirk J. Australian bush dermatitis. Contact Dermatitis. 1975;1:263-264. doi:10.1111/j.1600-0536.1975.tb05422.x
  6. Punchihewa N, Palmer A, Nixon R. Allergic contact dermatitis to Compositae: an Australian case series. Contact Dermatitis. 2022;87:356-362. doi:10.1111/cod.14162
  7. Chen KW, Marusciac L, Tamas PT, et al. Ragweed pollen allergy: burden, characteristics, and management of an imported allergen source in Europe. Int Arch Allergy Immunol. 2018;176:163-180. doi:10.1159/000487997
  8. Schloemer JA, Zirwas MJ, Burkhart CG. Airborne contact dermatitis: common causes in the USA. Int J Dermatol. 2015;54:271-274. doi:10.1111/ijd.12692
  9. Arlette J, Mitchell JC. Compositae dermatitis. current aspects. Contact Dermatitis. 1981;7:129-136. doi:10.1111/j.1600-0536.1981.tb04584.x
  10. Mitchell JC, Dupuis G. Allergic contact dermatitis from sesquiterpenoids of the Compositae family of plants. Br J Dermatol. 1971;84:139-150. doi:10.1111/j.1365-2133.1971.tb06857.x
  11. Salapovic H, Geier J, Reznicek G. Quantification of Sesquiterpene lactones in Asteraceae plant extracts: evaluation of their allergenic potential. Sci Pharm. 2013;81:807-818. doi:10.3797/scipharm.1306-17
  12. Paulsen E. Compositae dermatitis: a survey. Contact Dermatitis. 1992;26:76-86. doi:10.1111/j.1600-0536.1992.tb00888.x. Published correction appears in Contact Dermatitis. 1992;27:208.
  13. DeKoven JG, Silverberg JI, Warshaw EM, et al. North American Contact Dermatitis Group patch test results: 2017-2018. Dermatitis. 2021;32:111-123. doi:10.1097/DER.0000000000000729
  14. Paulsen E. Contact sensitization from Compositae-containing herbal remedies and cosmetics. Contact Dermatitis. 2002;47:189-198. doi:10.1034/j.1600-0536.2002.470401.x
  15. Frain-Bell W, Johnson BE. Contact allergic sensitivity to plants and the photosensitivity dermatitis and actinic reticuloid syndrome. Br J Dermatol. 1979;101:503-512.
  16. Paulsen E, Andersen KE. Clinical patterns of Compositae dermatitis in Danish monosensitized patients. Contact Dermatitis. 2018;78:185-193. doi:10.1111/cod.12916
  17. Jovanovic´ M, Poljacki M. Compositae dermatitis. Med Pregl. 2003;56:43-49. doi:10.2298/mpns0302043j
  18. Krook G. Occupational dermatitis from Lactuca sativa (lettuce) and Cichorium (endive). simultaneous occurrence of immediate and delayed allergy as a cause of contact dermatitis. Contact Dermatitis. 1977;3:27-36. doi:10.1111/j.1600-0536.1977.tb03583.x
  19. Paek SY, Lim HW. Chronic actinic dermatitis. Dermatol Clin. 2014;32:355-361, viii-ix. doi:10.1016/j.det.2014.03.007
  20. du P Menagé H, Hawk JL, White IR. Sesquiterpene lactone mix contact sensitivity and its relationship to chronic actinic dermatitis: a follow-up study. Contact Dermatitis. 1998;39:119-122. doi:10.1111/j.1600-0536.1998.tb05859.x
  21. Wang CX, Belsito DV. Chronic actinic dermatitis revisited. Dermatitis. 2020;31:68-74. doi:10.1097/DER.0000000000000531
  22. DeLeo VA, Adler BL, Warshaw EM, et al. Photopatch test results of the North American contact dermatitis group, 1999-2009. Photodermatol Photoimmunol Photomed. 2022;38:288-291. doi:10.1111/phpp.12742
  23. McGovern TW, LaWarre S. Botanical briefs: the scourge of India—Parthenium hysterophorus L. Cutis. 2001;67:27-34. Published correction appears in Cutis. 2001;67:154.
  24. Sharma VK, Verma P, Maharaja K. Parthenium dermatitis. Photochem Photobiol Sci. 2013;12:85-94. doi:10.1039/c2pp25186h
  25. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulse doses. Indian J Dermatol Venereol Leprol. 2006;72:24-27. doi:10.4103/0378-6323.19713
  26. Sharma VK, Bhat R, Sethuraman G, et al. Treatment of Parthenium dermatitis with methotrexate. Contact Dermatitis. 2007;57:118-119. doi:10.1111/j.1600-0536.2006.00950.x
  27. Burke DA, Corey G, Storrs FJ. Psoralen plus UVA protocol for Compositae photosensitivity. Am J Contact Dermat. 1996;7:171-176.
  28. Lovell CR. Allergic contact dermatitis due to plants. In: Plants and the Skin. Blackwell Scientific Publications; 1993:96-254.
  29. Dogra S, Parsad D, Handa S. Narrowband ultraviolet B in airborne contact dermatitis: a ray of hope! Br J Dermatol. 2004;150:373-374. doi:10.1111/j.1365-2133.2004.05724.x
  30. Lakshmi C, Srinivas CR, Jayaraman A. Ciclosporin in Parthenium dermatitis—a report of 2 cases. Contact Dermatitis. 2008;59:245-248. doi:10.1111/j.1600-0536.2007.01208.x
  31. Hendricks AJ, Yosipovitch G, Shi VY. Dupilumab use in dermatologic conditions beyond atopic dermatitis—a systematic review. J Dermatolog Treat. 2021;32:19-28. doi:10.1080/09546634.2019.1689227
  32. Napolitano M, Fabbrocini G, Patruno C. Allergic contact dermatitis to Compositae: a possible cause of dupilumab-associated facial and neck dermatitis in atopic dermatitis patients? Contact Dermatitis. 2021;85:473-474. doi:10.1111/cod.13898
  33. Muddebihal A, Sardana K, Sinha S, et al. Tofacitinib in refractory Parthenium-induced airborne allergic contact dermatitis. Contact Dermatitis. 2023;88:150-152. doi:10.1111/cod.14234
  34. Baltazar D, Shinamoto SR, Hamann CP, et al. Occupational airborne allergic contact dermatitis to invasive Compositae species treated with abrocitinib: a case report. Contact Dermatitis. 2022;87:542-544. doi:10.1111/cod.14204
References
  1. Morhardt S, Morhardt E. California Desert Flowers: An Introduction to Families, Genera, and Species. University of California Press; 2004.
  2. Gordon LA. Compositae dermatitis. Australas J Dermatol. 1999;40:123-130. doi:10.1046/j.1440-0960.1999.00341.x
  3. Denisow-Pietrzyk M, Pietrzyk Ł, Denisow B. Asteraceae species as potential environmental factors of allergy. Environ Sci Pollut Res Int. 2019;26:6290-6300. doi:10.1007/s11356-019-04146-w
  4. Paulsen E, Chistensen LP, Andersen KE. Cosmetics and herbal remedies with Compositae plant extracts—are they tolerated by Compositae-allergic patients? Contact Dermatitis. 2008;58:15-23. doi:10.1111/j.1600-0536.2007.01250.x
  5. Burry JN, Reid JG, Kirk J. Australian bush dermatitis. Contact Dermatitis. 1975;1:263-264. doi:10.1111/j.1600-0536.1975.tb05422.x
  6. Punchihewa N, Palmer A, Nixon R. Allergic contact dermatitis to Compositae: an Australian case series. Contact Dermatitis. 2022;87:356-362. doi:10.1111/cod.14162
  7. Chen KW, Marusciac L, Tamas PT, et al. Ragweed pollen allergy: burden, characteristics, and management of an imported allergen source in Europe. Int Arch Allergy Immunol. 2018;176:163-180. doi:10.1159/000487997
  8. Schloemer JA, Zirwas MJ, Burkhart CG. Airborne contact dermatitis: common causes in the USA. Int J Dermatol. 2015;54:271-274. doi:10.1111/ijd.12692
  9. Arlette J, Mitchell JC. Compositae dermatitis. current aspects. Contact Dermatitis. 1981;7:129-136. doi:10.1111/j.1600-0536.1981.tb04584.x
  10. Mitchell JC, Dupuis G. Allergic contact dermatitis from sesquiterpenoids of the Compositae family of plants. Br J Dermatol. 1971;84:139-150. doi:10.1111/j.1365-2133.1971.tb06857.x
  11. Salapovic H, Geier J, Reznicek G. Quantification of Sesquiterpene lactones in Asteraceae plant extracts: evaluation of their allergenic potential. Sci Pharm. 2013;81:807-818. doi:10.3797/scipharm.1306-17
  12. Paulsen E. Compositae dermatitis: a survey. Contact Dermatitis. 1992;26:76-86. doi:10.1111/j.1600-0536.1992.tb00888.x. Published correction appears in Contact Dermatitis. 1992;27:208.
  13. DeKoven JG, Silverberg JI, Warshaw EM, et al. North American Contact Dermatitis Group patch test results: 2017-2018. Dermatitis. 2021;32:111-123. doi:10.1097/DER.0000000000000729
  14. Paulsen E. Contact sensitization from Compositae-containing herbal remedies and cosmetics. Contact Dermatitis. 2002;47:189-198. doi:10.1034/j.1600-0536.2002.470401.x
  15. Frain-Bell W, Johnson BE. Contact allergic sensitivity to plants and the photosensitivity dermatitis and actinic reticuloid syndrome. Br J Dermatol. 1979;101:503-512.
  16. Paulsen E, Andersen KE. Clinical patterns of Compositae dermatitis in Danish monosensitized patients. Contact Dermatitis. 2018;78:185-193. doi:10.1111/cod.12916
  17. Jovanovic´ M, Poljacki M. Compositae dermatitis. Med Pregl. 2003;56:43-49. doi:10.2298/mpns0302043j
  18. Krook G. Occupational dermatitis from Lactuca sativa (lettuce) and Cichorium (endive). simultaneous occurrence of immediate and delayed allergy as a cause of contact dermatitis. Contact Dermatitis. 1977;3:27-36. doi:10.1111/j.1600-0536.1977.tb03583.x
  19. Paek SY, Lim HW. Chronic actinic dermatitis. Dermatol Clin. 2014;32:355-361, viii-ix. doi:10.1016/j.det.2014.03.007
  20. du P Menagé H, Hawk JL, White IR. Sesquiterpene lactone mix contact sensitivity and its relationship to chronic actinic dermatitis: a follow-up study. Contact Dermatitis. 1998;39:119-122. doi:10.1111/j.1600-0536.1998.tb05859.x
  21. Wang CX, Belsito DV. Chronic actinic dermatitis revisited. Dermatitis. 2020;31:68-74. doi:10.1097/DER.0000000000000531
  22. DeLeo VA, Adler BL, Warshaw EM, et al. Photopatch test results of the North American contact dermatitis group, 1999-2009. Photodermatol Photoimmunol Photomed. 2022;38:288-291. doi:10.1111/phpp.12742
  23. McGovern TW, LaWarre S. Botanical briefs: the scourge of India—Parthenium hysterophorus L. Cutis. 2001;67:27-34. Published correction appears in Cutis. 2001;67:154.
  24. Sharma VK, Verma P, Maharaja K. Parthenium dermatitis. Photochem Photobiol Sci. 2013;12:85-94. doi:10.1039/c2pp25186h
  25. Verma KK, Bansal A, Sethuraman G. Parthenium dermatitis treated with azathioprine weekly pulse doses. Indian J Dermatol Venereol Leprol. 2006;72:24-27. doi:10.4103/0378-6323.19713
  26. Sharma VK, Bhat R, Sethuraman G, et al. Treatment of Parthenium dermatitis with methotrexate. Contact Dermatitis. 2007;57:118-119. doi:10.1111/j.1600-0536.2006.00950.x
  27. Burke DA, Corey G, Storrs FJ. Psoralen plus UVA protocol for Compositae photosensitivity. Am J Contact Dermat. 1996;7:171-176.
  28. Lovell CR. Allergic contact dermatitis due to plants. In: Plants and the Skin. Blackwell Scientific Publications; 1993:96-254.
  29. Dogra S, Parsad D, Handa S. Narrowband ultraviolet B in airborne contact dermatitis: a ray of hope! Br J Dermatol. 2004;150:373-374. doi:10.1111/j.1365-2133.2004.05724.x
  30. Lakshmi C, Srinivas CR, Jayaraman A. Ciclosporin in Parthenium dermatitis—a report of 2 cases. Contact Dermatitis. 2008;59:245-248. doi:10.1111/j.1600-0536.2007.01208.x
  31. Hendricks AJ, Yosipovitch G, Shi VY. Dupilumab use in dermatologic conditions beyond atopic dermatitis—a systematic review. J Dermatolog Treat. 2021;32:19-28. doi:10.1080/09546634.2019.1689227
  32. Napolitano M, Fabbrocini G, Patruno C. Allergic contact dermatitis to Compositae: a possible cause of dupilumab-associated facial and neck dermatitis in atopic dermatitis patients? Contact Dermatitis. 2021;85:473-474. doi:10.1111/cod.13898
  33. Muddebihal A, Sardana K, Sinha S, et al. Tofacitinib in refractory Parthenium-induced airborne allergic contact dermatitis. Contact Dermatitis. 2023;88:150-152. doi:10.1111/cod.14234
  34. Baltazar D, Shinamoto SR, Hamann CP, et al. Occupational airborne allergic contact dermatitis to invasive Compositae species treated with abrocitinib: a case report. Contact Dermatitis. 2022;87:542-544. doi:10.1111/cod.14204
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Practice Points

  • Asteraceae dermatitis can occur from direct contact with plants of the Asteraceae family; through airborne pollen; or from exposure to topical medications, cooking products, and cosmetics.
  • Patient education on primary prevention, especially protective clothing, is crucial, as these plants are ubiquitous outdoors and have diverse phenotypes.
  • Management of mild Asteraceae dermatitis consists primarily of topical corticosteroids and calcineurin inhibitors, while systemic corticosteroids and other immunosuppressive agents are utilized for severe or recalcitrant cases.
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Atopic Dermatitis: Upadacitinib Effectiveness Maintained Through 76 weeks Among Adolescents

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Changed
Mon, 10/28/2024 - 12:09

 

TOPLINE:

Long-term treatment with upadacitinib in adolescents with moderate to severe atopic dermatitis (AD) demonstrated sustained efficacy and an acceptable safety profile through 76 weeks across three phase 3 trials.

METHODOLOGY:

  • Researchers conducted three double-blind, placebo-controlled phase 3 randomized clinical trials (Measure Up 1, Measure Up 2, and AD Up) involving 542 adolescents aged 12-17 years with moderate to severe AD.
  • Participants were randomized to receive the oral Janus kinase inhibitor upadacitinib (15 mg or 30 mg once daily) or placebo, with or without topical corticosteroids, for 16 weeks, followed by rerandomization of patients in the placebo group to upadacitinib for up to 76 weeks.
  • Study endpoints were at least a 75%, 90%, or 100% reduction in the Eczema Area and Severity Index (EASI-75, EASI-90, and EASI-100, respectively), Validated Investigator Global Assessment for AD (vIGA-AD) score of 0 or 1, and a ≥ 4-point improvement in the Worst Pruritus Numerical Rating Scale (WP-NRS).
  • Adverse events were monitored, including serious infections, herpes zoster, and creatine kinase elevation.

TAKEAWAY:

  • Among those who continued treatment on upadacitinib, 15 mg and 30 mg, EASI-75 response rates were maintained or improved through week 76 in all three studies. Patients who switched from placebo to upadacitinib also experienced improvements in EASI-75 through week 76.
  • The proportion of patients who achieved EASI-90 and EASI-100 responses increased, and in general, were maintained from week 16 through week 76 in all three studies; the proportion was numerically higher among patients on 30 mg for all three studies.
  • The proportion of adolescents achieving vIGA-AD score of 0 or 1 and WP-NRS improvement of ≥ 4 points was sustained or improved through 76 weeks.
  • Serious infections were reported in five patients or fewer in each treatment group for all three studies. All opportunistic infections were eczema herpeticum; most cases were not serious, or were mild or moderate, and in general, did not require stopping treatment.

IN PRACTICE:

“These results through 76 weeks demonstrated that upadacitinib, with a favorable benefit-risk profile, was an effective long-term treatment option for adolescents with moderate to severe AD,” the authors wrote.

SOURCE:

The study was led by Amy S. Paller, MD, professor and chair of dermatology, Northwestern University, Chicago, and was published online on October 23 in JAMA Dermatology.

LIMITATIONS: 

The study limitations included a small sample size, and the findings did not extend to patients under 12 years or those weighing < 40 kg.

DISCLOSURES:

This study was supported by AbbVie. Paller received grants and personal fees from pharmaceutical companies including AbbVie during the conduct of the study. Several authors reported financial ties with various sources, including AbbVie.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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TOPLINE:

Long-term treatment with upadacitinib in adolescents with moderate to severe atopic dermatitis (AD) demonstrated sustained efficacy and an acceptable safety profile through 76 weeks across three phase 3 trials.

METHODOLOGY:

  • Researchers conducted three double-blind, placebo-controlled phase 3 randomized clinical trials (Measure Up 1, Measure Up 2, and AD Up) involving 542 adolescents aged 12-17 years with moderate to severe AD.
  • Participants were randomized to receive the oral Janus kinase inhibitor upadacitinib (15 mg or 30 mg once daily) or placebo, with or without topical corticosteroids, for 16 weeks, followed by rerandomization of patients in the placebo group to upadacitinib for up to 76 weeks.
  • Study endpoints were at least a 75%, 90%, or 100% reduction in the Eczema Area and Severity Index (EASI-75, EASI-90, and EASI-100, respectively), Validated Investigator Global Assessment for AD (vIGA-AD) score of 0 or 1, and a ≥ 4-point improvement in the Worst Pruritus Numerical Rating Scale (WP-NRS).
  • Adverse events were monitored, including serious infections, herpes zoster, and creatine kinase elevation.

TAKEAWAY:

  • Among those who continued treatment on upadacitinib, 15 mg and 30 mg, EASI-75 response rates were maintained or improved through week 76 in all three studies. Patients who switched from placebo to upadacitinib also experienced improvements in EASI-75 through week 76.
  • The proportion of patients who achieved EASI-90 and EASI-100 responses increased, and in general, were maintained from week 16 through week 76 in all three studies; the proportion was numerically higher among patients on 30 mg for all three studies.
  • The proportion of adolescents achieving vIGA-AD score of 0 or 1 and WP-NRS improvement of ≥ 4 points was sustained or improved through 76 weeks.
  • Serious infections were reported in five patients or fewer in each treatment group for all three studies. All opportunistic infections were eczema herpeticum; most cases were not serious, or were mild or moderate, and in general, did not require stopping treatment.

IN PRACTICE:

“These results through 76 weeks demonstrated that upadacitinib, with a favorable benefit-risk profile, was an effective long-term treatment option for adolescents with moderate to severe AD,” the authors wrote.

SOURCE:

The study was led by Amy S. Paller, MD, professor and chair of dermatology, Northwestern University, Chicago, and was published online on October 23 in JAMA Dermatology.

LIMITATIONS: 

The study limitations included a small sample size, and the findings did not extend to patients under 12 years or those weighing < 40 kg.

DISCLOSURES:

This study was supported by AbbVie. Paller received grants and personal fees from pharmaceutical companies including AbbVie during the conduct of the study. Several authors reported financial ties with various sources, including AbbVie.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

 

TOPLINE:

Long-term treatment with upadacitinib in adolescents with moderate to severe atopic dermatitis (AD) demonstrated sustained efficacy and an acceptable safety profile through 76 weeks across three phase 3 trials.

METHODOLOGY:

  • Researchers conducted three double-blind, placebo-controlled phase 3 randomized clinical trials (Measure Up 1, Measure Up 2, and AD Up) involving 542 adolescents aged 12-17 years with moderate to severe AD.
  • Participants were randomized to receive the oral Janus kinase inhibitor upadacitinib (15 mg or 30 mg once daily) or placebo, with or without topical corticosteroids, for 16 weeks, followed by rerandomization of patients in the placebo group to upadacitinib for up to 76 weeks.
  • Study endpoints were at least a 75%, 90%, or 100% reduction in the Eczema Area and Severity Index (EASI-75, EASI-90, and EASI-100, respectively), Validated Investigator Global Assessment for AD (vIGA-AD) score of 0 or 1, and a ≥ 4-point improvement in the Worst Pruritus Numerical Rating Scale (WP-NRS).
  • Adverse events were monitored, including serious infections, herpes zoster, and creatine kinase elevation.

TAKEAWAY:

  • Among those who continued treatment on upadacitinib, 15 mg and 30 mg, EASI-75 response rates were maintained or improved through week 76 in all three studies. Patients who switched from placebo to upadacitinib also experienced improvements in EASI-75 through week 76.
  • The proportion of patients who achieved EASI-90 and EASI-100 responses increased, and in general, were maintained from week 16 through week 76 in all three studies; the proportion was numerically higher among patients on 30 mg for all three studies.
  • The proportion of adolescents achieving vIGA-AD score of 0 or 1 and WP-NRS improvement of ≥ 4 points was sustained or improved through 76 weeks.
  • Serious infections were reported in five patients or fewer in each treatment group for all three studies. All opportunistic infections were eczema herpeticum; most cases were not serious, or were mild or moderate, and in general, did not require stopping treatment.

IN PRACTICE:

“These results through 76 weeks demonstrated that upadacitinib, with a favorable benefit-risk profile, was an effective long-term treatment option for adolescents with moderate to severe AD,” the authors wrote.

SOURCE:

The study was led by Amy S. Paller, MD, professor and chair of dermatology, Northwestern University, Chicago, and was published online on October 23 in JAMA Dermatology.

LIMITATIONS: 

The study limitations included a small sample size, and the findings did not extend to patients under 12 years or those weighing < 40 kg.

DISCLOSURES:

This study was supported by AbbVie. Paller received grants and personal fees from pharmaceutical companies including AbbVie during the conduct of the study. Several authors reported financial ties with various sources, including AbbVie.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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Study Compares Punch Excision vs. Core Excision for Recalcitrant Keloids

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Mon, 10/28/2024 - 12:03

Punch excision (PE) followed by immediate cryotherapy could be a viable and simpler alternative to core excision (CE) for the treatment of recalcitrant keloids, according to the results of a small retrospective study.

The method “offers similar efficacy, faster healing, and fewer complications,” one of the study authors, Jinwoong Jung, MD, said in an interview following the annual meeting of the American Society for Dermatologic Surgery, where he presented the study results during an oral abstract session.

For the study, Jung, a dermatologist at Yonsei University College of Medicine, Seoul, South Korea, and colleagues retrospectively analyzed 22 patients with recalcitrant keloids treated with cryotherapy immediately following either PE or CE between May 2019 and March 2024. They used the Vancouver Scar Scale (VSS) to assess treatment efficacy.

Of the 22 patients, 16 underwent treatment with CE and 6 underwent treatment with PE. Pretreatment VSS scores showed no significant differences between the groups (P = .535). The CE group had a reduction in the VSS score from 8.13 to 4.00, while the PE group had a reduction from 7.83 to 3.67, but these declines did not differ significantly (P = .737). The PE group exhibited a shorter healing time than the CE group (a mean of 43.5 vs 63.87 days, respectively), though this difference was not statistically significant (P = .129).

“The uniqueness of this work lies in its simplified use of PE for recalcitrant keloids, which demonstrated efficacy comparable to CE, with the potential advantage of faster healing times,” Jung said. “Future studies with larger sample sizes and extended follow-up periods could help establish this approach as a standard treatment method.”

He acknowledged certain limitations of the study, including its small sample size and the lack of long-term follow-up data. The researchers reported having no relevant disclosures.

A version of this article first appeared on Medscape.com.

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Punch excision (PE) followed by immediate cryotherapy could be a viable and simpler alternative to core excision (CE) for the treatment of recalcitrant keloids, according to the results of a small retrospective study.

The method “offers similar efficacy, faster healing, and fewer complications,” one of the study authors, Jinwoong Jung, MD, said in an interview following the annual meeting of the American Society for Dermatologic Surgery, where he presented the study results during an oral abstract session.

For the study, Jung, a dermatologist at Yonsei University College of Medicine, Seoul, South Korea, and colleagues retrospectively analyzed 22 patients with recalcitrant keloids treated with cryotherapy immediately following either PE or CE between May 2019 and March 2024. They used the Vancouver Scar Scale (VSS) to assess treatment efficacy.

Of the 22 patients, 16 underwent treatment with CE and 6 underwent treatment with PE. Pretreatment VSS scores showed no significant differences between the groups (P = .535). The CE group had a reduction in the VSS score from 8.13 to 4.00, while the PE group had a reduction from 7.83 to 3.67, but these declines did not differ significantly (P = .737). The PE group exhibited a shorter healing time than the CE group (a mean of 43.5 vs 63.87 days, respectively), though this difference was not statistically significant (P = .129).

“The uniqueness of this work lies in its simplified use of PE for recalcitrant keloids, which demonstrated efficacy comparable to CE, with the potential advantage of faster healing times,” Jung said. “Future studies with larger sample sizes and extended follow-up periods could help establish this approach as a standard treatment method.”

He acknowledged certain limitations of the study, including its small sample size and the lack of long-term follow-up data. The researchers reported having no relevant disclosures.

A version of this article first appeared on Medscape.com.

Punch excision (PE) followed by immediate cryotherapy could be a viable and simpler alternative to core excision (CE) for the treatment of recalcitrant keloids, according to the results of a small retrospective study.

The method “offers similar efficacy, faster healing, and fewer complications,” one of the study authors, Jinwoong Jung, MD, said in an interview following the annual meeting of the American Society for Dermatologic Surgery, where he presented the study results during an oral abstract session.

For the study, Jung, a dermatologist at Yonsei University College of Medicine, Seoul, South Korea, and colleagues retrospectively analyzed 22 patients with recalcitrant keloids treated with cryotherapy immediately following either PE or CE between May 2019 and March 2024. They used the Vancouver Scar Scale (VSS) to assess treatment efficacy.

Of the 22 patients, 16 underwent treatment with CE and 6 underwent treatment with PE. Pretreatment VSS scores showed no significant differences between the groups (P = .535). The CE group had a reduction in the VSS score from 8.13 to 4.00, while the PE group had a reduction from 7.83 to 3.67, but these declines did not differ significantly (P = .737). The PE group exhibited a shorter healing time than the CE group (a mean of 43.5 vs 63.87 days, respectively), though this difference was not statistically significant (P = .129).

“The uniqueness of this work lies in its simplified use of PE for recalcitrant keloids, which demonstrated efficacy comparable to CE, with the potential advantage of faster healing times,” Jung said. “Future studies with larger sample sizes and extended follow-up periods could help establish this approach as a standard treatment method.”

He acknowledged certain limitations of the study, including its small sample size and the lack of long-term follow-up data. The researchers reported having no relevant disclosures.

A version of this article first appeared on Medscape.com.

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FDA Approves OnabotulinumtoxinA for Improving Platysma Bands

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Mon, 10/28/2024 - 09:51

The Food and Drug Administration (FDA) has approved onabotulinumtoxinA (Botox Cosmetic) for temporary improvement in the appearance of moderate to severe platysma bands in adults.

According to a press release from Allergan Aesthetics, which developed onabotulinumtoxinA, by injecting along the jawline and the vertical bands connecting the jaw and neck with one of the FDA-approved doses of the product based on severity, onabotulinumtoxinA temporarily reduces underlying muscle activity.

The company cited results from phase 3 clinical studies, which demonstrated statistical significance for the improvement in appearance of platysma bands from baseline with onabotulinumtoxinA compared with placebo on both investigator and patient assessment (P < .0001).

All secondary endpoints were also met, as measured by multiple validated, proprietary patient-reported outcome instruments. In two of the clinical studies, for example, 65% and 62% of patients reported being “very satisfied” or “satisfied,” respectively, with their neck and jawline definition 14 days after treatment with a dose of 26, 31, or 36 units of onabotulinumtoxinA, compared with 12% with placebo in both studies.

The development marks the fourth indication for onabotulinumtoxinA. The others are for moderate to severe glabellar lines associated with corrugator and/or procerus muscle activity, moderate to severe lateral canthal lines associated with orbicularis oculi activity, and moderate to severe forehead lines associated with frontalis activity.

A version of this article appeared on Medscape.com.

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The Food and Drug Administration (FDA) has approved onabotulinumtoxinA (Botox Cosmetic) for temporary improvement in the appearance of moderate to severe platysma bands in adults.

According to a press release from Allergan Aesthetics, which developed onabotulinumtoxinA, by injecting along the jawline and the vertical bands connecting the jaw and neck with one of the FDA-approved doses of the product based on severity, onabotulinumtoxinA temporarily reduces underlying muscle activity.

The company cited results from phase 3 clinical studies, which demonstrated statistical significance for the improvement in appearance of platysma bands from baseline with onabotulinumtoxinA compared with placebo on both investigator and patient assessment (P < .0001).

All secondary endpoints were also met, as measured by multiple validated, proprietary patient-reported outcome instruments. In two of the clinical studies, for example, 65% and 62% of patients reported being “very satisfied” or “satisfied,” respectively, with their neck and jawline definition 14 days after treatment with a dose of 26, 31, or 36 units of onabotulinumtoxinA, compared with 12% with placebo in both studies.

The development marks the fourth indication for onabotulinumtoxinA. The others are for moderate to severe glabellar lines associated with corrugator and/or procerus muscle activity, moderate to severe lateral canthal lines associated with orbicularis oculi activity, and moderate to severe forehead lines associated with frontalis activity.

A version of this article appeared on Medscape.com.

The Food and Drug Administration (FDA) has approved onabotulinumtoxinA (Botox Cosmetic) for temporary improvement in the appearance of moderate to severe platysma bands in adults.

According to a press release from Allergan Aesthetics, which developed onabotulinumtoxinA, by injecting along the jawline and the vertical bands connecting the jaw and neck with one of the FDA-approved doses of the product based on severity, onabotulinumtoxinA temporarily reduces underlying muscle activity.

The company cited results from phase 3 clinical studies, which demonstrated statistical significance for the improvement in appearance of platysma bands from baseline with onabotulinumtoxinA compared with placebo on both investigator and patient assessment (P < .0001).

All secondary endpoints were also met, as measured by multiple validated, proprietary patient-reported outcome instruments. In two of the clinical studies, for example, 65% and 62% of patients reported being “very satisfied” or “satisfied,” respectively, with their neck and jawline definition 14 days after treatment with a dose of 26, 31, or 36 units of onabotulinumtoxinA, compared with 12% with placebo in both studies.

The development marks the fourth indication for onabotulinumtoxinA. The others are for moderate to severe glabellar lines associated with corrugator and/or procerus muscle activity, moderate to severe lateral canthal lines associated with orbicularis oculi activity, and moderate to severe forehead lines associated with frontalis activity.

A version of this article appeared on Medscape.com.

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A 51-year-old woman presented for a routine full body skin exam after vacationing in Hawaii.

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Fri, 10/25/2024 - 12:56

Primary adrenal insufficiency (Addison’s disease) results from a dysfunction of the adrenal glands, which may be secondary to autoimmune diseases, genetic conditions, infections, and vasculopathies,or may be drug-induced (e.g. checkpoint inhibitors), among others . In contrast, secondary adrenal insufficiency results from pituitary dysfunction of low adrenocorticotropic hormone (ACTH). The most common cause of primary adrenal insufficiency in developed countries is autoimmune adrenalitis, which accounts for upwards of 90% of cases. Typically, 21-hydroxylase autoantibodies are identified and account for destruction of the adrenal cortex through cell-mediated and humoral immune responses.

Dr. Sophia M. Akhiyat


Dermatological findings of primary adrenal insufficiency can include hyperpigmentation of the mucocutaneous surfaces and nails, most prominently affecting the head, neck, and hands. Palmar creases, subungual surfaces, sites of trauma, and joint spaces (including the knees, spine, elbows, and shoulders) are commonly affected. Hair depletes in the pubic area and axillary vaults. Nevi may also appear darker. In patients with autoimmune adrenalitis, vitiligo may be seen secondary to autoimmune destruction of melanocytes.

Diagnosis may be difficult in the early stages, but historical findings of fatigue and clinical findings of hyperpigmentation in classic areas may prompt appropriate lab screening workup. It is essential to determine whether adrenal insufficiency is primary or secondary. Evaluation of decreased cortisol production, determination of whether production is ACTH-dependent or -independent, and evaluation for the underlying causes of adrenal dysfunction are important. Lab screening includes morning serum cortisol, morning ACTH (cosyntropin) stimulation test, fasting CBC with differential, and CMP to evaluate for normocytic normochromic anemia, hyponatremia, hyperkalemia, hypoglycemia, plasma renin/aldosterone ratio, and 21-hydroxylase autoantibodies.

Dr. Sophia M. Akhiyat


Management strategies of primary adrenal insufficiency require corticosteroid supplementation and multidisciplinary collaboration with endocrinology. If untreated, primary adrenal insufficiency can be fatal. Adrenal crisis is a critical condition following a precipitating event, such as GI infection, fever, acute stress, and/or untreated adrenal or pituitary disorders. Clinical findings include acute shock with hypotension, nausea, vomiting, abdominal pain, back or leg pain, and a change in mental status. In this scenario, increasing the dose of corticosteroid supplementation is essential for reducing mortality.

Upon examining this patient’s new skin findings of hyperpigmentation and discussing her fatigue, primary adrenal insufficiency was suspected. With further prompting, the patient reported an ICU hospitalization several months prior because of sepsis originating from a peritonsillar abscess. With these clinical and historical findings, preliminary workup was conducted by dermatology, which included morning cortisol level, ACTH, CBC with differential, CMP, plasma renin-aldosterone ratio, and 21-hydroxylase autoantibodies. Work up demonstrated a low morning cortisol level of 1.3 mcg/dL, an elevated ACTH of 2,739 pg/mL, and positive 21-hydroxylase autoantibodies. The patient was urgently referred to endocrinology and started on oral hydrocortisone. Her fatigue immediately improved, and at 1-year follow-up with dermatology, her mucocutaneous hyperpigmentation had subsided dramatically.

Dr. Donna Bilu Martin


Dermatologists can play a major role in the early diagnosis of primary adrenal insufficiency, which is essential for reducing patient morbidity and mortality. Skin findings on full body skin exams can clue in dermatologists for ordering preliminary workup to expedite care for these patients.

The case and photos were submitted by Dr. Akhiyat, Scripps Clinic Medical Group, La Jolla, California. Donna Bilu Martin, MD, edited the column.
 

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

J Am Acad Dermatol. 2014 May;70(5):Supplement 1AB118. doi: 10.1016/j.jaad.2014.01.491.

Michels A, Michels N. Am Fam Physician. 2014 Apr 1;89(7):563-568.

Kauzman A et al. J Can Dent Assoc. 2004 Nov;70(10):682-683.

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Primary adrenal insufficiency (Addison’s disease) results from a dysfunction of the adrenal glands, which may be secondary to autoimmune diseases, genetic conditions, infections, and vasculopathies,or may be drug-induced (e.g. checkpoint inhibitors), among others . In contrast, secondary adrenal insufficiency results from pituitary dysfunction of low adrenocorticotropic hormone (ACTH). The most common cause of primary adrenal insufficiency in developed countries is autoimmune adrenalitis, which accounts for upwards of 90% of cases. Typically, 21-hydroxylase autoantibodies are identified and account for destruction of the adrenal cortex through cell-mediated and humoral immune responses.

Dr. Sophia M. Akhiyat


Dermatological findings of primary adrenal insufficiency can include hyperpigmentation of the mucocutaneous surfaces and nails, most prominently affecting the head, neck, and hands. Palmar creases, subungual surfaces, sites of trauma, and joint spaces (including the knees, spine, elbows, and shoulders) are commonly affected. Hair depletes in the pubic area and axillary vaults. Nevi may also appear darker. In patients with autoimmune adrenalitis, vitiligo may be seen secondary to autoimmune destruction of melanocytes.

Diagnosis may be difficult in the early stages, but historical findings of fatigue and clinical findings of hyperpigmentation in classic areas may prompt appropriate lab screening workup. It is essential to determine whether adrenal insufficiency is primary or secondary. Evaluation of decreased cortisol production, determination of whether production is ACTH-dependent or -independent, and evaluation for the underlying causes of adrenal dysfunction are important. Lab screening includes morning serum cortisol, morning ACTH (cosyntropin) stimulation test, fasting CBC with differential, and CMP to evaluate for normocytic normochromic anemia, hyponatremia, hyperkalemia, hypoglycemia, plasma renin/aldosterone ratio, and 21-hydroxylase autoantibodies.

Dr. Sophia M. Akhiyat


Management strategies of primary adrenal insufficiency require corticosteroid supplementation and multidisciplinary collaboration with endocrinology. If untreated, primary adrenal insufficiency can be fatal. Adrenal crisis is a critical condition following a precipitating event, such as GI infection, fever, acute stress, and/or untreated adrenal or pituitary disorders. Clinical findings include acute shock with hypotension, nausea, vomiting, abdominal pain, back or leg pain, and a change in mental status. In this scenario, increasing the dose of corticosteroid supplementation is essential for reducing mortality.

Upon examining this patient’s new skin findings of hyperpigmentation and discussing her fatigue, primary adrenal insufficiency was suspected. With further prompting, the patient reported an ICU hospitalization several months prior because of sepsis originating from a peritonsillar abscess. With these clinical and historical findings, preliminary workup was conducted by dermatology, which included morning cortisol level, ACTH, CBC with differential, CMP, plasma renin-aldosterone ratio, and 21-hydroxylase autoantibodies. Work up demonstrated a low morning cortisol level of 1.3 mcg/dL, an elevated ACTH of 2,739 pg/mL, and positive 21-hydroxylase autoantibodies. The patient was urgently referred to endocrinology and started on oral hydrocortisone. Her fatigue immediately improved, and at 1-year follow-up with dermatology, her mucocutaneous hyperpigmentation had subsided dramatically.

Dr. Donna Bilu Martin


Dermatologists can play a major role in the early diagnosis of primary adrenal insufficiency, which is essential for reducing patient morbidity and mortality. Skin findings on full body skin exams can clue in dermatologists for ordering preliminary workup to expedite care for these patients.

The case and photos were submitted by Dr. Akhiyat, Scripps Clinic Medical Group, La Jolla, California. Donna Bilu Martin, MD, edited the column.
 

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

J Am Acad Dermatol. 2014 May;70(5):Supplement 1AB118. doi: 10.1016/j.jaad.2014.01.491.

Michels A, Michels N. Am Fam Physician. 2014 Apr 1;89(7):563-568.

Kauzman A et al. J Can Dent Assoc. 2004 Nov;70(10):682-683.

Primary adrenal insufficiency (Addison’s disease) results from a dysfunction of the adrenal glands, which may be secondary to autoimmune diseases, genetic conditions, infections, and vasculopathies,or may be drug-induced (e.g. checkpoint inhibitors), among others . In contrast, secondary adrenal insufficiency results from pituitary dysfunction of low adrenocorticotropic hormone (ACTH). The most common cause of primary adrenal insufficiency in developed countries is autoimmune adrenalitis, which accounts for upwards of 90% of cases. Typically, 21-hydroxylase autoantibodies are identified and account for destruction of the adrenal cortex through cell-mediated and humoral immune responses.

Dr. Sophia M. Akhiyat


Dermatological findings of primary adrenal insufficiency can include hyperpigmentation of the mucocutaneous surfaces and nails, most prominently affecting the head, neck, and hands. Palmar creases, subungual surfaces, sites of trauma, and joint spaces (including the knees, spine, elbows, and shoulders) are commonly affected. Hair depletes in the pubic area and axillary vaults. Nevi may also appear darker. In patients with autoimmune adrenalitis, vitiligo may be seen secondary to autoimmune destruction of melanocytes.

Diagnosis may be difficult in the early stages, but historical findings of fatigue and clinical findings of hyperpigmentation in classic areas may prompt appropriate lab screening workup. It is essential to determine whether adrenal insufficiency is primary or secondary. Evaluation of decreased cortisol production, determination of whether production is ACTH-dependent or -independent, and evaluation for the underlying causes of adrenal dysfunction are important. Lab screening includes morning serum cortisol, morning ACTH (cosyntropin) stimulation test, fasting CBC with differential, and CMP to evaluate for normocytic normochromic anemia, hyponatremia, hyperkalemia, hypoglycemia, plasma renin/aldosterone ratio, and 21-hydroxylase autoantibodies.

Dr. Sophia M. Akhiyat


Management strategies of primary adrenal insufficiency require corticosteroid supplementation and multidisciplinary collaboration with endocrinology. If untreated, primary adrenal insufficiency can be fatal. Adrenal crisis is a critical condition following a precipitating event, such as GI infection, fever, acute stress, and/or untreated adrenal or pituitary disorders. Clinical findings include acute shock with hypotension, nausea, vomiting, abdominal pain, back or leg pain, and a change in mental status. In this scenario, increasing the dose of corticosteroid supplementation is essential for reducing mortality.

Upon examining this patient’s new skin findings of hyperpigmentation and discussing her fatigue, primary adrenal insufficiency was suspected. With further prompting, the patient reported an ICU hospitalization several months prior because of sepsis originating from a peritonsillar abscess. With these clinical and historical findings, preliminary workup was conducted by dermatology, which included morning cortisol level, ACTH, CBC with differential, CMP, plasma renin-aldosterone ratio, and 21-hydroxylase autoantibodies. Work up demonstrated a low morning cortisol level of 1.3 mcg/dL, an elevated ACTH of 2,739 pg/mL, and positive 21-hydroxylase autoantibodies. The patient was urgently referred to endocrinology and started on oral hydrocortisone. Her fatigue immediately improved, and at 1-year follow-up with dermatology, her mucocutaneous hyperpigmentation had subsided dramatically.

Dr. Donna Bilu Martin


Dermatologists can play a major role in the early diagnosis of primary adrenal insufficiency, which is essential for reducing patient morbidity and mortality. Skin findings on full body skin exams can clue in dermatologists for ordering preliminary workup to expedite care for these patients.

The case and photos were submitted by Dr. Akhiyat, Scripps Clinic Medical Group, La Jolla, California. Donna Bilu Martin, MD, edited the column.
 

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Florida. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.

References

J Am Acad Dermatol. 2014 May;70(5):Supplement 1AB118. doi: 10.1016/j.jaad.2014.01.491.

Michels A, Michels N. Am Fam Physician. 2014 Apr 1;89(7):563-568.

Kauzman A et al. J Can Dent Assoc. 2004 Nov;70(10):682-683.

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Dr. Sophia M. Akhiyat
A 51-year-old woman presented for a routine full body skin exam after vacationing in Hawaii. The patient reported significant tanning during her vacation and fatigue, accounting it to jet lag. Hyperpigmented macules coalescing into reticular patches were noted on her lips and ears, which the patient reports have been present for months and become darker after tanning.

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