Mixed Topics

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.

THE DIAGNOSIS: Black Dermographism

Black dermographism is characterized by asymptomatic black discoloration on the skin caused by contact with various metals, most commonly gold but also silver, nickel, zinc, lead, and aluminum.¹ These metallic particles have a black appearance as they do not reflect light.² Our patient was wearing gold hoop earrings at presentation, which were near the black patches. Certain topical products (eg, makeup, sunscreens [especially those containing zinc oxide or titanium oxide], toothpaste) can abrade metal, causing it to deposit on the skin and absorb light.³ The black discoloration is not permanent and can be prevented by avoiding contact between inciting products and metals.² No further diagnostic testing is necessary, and the patches will self-resolve if contact with the product is avoided.

Our patient noted that she wore a physical sunscreen daily, but the black patches were present only when she wore the gold hoop earrings. Given this history and physical examination findings in the office, it was suspected she had black dermographism due to her gold earrings and topical sunscreen. The patient was advised to avoid wearing the gold earrings.

Black dermographism is a misnomer because it is not a true urticarial reaction but rather a false dermographism; therefore, patients will not experience pruritus or erythema.¹ True dermographism is an inducible urticarial eruption from pressure or trauma to the skin. The clinical appearance is notable for erythematous wheals in the shape of the external force applied.⁴ Two other types of false dermographism include white dermographism, which occurs secondary to allergic contact dermatitis, and yellow dermographism, which is caused by bile deposits on the skin.⁴

Additional diagnoses were able to be ruled out for the following reasons: cutaneous mastocytosis can manifest with red-brown maculopapular lesions often accompanied by the Darier sign, which includes swelling, pruritus, and erythema but was not present in our patient.⁴ Allergic contact dermatitis manifests as a delayed eczematous reaction around 48 to 72 hours after exposure to an allergen. Our patient’s lesions formed while wearing gold earrings but did not manifest with a hypersensitivity reaction. Of note, symptomatic dermographism has been reported to mimic latex allergy.⁵ Ecchymosis may appear as erythematous, violaceous, or yellow-green patches depending on the stage but develops due to leakage from broken blood vessels secondary to trauma, which was not reported in our patient. Type I hypersensitivity reactions can occur minutes to hours after exposure to an allergen but typically manifest with a wheal-and-flare presentation.

Black dermographism from gold earrings can mimic concerning skin disorders or poor hygiene, causing unnecessary anxiety. Understanding that it is a harmless reaction between gold and certain topical products can reassure patients and prevent unnecessary testing or treatments.

THE DIAGNOSIS: Black Dermographism

Black dermographism is characterized by asymptomatic black discoloration on the skin caused by contact with various metals, most commonly gold but also silver, nickel, zinc, lead, and aluminum.¹ These metallic particles have a black appearance as they do not reflect light.² Our patient was wearing gold hoop earrings at presentation, which were near the black patches. Certain topical products (eg, makeup, sunscreens [especially those containing zinc oxide or titanium oxide], toothpaste) can abrade metal, causing it to deposit on the skin and absorb light.³ The black discoloration is not permanent and can be prevented by avoiding contact between inciting products and metals.² No further diagnostic testing is necessary, and the patches will self-resolve if contact with the product is avoided.

Our patient noted that she wore a physical sunscreen daily, but the black patches were present only when she wore the gold hoop earrings. Given this history and physical examination findings in the office, it was suspected she had black dermographism due to her gold earrings and topical sunscreen. The patient was advised to avoid wearing the gold earrings.

Black dermographism is a misnomer because it is not a true urticarial reaction but rather a false dermographism; therefore, patients will not experience pruritus or erythema.¹ True dermographism is an inducible urticarial eruption from pressure or trauma to the skin. The clinical appearance is notable for erythematous wheals in the shape of the external force applied.⁴ Two other types of false dermographism include white dermographism, which occurs secondary to allergic contact dermatitis, and yellow dermographism, which is caused by bile deposits on the skin.⁴

Additional diagnoses were able to be ruled out for the following reasons: cutaneous mastocytosis can manifest with red-brown maculopapular lesions often accompanied by the Darier sign, which includes swelling, pruritus, and erythema but was not present in our patient.⁴ Allergic contact dermatitis manifests as a delayed eczematous reaction around 48 to 72 hours after exposure to an allergen. Our patient’s lesions formed while wearing gold earrings but did not manifest with a hypersensitivity reaction. Of note, symptomatic dermographism has been reported to mimic latex allergy.⁵ Ecchymosis may appear as erythematous, violaceous, or yellow-green patches depending on the stage but develops due to leakage from broken blood vessels secondary to trauma, which was not reported in our patient. Type I hypersensitivity reactions can occur minutes to hours after exposure to an allergen but typically manifest with a wheal-and-flare presentation.

Black dermographism from gold earrings can mimic concerning skin disorders or poor hygiene, causing unnecessary anxiety. Understanding that it is a harmless reaction between gold and certain topical products can reassure patients and prevent unnecessary testing or treatments.

THE DIAGNOSIS: Black Dermographism

Black dermographism is characterized by asymptomatic black discoloration on the skin caused by contact with various metals, most commonly gold but also silver, nickel, zinc, lead, and aluminum.¹ These metallic particles have a black appearance as they do not reflect light.² Our patient was wearing gold hoop earrings at presentation, which were near the black patches. Certain topical products (eg, makeup, sunscreens [especially those containing zinc oxide or titanium oxide], toothpaste) can abrade metal, causing it to deposit on the skin and absorb light.³ The black discoloration is not permanent and can be prevented by avoiding contact between inciting products and metals.² No further diagnostic testing is necessary, and the patches will self-resolve if contact with the product is avoided.

Our patient noted that she wore a physical sunscreen daily, but the black patches were present only when she wore the gold hoop earrings. Given this history and physical examination findings in the office, it was suspected she had black dermographism due to her gold earrings and topical sunscreen. The patient was advised to avoid wearing the gold earrings.

Black dermographism is a misnomer because it is not a true urticarial reaction but rather a false dermographism; therefore, patients will not experience pruritus or erythema.¹ True dermographism is an inducible urticarial eruption from pressure or trauma to the skin. The clinical appearance is notable for erythematous wheals in the shape of the external force applied.⁴ Two other types of false dermographism include white dermographism, which occurs secondary to allergic contact dermatitis, and yellow dermographism, which is caused by bile deposits on the skin.⁴

Additional diagnoses were able to be ruled out for the following reasons: cutaneous mastocytosis can manifest with red-brown maculopapular lesions often accompanied by the Darier sign, which includes swelling, pruritus, and erythema but was not present in our patient.⁴ Allergic contact dermatitis manifests as a delayed eczematous reaction around 48 to 72 hours after exposure to an allergen. Our patient’s lesions formed while wearing gold earrings but did not manifest with a hypersensitivity reaction. Of note, symptomatic dermographism has been reported to mimic latex allergy.⁵ Ecchymosis may appear as erythematous, violaceous, or yellow-green patches depending on the stage but develops due to leakage from broken blood vessels secondary to trauma, which was not reported in our patient. Type I hypersensitivity reactions can occur minutes to hours after exposure to an allergen but typically manifest with a wheal-and-flare presentation.

Black dermographism from gold earrings can mimic concerning skin disorders or poor hygiene, causing unnecessary anxiety. Understanding that it is a harmless reaction between gold and certain topical products can reassure patients and prevent unnecessary testing or treatments.

THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund¹ in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.^2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.^3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.² Recurrent remission and exacerbation occurs in many patients.³

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.³

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.⁵ Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.⁶ Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.⁷ Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.^8-10

THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund¹ in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.^2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.^3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.² Recurrent remission and exacerbation occurs in many patients.³

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.³

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.⁵ Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.⁶ Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.⁷ Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.^8-10

THE DIAGNOSIS: Disseminate and Recurrent Infundibulofolliculitis

Histopathology demonstrated a lymphocyte-predominant infundibular infiltrate with mild spongiosis and lymphocytic exocytosis; a mild, superficial perivascular infiltrate also was present. The surrounding skin was largely normal with no notable papillomatosis, acanthosis, or hyperkeratosis (Figure 1). The clinical presentation and histopathologic findings led to the diagnosis of disseminate and recurrent infundibulofolliculitis (DRIF). The patient was started on a 2-week course of once-daily ammonium lactate lotion 12% and urea cream 40% and twice-daily triamcinolone ointment 0.1%. The patient was instructed to take a 1-week break before this regimen was repeated. Isotretinoin 0.5 mg/kg/d for 2 to 4 months was considered and will be an option if there is no improvement at follow-up.

Disseminate and recurrent infundibulofolliculitis is a rare noninfectious folliculitis that initially was described by Hitch and Lund¹ in 1968. Males of African descent are most commonly affected by DRIF, but the condition is not limited to this population.^2,3 It manifests as asymptomatic, flesh-colored, monomorphic, follicular papules distributed on the trunk and proximal extremities. Pustules can be present, and hair may be seen protruding from them. As the name suggests, DRIF is associated with histopathologic changes that are prominent at the infundibulum of hair follicles.^3,4 Disseminate and recurrent infundibulofolliculitis can persist for months to years because it often is resistant to treatment. Treatments include topical monotherapies such as corticosteroids, calcineurin inhibitors, or retinoids; combination topical treatments; antibiotics; and isotretinoin.² Recurrent remission and exacerbation occurs in many patients.³

The classic manifestations of DRIF, including follicular, monomorphic, flesh-colored papules distributed on the neck, trunk, and proximal upper extremities, were seen in our patient (Figure 2). These findings along with the skin biopsy identifying a lymphocytic infundibular infiltrate led to the diagnosis of DRIF. The papules associated with DRIF can be recurrent or chronic. The lesions in this patient were chronic and persistent.

Despite limited evidence, it has been suggested that DRIF may be a manifestation of atopic dermatitis in patients with darker skin tones. In our case, the patient had a history of childhood eczema. Other hypotheses have proposed that DRIF could be a nonspecific reaction to a currently unknown antigen. A causative infectious agent has not been identified, although the search continues. There is speculation that DRIF could be an overt expression of normal follicular prominence, but the presence of occasional pustules and lymphocyte- predominant infundibular infiltrate negates that.³

Confluent and reticulated papillomatosis was included in the differential for our patient and manifests as asymptomatic hyperpigmented papules and plaques frequently occurring on the upper trunk, neck, and axilla; however, these lesions have a peripheral netlike configuration, as the name suggests. Additionally, this condition is thought to have an infectious component (Dietzia papillomatosis) and responds to antibiotic treatment.⁵ Follicular eczema also was high in the differential diagnosis but usually is seasonal and pruritic, and histopathology typically shows the features of spongiotic dermatitis. It also would respond well to topical steroids.⁶ Another condition high on the differential was juxtaclavicular beaded lines, which also manifests as flesh-colored follicular papules distributed on the upper trunk; however, histopathology usually shows features of hyperplastic pilosebaceous units along with spongiosis and exocytosis.⁷ Pityrosporum folliculitis initially was considered, but the patient only endorsed occasional pruritus. Additionally, no fungal elements were observed.

Currently, there are no definitive treatments for DRIF. The topical treatments available include midpotency corticosteroids, tretinoin, calcineurin inhibitors, 12% lactic acid, and 20% to 40% urea. The systemic therapies are high-dose oral vitamin A (100,000 IU/d), isotretinoin, and psoralen plus UVA.^8-10

Practice Gap

Intralesional cryosurgery is a highly effective treatment for dermatologic conditions, notably keloids and hypertrophic scars.¹ Conventional methods typically use specialized double-lumen intralesional probes or Luer lock adapters connected to hypodermic or lumbar puncture needles, allowing cryogen to flow internally to cool the probe or needle and treat the lesion via conduction.² However, specialized intralesional probes are expensive and often are difficult to obtain. Furthermore, Luer lock adapters with needles directly attached to the handle unit can be ergonomically challenging, as the procedure requires simultaneous maintenance of a perpendicular handheld position, precise needle passage through the exact center of the lesion, and protection of the surrounding perilesional healthy skin from cold injury. Consequently, these limitations restrict widespread adoption, necessitating simpler, more accessible, and cost-effective alternatives. Herein, we present a novel, practical, and economical cryogen delivery method that adapts a disposable infusion set to a standard cryospray nozzle.

The Technique

This technique involves detaching the infusion set tubing and securely connecting it to the cryospray nozzle (Figure 1). Brief activation of the cryospray to constrict the nozzle or a small incision in the tubing may be required to ensure a tight fit, which can be secured with medical tape to maintain consistent cryogen flow. Local anesthesia is administered directly into and around the lesion, particularly translesionally for keloids, to avoid unnecessary trauma to the surrounding healthy skin, which could trigger further keloid formation. A needle is inserted through the lesion with the tip extending beyond its distal boundary, ensuring the tip remains outside the lesion during cryogen application to prevent cryoinsufflation. If necessary, gentle bending of the needle helps ensure optimal cryogen distribution within the lesion (Figures 2A and 2B). However, this may slightly reduce flow and extend freezing duration; therefore, bending the needle should be performed cautiously and is specifically recommended for effectively treating lesions on curved anatomic sites (eg, the auricle of the ear) to optimize freezing and protect surrounding tissues.

During initial cryogen release, covering the needle tip with gauze prevents aerosolization of biological debris, while placing a wooden tongue depressor between the needle tip and the patient’s skin prevents inadvertent cold injury. After cryogen flow is initiated, the lesion begins to freeze at both the needle entry and exit points, forming what is referred to as ice balls. Over time, typically within several seconds to a few minutes depending on lesion size and tissue characteristics, these ice balls merge centrally, forming a single ice ball encompassing the entire lesion (Figure 2C). Cryogen flow should be maintained during a single application until the unified ice ball appearance is achieved, confirming effective cooling.

Practice Implications

Studies have consistently shown that intralesional cryosurgery is associated with a reduction in the size and symptoms of hypertrophic scars and keloids.^1,2 Multimodal treatment approaches, including intralesional methods, are especially valued for their targeted efficacy and minimal adverse effects. Our simplified method offers practical economic advantages, making it highly suitable for broad adoption across diverse clinical settings, particularly those that are resource limited. Clinicians can safely and effectively utilize this technique without specialized or costly equipment, considerably enhancing clinical efficiency and accessibility. The straightforwardness of this method also facilitates the training of medical personnel, enabling rapid integration into clinical practice and the flexibility to treat various lesion types and sizes effectively.

Practice Gap

Intralesional cryosurgery is a highly effective treatment for dermatologic conditions, notably keloids and hypertrophic scars.¹ Conventional methods typically use specialized double-lumen intralesional probes or Luer lock adapters connected to hypodermic or lumbar puncture needles, allowing cryogen to flow internally to cool the probe or needle and treat the lesion via conduction.² However, specialized intralesional probes are expensive and often are difficult to obtain. Furthermore, Luer lock adapters with needles directly attached to the handle unit can be ergonomically challenging, as the procedure requires simultaneous maintenance of a perpendicular handheld position, precise needle passage through the exact center of the lesion, and protection of the surrounding perilesional healthy skin from cold injury. Consequently, these limitations restrict widespread adoption, necessitating simpler, more accessible, and cost-effective alternatives. Herein, we present a novel, practical, and economical cryogen delivery method that adapts a disposable infusion set to a standard cryospray nozzle.

The Technique

This technique involves detaching the infusion set tubing and securely connecting it to the cryospray nozzle (Figure 1). Brief activation of the cryospray to constrict the nozzle or a small incision in the tubing may be required to ensure a tight fit, which can be secured with medical tape to maintain consistent cryogen flow. Local anesthesia is administered directly into and around the lesion, particularly translesionally for keloids, to avoid unnecessary trauma to the surrounding healthy skin, which could trigger further keloid formation. A needle is inserted through the lesion with the tip extending beyond its distal boundary, ensuring the tip remains outside the lesion during cryogen application to prevent cryoinsufflation. If necessary, gentle bending of the needle helps ensure optimal cryogen distribution within the lesion (Figures 2A and 2B). However, this may slightly reduce flow and extend freezing duration; therefore, bending the needle should be performed cautiously and is specifically recommended for effectively treating lesions on curved anatomic sites (eg, the auricle of the ear) to optimize freezing and protect surrounding tissues.

During initial cryogen release, covering the needle tip with gauze prevents aerosolization of biological debris, while placing a wooden tongue depressor between the needle tip and the patient’s skin prevents inadvertent cold injury. After cryogen flow is initiated, the lesion begins to freeze at both the needle entry and exit points, forming what is referred to as ice balls. Over time, typically within several seconds to a few minutes depending on lesion size and tissue characteristics, these ice balls merge centrally, forming a single ice ball encompassing the entire lesion (Figure 2C). Cryogen flow should be maintained during a single application until the unified ice ball appearance is achieved, confirming effective cooling.

Practice Implications

Studies have consistently shown that intralesional cryosurgery is associated with a reduction in the size and symptoms of hypertrophic scars and keloids.^1,2 Multimodal treatment approaches, including intralesional methods, are especially valued for their targeted efficacy and minimal adverse effects. Our simplified method offers practical economic advantages, making it highly suitable for broad adoption across diverse clinical settings, particularly those that are resource limited. Clinicians can safely and effectively utilize this technique without specialized or costly equipment, considerably enhancing clinical efficiency and accessibility. The straightforwardness of this method also facilitates the training of medical personnel, enabling rapid integration into clinical practice and the flexibility to treat various lesion types and sizes effectively.

Practice Gap

Intralesional cryosurgery is a highly effective treatment for dermatologic conditions, notably keloids and hypertrophic scars.¹ Conventional methods typically use specialized double-lumen intralesional probes or Luer lock adapters connected to hypodermic or lumbar puncture needles, allowing cryogen to flow internally to cool the probe or needle and treat the lesion via conduction.² However, specialized intralesional probes are expensive and often are difficult to obtain. Furthermore, Luer lock adapters with needles directly attached to the handle unit can be ergonomically challenging, as the procedure requires simultaneous maintenance of a perpendicular handheld position, precise needle passage through the exact center of the lesion, and protection of the surrounding perilesional healthy skin from cold injury. Consequently, these limitations restrict widespread adoption, necessitating simpler, more accessible, and cost-effective alternatives. Herein, we present a novel, practical, and economical cryogen delivery method that adapts a disposable infusion set to a standard cryospray nozzle.

The Technique

This technique involves detaching the infusion set tubing and securely connecting it to the cryospray nozzle (Figure 1). Brief activation of the cryospray to constrict the nozzle or a small incision in the tubing may be required to ensure a tight fit, which can be secured with medical tape to maintain consistent cryogen flow. Local anesthesia is administered directly into and around the lesion, particularly translesionally for keloids, to avoid unnecessary trauma to the surrounding healthy skin, which could trigger further keloid formation. A needle is inserted through the lesion with the tip extending beyond its distal boundary, ensuring the tip remains outside the lesion during cryogen application to prevent cryoinsufflation. If necessary, gentle bending of the needle helps ensure optimal cryogen distribution within the lesion (Figures 2A and 2B). However, this may slightly reduce flow and extend freezing duration; therefore, bending the needle should be performed cautiously and is specifically recommended for effectively treating lesions on curved anatomic sites (eg, the auricle of the ear) to optimize freezing and protect surrounding tissues.

During initial cryogen release, covering the needle tip with gauze prevents aerosolization of biological debris, while placing a wooden tongue depressor between the needle tip and the patient’s skin prevents inadvertent cold injury. After cryogen flow is initiated, the lesion begins to freeze at both the needle entry and exit points, forming what is referred to as ice balls. Over time, typically within several seconds to a few minutes depending on lesion size and tissue characteristics, these ice balls merge centrally, forming a single ice ball encompassing the entire lesion (Figure 2C). Cryogen flow should be maintained during a single application until the unified ice ball appearance is achieved, confirming effective cooling.

Practice Implications

Studies have consistently shown that intralesional cryosurgery is associated with a reduction in the size and symptoms of hypertrophic scars and keloids.^1,2 Multimodal treatment approaches, including intralesional methods, are especially valued for their targeted efficacy and minimal adverse effects. Our simplified method offers practical economic advantages, making it highly suitable for broad adoption across diverse clinical settings, particularly those that are resource limited. Clinicians can safely and effectively utilize this technique without specialized or costly equipment, considerably enhancing clinical efficiency and accessibility. The straightforwardness of this method also facilitates the training of medical personnel, enabling rapid integration into clinical practice and the flexibility to treat various lesion types and sizes effectively.

To the Editor:

The widespread availability and popularity of ChatGPT (OpenAI) have sparked interest in its potential applications within various fields, including medical diagnostics.¹ In dermatology, large language models (LLMs) already are being cited as a possible way to reliably respond to common patient queries and produce concise patient education materials.^2,3 That being said, there is skepticism regarding the technology’s efficacy and reliability in producing accurate treatment plans, with variability among popular LLMs; for example, a recent study by Chau et al⁴ demonstrated that ChatGPT was best at providing specific and accurate information regarding patient-facing responses to questions about 5 dermatologic diagnoses compared to Google Bard (now rebranded as Google Gemini) and Bing AI (now rebranded as Microsoft Copilot), which more often produced inaccurate or nonspecific responses. Google Bard also declined to answer one prompt.⁴ Large language models also have been evaluated in diagnosing skin lesions. In 2024, SkinGPT-4 (a pretrained multimodel LLM developed by Zhou et al⁵) achieved just over 80% accuracy in interpreting images of skin lesions and was considered informative by 82.5% of board-certified dermatologists, demonstrating that LLMs may have the potential to become integrated into clinical practice.⁵

Our study aimed to evaluate the performance of GPT-4o (OpenAI)—a widely accessible, low-cost LLM—in diagnosing dermatologic conditions using the HAM10000 dataset, a well-curated collection of dermatoscopic images developed for training and benchmarking artificial intelligence (AI) algorithms.⁶ HAM10000 comprises images representing 7 distinct skin conditions: actinic keratoses (ak), basal cell carcinoma (bcc), benign keratosis (bk), dermatofibroma (df), melanoma (mel), melanocytic nevi (nv), and vascular skin lesions (vsl), providing a robust platform for multiclass classification assessment. We evaluated GPT-4o using 100 dermatoscopic images per condition to assess diagnostic accuracy, potential biases, and limitations in skin lesion identification. The HAM10000 dataset was selected because it offers a large standardized reference set of dermatoscopic (rather than conventional clinical) images commonly used in dermatologic AI research. GPT-4o was chosen due to its patient-friendly interface, widespread use, and prior reports suggesting greater reliability in skin lesion assessment compared with other LLMs.

One hundred images from each of the 7 dermatologic categories were randomly selected for use in our analysis in 2024. The images were selected by our data scientist (J.C.) through random sampling from the dataset. Each image was separately presented to GPT-4o without any preprocessing or modification alongside 2 prompts designed to evaluate the diagnostic capabilities of GPT-4o. Both prompts included the same list of 7 dermatologic conditions for answer choices but differed in contextual information, where prompt 1 provided patient demographic information and localization of the dermatological condition but prompt 2 did not provide these details (Table). No follow-up questions were presented.

For prompt 1, the confusion matrix showed a strong bias toward detecting mel and bcc, with high true positives (mel, 83%; bcc, 37%)(eFigure 1). This pattern possibly suggests a tendency to favor malignant labels (eg, mel, BCC) when uncertainty is present. Interestingly, df and vsl also had notable true positives (46% and 37%, respectively), which is unexpected for less critical conditions because the model’s correct classifications were uneven across benign lesions. Actinic keratoses and nv showed higher misclassification rates, suggesting the model struggled to distinguish them from other lesions.

As shown in eTable 1, prompt 1 exhibited the highest recall for mel at 0.83 but performed worse in precision (0.242) and specificity (0.567) compared to ak, which had an extremely low recall (0.03) but very high specificity (0.992) and moderate precision score (0.375). The highest precision score was seen with vsl (0.738), which also achieved high scores in specificity (0.982) and accuracy (0.88) and performed moderately well in recall (0.31). All performance metrics are reported as proportions (0-1.0), wherein 1.0 indicates 100.

For prompt 2, the second confusion matrix followed similar trends as prompt 1 but still differed in key areas (eFigure 2). Melanoma detection remained strong (true positives, 95%), while bcc shows slightly fewer true positives (24%). Vascular skin lesions improve in true positives (40%), and df dropped slightly (33%). The model continues to struggle with ak and nv, with notable misclassifications observed across other categories

Similar to prompt 1, prompt 2 achieved its highest recall for mel (0.95%), but demonstrated lower precision (0.223%) and specificity (0.488%) for this class. Prompt 2 also produced the highest accuracy for vascular skin lesions (0.90%). The highest specificity was observed for both bk and ak (0.992% each); however, ak again demonstrated the lowest recall, with a value of 0.01%.

A previous study utilizing a model of binary classification to distinguish between mel and benign dermatologic conditions demonstrated poor performance.¹ Additionally, prior studies have employed a less-strict, open-ended style question approach to examine ChatGPT’s ability to diagnose mel with limited efficacy.⁷ The HAM10000 dataset was specifically selected despite its limitations (including the absence of clinical images and limited diversity in skin tones) due to its comprehensive nature, robust annotation standards, and widespread acceptance in dermatologic AI research. Compared to the Diverse Dermatology Images dataset, which notably lacks skin tone diversity, HAM10000 provides a balanced representation of several dermatologic conditions crucial for multiclass classification tasks, making it suitable for benchmarking AI performance. This study aimed to eliminate these limitations by employing a multiclass classification approach; however, despite this switch, our results indicate continued and major limitations of the diagnostic capabilities of GPT-4o.

In its current form, GPT-4o appeared to demonstrate a clear accuracy bias toward correctly identifying specific and severe dermatologic conditions (eg, mel, bcc) but showed low and variable class-level performance for other categories (eg, ak, nv, df, vsl), with frequent misclassification into melanoma or basal cell carcinoma and low recall for some classes (eTables 1 and 2). This finding emphasized that GPT-4o currently lacks the reliability needed for real-life clinical applications in dermatology, as both binary and multiclass models fail to achieve consistent accurate performance across all skin conditions. Notably, GPT-4o may generate false-positive malignant classifications among patients due to its skew in predicted labels toward labeling benign lesions as malignant.

From the patient perspective, younger individuals may upload images of benign nevi only to unnecessarily fear a mel diagnosis after receiving GPT-4o results. Statistically, younger patients are less likely than older patients to have malignant lesions and more likely to instead present with common vsl or df—lesions that GPT-4o appears likely to identify correctly.⁸ For older users, however, the situation may differ. Beyond ak being misclassified as bcc, older patients also may encounter GPT-4o outputs that mislabel lesions as mel, raising concerns and heightening anxiety. Given the technology’s tendency to overestimate the risk of serious dermatologic conditions, this behavior poses a considerable challenge in its current state and may inadvertently intensify public anxiety around mel.

A notable limitation of our study was that, compared to publicly available datasets, the HAM10000 dataset includes only dermatoscopic images rather than a combination of clinical and dermatoscopic images. Furthermore, the HAM10000 dataset comprises images primarily from White patients, whereas other diverse databases (eg, the Diverse Dermatology Images dataset) may be more suitable for training AI algorithms to accurately diagnose skin lesions in individuals with a variety of skin tones.⁹

Ultimately, our results signal that major advancements in the design and training of LLMs such as GPT-4o are necessary before these systems can be integrated into dermatologic diagnostic decision-making to offer benefit rather than cause harm. Consulting a health care professional rather than relying solely on AI, which might otherwise lead to avoidable stress, unnecessary alarm, and potentially increased health care costs due to unwarranted follow-up and testing, should remain the recommended standard of care for patients suspecting a skin lesion.

To the Editor:

The widespread availability and popularity of ChatGPT (OpenAI) have sparked interest in its potential applications within various fields, including medical diagnostics.¹ In dermatology, large language models (LLMs) already are being cited as a possible way to reliably respond to common patient queries and produce concise patient education materials.^2,3 That being said, there is skepticism regarding the technology’s efficacy and reliability in producing accurate treatment plans, with variability among popular LLMs; for example, a recent study by Chau et al⁴ demonstrated that ChatGPT was best at providing specific and accurate information regarding patient-facing responses to questions about 5 dermatologic diagnoses compared to Google Bard (now rebranded as Google Gemini) and Bing AI (now rebranded as Microsoft Copilot), which more often produced inaccurate or nonspecific responses. Google Bard also declined to answer one prompt.⁴ Large language models also have been evaluated in diagnosing skin lesions. In 2024, SkinGPT-4 (a pretrained multimodel LLM developed by Zhou et al⁵) achieved just over 80% accuracy in interpreting images of skin lesions and was considered informative by 82.5% of board-certified dermatologists, demonstrating that LLMs may have the potential to become integrated into clinical practice.⁵

Our study aimed to evaluate the performance of GPT-4o (OpenAI)—a widely accessible, low-cost LLM—in diagnosing dermatologic conditions using the HAM10000 dataset, a well-curated collection of dermatoscopic images developed for training and benchmarking artificial intelligence (AI) algorithms.⁶ HAM10000 comprises images representing 7 distinct skin conditions: actinic keratoses (ak), basal cell carcinoma (bcc), benign keratosis (bk), dermatofibroma (df), melanoma (mel), melanocytic nevi (nv), and vascular skin lesions (vsl), providing a robust platform for multiclass classification assessment. We evaluated GPT-4o using 100 dermatoscopic images per condition to assess diagnostic accuracy, potential biases, and limitations in skin lesion identification. The HAM10000 dataset was selected because it offers a large standardized reference set of dermatoscopic (rather than conventional clinical) images commonly used in dermatologic AI research. GPT-4o was chosen due to its patient-friendly interface, widespread use, and prior reports suggesting greater reliability in skin lesion assessment compared with other LLMs.

One hundred images from each of the 7 dermatologic categories were randomly selected for use in our analysis in 2024. The images were selected by our data scientist (J.C.) through random sampling from the dataset. Each image was separately presented to GPT-4o without any preprocessing or modification alongside 2 prompts designed to evaluate the diagnostic capabilities of GPT-4o. Both prompts included the same list of 7 dermatologic conditions for answer choices but differed in contextual information, where prompt 1 provided patient demographic information and localization of the dermatological condition but prompt 2 did not provide these details (Table). No follow-up questions were presented.

For prompt 1, the confusion matrix showed a strong bias toward detecting mel and bcc, with high true positives (mel, 83%; bcc, 37%)(eFigure 1). This pattern possibly suggests a tendency to favor malignant labels (eg, mel, BCC) when uncertainty is present. Interestingly, df and vsl also had notable true positives (46% and 37%, respectively), which is unexpected for less critical conditions because the model’s correct classifications were uneven across benign lesions. Actinic keratoses and nv showed higher misclassification rates, suggesting the model struggled to distinguish them from other lesions.

As shown in eTable 1, prompt 1 exhibited the highest recall for mel at 0.83 but performed worse in precision (0.242) and specificity (0.567) compared to ak, which had an extremely low recall (0.03) but very high specificity (0.992) and moderate precision score (0.375). The highest precision score was seen with vsl (0.738), which also achieved high scores in specificity (0.982) and accuracy (0.88) and performed moderately well in recall (0.31). All performance metrics are reported as proportions (0-1.0), wherein 1.0 indicates 100.

For prompt 2, the second confusion matrix followed similar trends as prompt 1 but still differed in key areas (eFigure 2). Melanoma detection remained strong (true positives, 95%), while bcc shows slightly fewer true positives (24%). Vascular skin lesions improve in true positives (40%), and df dropped slightly (33%). The model continues to struggle with ak and nv, with notable misclassifications observed across other categories

Similar to prompt 1, prompt 2 achieved its highest recall for mel (0.95%), but demonstrated lower precision (0.223%) and specificity (0.488%) for this class. Prompt 2 also produced the highest accuracy for vascular skin lesions (0.90%). The highest specificity was observed for both bk and ak (0.992% each); however, ak again demonstrated the lowest recall, with a value of 0.01%.

A previous study utilizing a model of binary classification to distinguish between mel and benign dermatologic conditions demonstrated poor performance.¹ Additionally, prior studies have employed a less-strict, open-ended style question approach to examine ChatGPT’s ability to diagnose mel with limited efficacy.⁷ The HAM10000 dataset was specifically selected despite its limitations (including the absence of clinical images and limited diversity in skin tones) due to its comprehensive nature, robust annotation standards, and widespread acceptance in dermatologic AI research. Compared to the Diverse Dermatology Images dataset, which notably lacks skin tone diversity, HAM10000 provides a balanced representation of several dermatologic conditions crucial for multiclass classification tasks, making it suitable for benchmarking AI performance. This study aimed to eliminate these limitations by employing a multiclass classification approach; however, despite this switch, our results indicate continued and major limitations of the diagnostic capabilities of GPT-4o.

In its current form, GPT-4o appeared to demonstrate a clear accuracy bias toward correctly identifying specific and severe dermatologic conditions (eg, mel, bcc) but showed low and variable class-level performance for other categories (eg, ak, nv, df, vsl), with frequent misclassification into melanoma or basal cell carcinoma and low recall for some classes (eTables 1 and 2). This finding emphasized that GPT-4o currently lacks the reliability needed for real-life clinical applications in dermatology, as both binary and multiclass models fail to achieve consistent accurate performance across all skin conditions. Notably, GPT-4o may generate false-positive malignant classifications among patients due to its skew in predicted labels toward labeling benign lesions as malignant.

From the patient perspective, younger individuals may upload images of benign nevi only to unnecessarily fear a mel diagnosis after receiving GPT-4o results. Statistically, younger patients are less likely than older patients to have malignant lesions and more likely to instead present with common vsl or df—lesions that GPT-4o appears likely to identify correctly.⁸ For older users, however, the situation may differ. Beyond ak being misclassified as bcc, older patients also may encounter GPT-4o outputs that mislabel lesions as mel, raising concerns and heightening anxiety. Given the technology’s tendency to overestimate the risk of serious dermatologic conditions, this behavior poses a considerable challenge in its current state and may inadvertently intensify public anxiety around mel.

A notable limitation of our study was that, compared to publicly available datasets, the HAM10000 dataset includes only dermatoscopic images rather than a combination of clinical and dermatoscopic images. Furthermore, the HAM10000 dataset comprises images primarily from White patients, whereas other diverse databases (eg, the Diverse Dermatology Images dataset) may be more suitable for training AI algorithms to accurately diagnose skin lesions in individuals with a variety of skin tones.⁹

Ultimately, our results signal that major advancements in the design and training of LLMs such as GPT-4o are necessary before these systems can be integrated into dermatologic diagnostic decision-making to offer benefit rather than cause harm. Consulting a health care professional rather than relying solely on AI, which might otherwise lead to avoidable stress, unnecessary alarm, and potentially increased health care costs due to unwarranted follow-up and testing, should remain the recommended standard of care for patients suspecting a skin lesion.

To the Editor:

The widespread availability and popularity of ChatGPT (OpenAI) have sparked interest in its potential applications within various fields, including medical diagnostics.¹ In dermatology, large language models (LLMs) already are being cited as a possible way to reliably respond to common patient queries and produce concise patient education materials.^2,3 That being said, there is skepticism regarding the technology’s efficacy and reliability in producing accurate treatment plans, with variability among popular LLMs; for example, a recent study by Chau et al⁴ demonstrated that ChatGPT was best at providing specific and accurate information regarding patient-facing responses to questions about 5 dermatologic diagnoses compared to Google Bard (now rebranded as Google Gemini) and Bing AI (now rebranded as Microsoft Copilot), which more often produced inaccurate or nonspecific responses. Google Bard also declined to answer one prompt.⁴ Large language models also have been evaluated in diagnosing skin lesions. In 2024, SkinGPT-4 (a pretrained multimodel LLM developed by Zhou et al⁵) achieved just over 80% accuracy in interpreting images of skin lesions and was considered informative by 82.5% of board-certified dermatologists, demonstrating that LLMs may have the potential to become integrated into clinical practice.⁵

Our study aimed to evaluate the performance of GPT-4o (OpenAI)—a widely accessible, low-cost LLM—in diagnosing dermatologic conditions using the HAM10000 dataset, a well-curated collection of dermatoscopic images developed for training and benchmarking artificial intelligence (AI) algorithms.⁶ HAM10000 comprises images representing 7 distinct skin conditions: actinic keratoses (ak), basal cell carcinoma (bcc), benign keratosis (bk), dermatofibroma (df), melanoma (mel), melanocytic nevi (nv), and vascular skin lesions (vsl), providing a robust platform for multiclass classification assessment. We evaluated GPT-4o using 100 dermatoscopic images per condition to assess diagnostic accuracy, potential biases, and limitations in skin lesion identification. The HAM10000 dataset was selected because it offers a large standardized reference set of dermatoscopic (rather than conventional clinical) images commonly used in dermatologic AI research. GPT-4o was chosen due to its patient-friendly interface, widespread use, and prior reports suggesting greater reliability in skin lesion assessment compared with other LLMs.

One hundred images from each of the 7 dermatologic categories were randomly selected for use in our analysis in 2024. The images were selected by our data scientist (J.C.) through random sampling from the dataset. Each image was separately presented to GPT-4o without any preprocessing or modification alongside 2 prompts designed to evaluate the diagnostic capabilities of GPT-4o. Both prompts included the same list of 7 dermatologic conditions for answer choices but differed in contextual information, where prompt 1 provided patient demographic information and localization of the dermatological condition but prompt 2 did not provide these details (Table). No follow-up questions were presented.

For prompt 1, the confusion matrix showed a strong bias toward detecting mel and bcc, with high true positives (mel, 83%; bcc, 37%)(eFigure 1). This pattern possibly suggests a tendency to favor malignant labels (eg, mel, BCC) when uncertainty is present. Interestingly, df and vsl also had notable true positives (46% and 37%, respectively), which is unexpected for less critical conditions because the model’s correct classifications were uneven across benign lesions. Actinic keratoses and nv showed higher misclassification rates, suggesting the model struggled to distinguish them from other lesions.

As shown in eTable 1, prompt 1 exhibited the highest recall for mel at 0.83 but performed worse in precision (0.242) and specificity (0.567) compared to ak, which had an extremely low recall (0.03) but very high specificity (0.992) and moderate precision score (0.375). The highest precision score was seen with vsl (0.738), which also achieved high scores in specificity (0.982) and accuracy (0.88) and performed moderately well in recall (0.31). All performance metrics are reported as proportions (0-1.0), wherein 1.0 indicates 100.

For prompt 2, the second confusion matrix followed similar trends as prompt 1 but still differed in key areas (eFigure 2). Melanoma detection remained strong (true positives, 95%), while bcc shows slightly fewer true positives (24%). Vascular skin lesions improve in true positives (40%), and df dropped slightly (33%). The model continues to struggle with ak and nv, with notable misclassifications observed across other categories

Similar to prompt 1, prompt 2 achieved its highest recall for mel (0.95%), but demonstrated lower precision (0.223%) and specificity (0.488%) for this class. Prompt 2 also produced the highest accuracy for vascular skin lesions (0.90%). The highest specificity was observed for both bk and ak (0.992% each); however, ak again demonstrated the lowest recall, with a value of 0.01%.

A previous study utilizing a model of binary classification to distinguish between mel and benign dermatologic conditions demonstrated poor performance.¹ Additionally, prior studies have employed a less-strict, open-ended style question approach to examine ChatGPT’s ability to diagnose mel with limited efficacy.⁷ The HAM10000 dataset was specifically selected despite its limitations (including the absence of clinical images and limited diversity in skin tones) due to its comprehensive nature, robust annotation standards, and widespread acceptance in dermatologic AI research. Compared to the Diverse Dermatology Images dataset, which notably lacks skin tone diversity, HAM10000 provides a balanced representation of several dermatologic conditions crucial for multiclass classification tasks, making it suitable for benchmarking AI performance. This study aimed to eliminate these limitations by employing a multiclass classification approach; however, despite this switch, our results indicate continued and major limitations of the diagnostic capabilities of GPT-4o.

In its current form, GPT-4o appeared to demonstrate a clear accuracy bias toward correctly identifying specific and severe dermatologic conditions (eg, mel, bcc) but showed low and variable class-level performance for other categories (eg, ak, nv, df, vsl), with frequent misclassification into melanoma or basal cell carcinoma and low recall for some classes (eTables 1 and 2). This finding emphasized that GPT-4o currently lacks the reliability needed for real-life clinical applications in dermatology, as both binary and multiclass models fail to achieve consistent accurate performance across all skin conditions. Notably, GPT-4o may generate false-positive malignant classifications among patients due to its skew in predicted labels toward labeling benign lesions as malignant.

From the patient perspective, younger individuals may upload images of benign nevi only to unnecessarily fear a mel diagnosis after receiving GPT-4o results. Statistically, younger patients are less likely than older patients to have malignant lesions and more likely to instead present with common vsl or df—lesions that GPT-4o appears likely to identify correctly.⁸ For older users, however, the situation may differ. Beyond ak being misclassified as bcc, older patients also may encounter GPT-4o outputs that mislabel lesions as mel, raising concerns and heightening anxiety. Given the technology’s tendency to overestimate the risk of serious dermatologic conditions, this behavior poses a considerable challenge in its current state and may inadvertently intensify public anxiety around mel.

A notable limitation of our study was that, compared to publicly available datasets, the HAM10000 dataset includes only dermatoscopic images rather than a combination of clinical and dermatoscopic images. Furthermore, the HAM10000 dataset comprises images primarily from White patients, whereas other diverse databases (eg, the Diverse Dermatology Images dataset) may be more suitable for training AI algorithms to accurately diagnose skin lesions in individuals with a variety of skin tones.⁹

Ultimately, our results signal that major advancements in the design and training of LLMs such as GPT-4o are necessary before these systems can be integrated into dermatologic diagnostic decision-making to offer benefit rather than cause harm. Consulting a health care professional rather than relying solely on AI, which might otherwise lead to avoidable stress, unnecessary alarm, and potentially increased health care costs due to unwarranted follow-up and testing, should remain the recommended standard of care for patients suspecting a skin lesion.

To the Editor:

It is known that dermatologist evaluation of skin conditions in hospitalized patients confers enhanced diagnostic accuracy, timely and appropriate treatment, and an overall reduction in readmissions compared to assessments by nondermatology hospitalists.¹ Dermatology consultations have been shown to alter diagnoses in up to 50% of cases and lead to changes in management in nearly 75% of cases, even for prevalent dermatologic conditions such as drug rashes, cellulitis, and stasis dermatitis.^1,2 Previous studies have observed a multiday reduction in length of hospital stay, a 10-fold reduction in readmission rate, and lower 30-day mortality, all leading to a reduction in patient morbidity and costs to both the patient and the health care system.^3,4 Despite these benefits, there has been a decrease in the number of dermatologists providing inpatient services and a reduction in medical centers offering dermatology consultations over the past several years.⁵ To better appreciate current trends of declining dermatology inpatient and consultative services within our region, we evaluated the availability of dermatology care at hospitals across Virginia.

A simple telephone survey was conducted across community hospitals in Virginia wherein medical staff administrators were asked to provide details regarding their dermatology staffing. The following figures were collected: number of dermatologists on staff, number of dermatologists with consulting privileges, number of affiliated dermatologists, and number of advanced-practice dermatology providers. Follow-up calls were carried out to elaborate on how dermatologists (when available) were integrated into inpatient care workflow and made accessible to hospitalists and emergency medicine departments. Academic centers, military hospitals, and specialty hospitals were excluded from the survey.

To better appreciate the relationships between hospital and population characteristics and the availability of dermatology care, publicly available data were collected on hospital bed counts and regional population density for each facility.^6-9 Spearman rank correlation analyses were conducted in Microsoft Excel to evaluate the association between the number of dermatologists on staff, number of consulting dermatologists, staffed inpatient beds, and population size.

Sixty-four hospitals—more than 70% of the 90 eligible community hospitals—responded to the survey between May and August 2024 and were included in the study. On-staff dermatologists were present at 8 (12.5%) of the hospitals surveyed; of these, 4 (50.0%) hospitals had between 1 and 5 dermatologists, 3 (37.5%) had between 6 and 10 dermatologists, and 1 (12.5%) had between 11 and 15 dermatologists. An additional 4 (6.3%) hospitals provided consultative dermatology services from outside dermatology clinics. Urban hospitals accounted for 9 of 12 (75%) hospitals offering in-house dermatology services, either through on-staff physicians or consultations with clinic-based providers.

Based on Spearman rank correlation analysis, there was a positive correlation between the number of dermatologists on staff and the number of staffed hospital beds (r=0.61; P <.001). Similarly, there was a positive correlation between the number of dermatologists on staff and the population density of the affiliated region (r=0.58; P <.001). Finally, there was a positive correlation between the number of dermatologists on staff and the number of available consulting dermatologists (r=0.89; P <.001).

At facilities with only consultative dermatology services accessible, there often was no formal dermatology team or department present. Rather, the hospitals relied on a loosely affiliated network of dermatology providers or navigated inpatient dermatology needs almost exclusively via internal medicine hospitalists or emergency medicine physicians. When available, dermatology support from dermatology physicians often was provided through teledermatology platforms. Although teledermatology has a large role in increasing access to care within underserved areas, its reliance on images and second-hand case descriptions can limit the provider’s ability to perform a comprehensive examination and assessment. Moreover, it was noted that few hospital representatives could offer clarity on how dermatologists were integrated into the inpatient setting. It remained unclear whether dermatologists were practically accessible to the inpatient care teams in a structured manner.

The uneven distribution and limited availability of dermatology inpatient care in Virginia reflect national trends and underscore ongoing access issues for patients. Without intentional intervention, these trends are expected to continue, contributing to a glaring gap in hospital services as well as to patient morbidity and mortality. The correlation data obtained in our study further qualify these disparities. The positive correlations between dermatologist availability and hospital size and population density suggest that larger, more urban facilities are more likely to offer inpatient dermatology care, whether through staffing or consultation. This relationship is not unexpected, given the greater financial resources and specialist networks available to facilities with large patient volumes. This suggests that dermatology care is shaped by institutional capacity and geographic leverage rather than clinical need, reinforcing existing disparities.

Importantly, it should be noted that the data may overestimate the true availability of dermatologists to these patients. As revealed via follow-up survey calls, respondent facilities that provided dermatology via consultative services often did not have a defined structure for integrating this care into the inpatient workflow. In some instances, dermatologists were technically affiliated with the hospital but had varying levels of practical interaction with the hospital providers and their patients. Administrative staff's differing awareness regarding dermatology interaction with the hospital facility may reveal systemic underutilization and opportunities to improve coordination to achieve the greatest benefit from dermatology services. These observations are further informed by the scope of our study, which focused specifically on community hospitals. The exclusion of academic and military institutions—and the tendency of these to exist in more densely populated areas—may have limited how broadly our findings reflect nationwide dermatology access by omitting more established dermatology departments and specialty care. As a result, regional variations in predominant facility type should be considered when interpreting the implications of these results beyond Virginia’s community hospital system.

In response to access limitations and differences in availability, facilities are turning to integrated teledermatology as a valuable tool to expand the reach of specialist care, particularly in rural or resource-limited settings. This modality acts as an important step toward improving equity in care by beginning to bridge geographic gaps; however, along with these logistical advantages, teledermatology also confers diagnostic limitations and clinical trade-offs that should be thoughtfully considered. Our findings highlight the need to expand access in a way that integrates technological advances with in-person care to build a sustainable and effective path forward without compromising the quality of care patients receive. We present these outcomes to emphasize the importance of increasing dermatology involvement in the care of hospitalized patients, which is a promising strategy to improve patient outcomes and reduce existing disparities in Virginia and nationwide.

To the Editor:

It is known that dermatologist evaluation of skin conditions in hospitalized patients confers enhanced diagnostic accuracy, timely and appropriate treatment, and an overall reduction in readmissions compared to assessments by nondermatology hospitalists.¹ Dermatology consultations have been shown to alter diagnoses in up to 50% of cases and lead to changes in management in nearly 75% of cases, even for prevalent dermatologic conditions such as drug rashes, cellulitis, and stasis dermatitis.^1,2 Previous studies have observed a multiday reduction in length of hospital stay, a 10-fold reduction in readmission rate, and lower 30-day mortality, all leading to a reduction in patient morbidity and costs to both the patient and the health care system.^3,4 Despite these benefits, there has been a decrease in the number of dermatologists providing inpatient services and a reduction in medical centers offering dermatology consultations over the past several years.⁵ To better appreciate current trends of declining dermatology inpatient and consultative services within our region, we evaluated the availability of dermatology care at hospitals across Virginia.

A simple telephone survey was conducted across community hospitals in Virginia wherein medical staff administrators were asked to provide details regarding their dermatology staffing. The following figures were collected: number of dermatologists on staff, number of dermatologists with consulting privileges, number of affiliated dermatologists, and number of advanced-practice dermatology providers. Follow-up calls were carried out to elaborate on how dermatologists (when available) were integrated into inpatient care workflow and made accessible to hospitalists and emergency medicine departments. Academic centers, military hospitals, and specialty hospitals were excluded from the survey.

To better appreciate the relationships between hospital and population characteristics and the availability of dermatology care, publicly available data were collected on hospital bed counts and regional population density for each facility.^6-9 Spearman rank correlation analyses were conducted in Microsoft Excel to evaluate the association between the number of dermatologists on staff, number of consulting dermatologists, staffed inpatient beds, and population size.

Sixty-four hospitals—more than 70% of the 90 eligible community hospitals—responded to the survey between May and August 2024 and were included in the study. On-staff dermatologists were present at 8 (12.5%) of the hospitals surveyed; of these, 4 (50.0%) hospitals had between 1 and 5 dermatologists, 3 (37.5%) had between 6 and 10 dermatologists, and 1 (12.5%) had between 11 and 15 dermatologists. An additional 4 (6.3%) hospitals provided consultative dermatology services from outside dermatology clinics. Urban hospitals accounted for 9 of 12 (75%) hospitals offering in-house dermatology services, either through on-staff physicians or consultations with clinic-based providers.

Based on Spearman rank correlation analysis, there was a positive correlation between the number of dermatologists on staff and the number of staffed hospital beds (r=0.61; P <.001). Similarly, there was a positive correlation between the number of dermatologists on staff and the population density of the affiliated region (r=0.58; P <.001). Finally, there was a positive correlation between the number of dermatologists on staff and the number of available consulting dermatologists (r=0.89; P <.001).

At facilities with only consultative dermatology services accessible, there often was no formal dermatology team or department present. Rather, the hospitals relied on a loosely affiliated network of dermatology providers or navigated inpatient dermatology needs almost exclusively via internal medicine hospitalists or emergency medicine physicians. When available, dermatology support from dermatology physicians often was provided through teledermatology platforms. Although teledermatology has a large role in increasing access to care within underserved areas, its reliance on images and second-hand case descriptions can limit the provider’s ability to perform a comprehensive examination and assessment. Moreover, it was noted that few hospital representatives could offer clarity on how dermatologists were integrated into the inpatient setting. It remained unclear whether dermatologists were practically accessible to the inpatient care teams in a structured manner.

The uneven distribution and limited availability of dermatology inpatient care in Virginia reflect national trends and underscore ongoing access issues for patients. Without intentional intervention, these trends are expected to continue, contributing to a glaring gap in hospital services as well as to patient morbidity and mortality. The correlation data obtained in our study further qualify these disparities. The positive correlations between dermatologist availability and hospital size and population density suggest that larger, more urban facilities are more likely to offer inpatient dermatology care, whether through staffing or consultation. This relationship is not unexpected, given the greater financial resources and specialist networks available to facilities with large patient volumes. This suggests that dermatology care is shaped by institutional capacity and geographic leverage rather than clinical need, reinforcing existing disparities.

Importantly, it should be noted that the data may overestimate the true availability of dermatologists to these patients. As revealed via follow-up survey calls, respondent facilities that provided dermatology via consultative services often did not have a defined structure for integrating this care into the inpatient workflow. In some instances, dermatologists were technically affiliated with the hospital but had varying levels of practical interaction with the hospital providers and their patients. Administrative staff's differing awareness regarding dermatology interaction with the hospital facility may reveal systemic underutilization and opportunities to improve coordination to achieve the greatest benefit from dermatology services. These observations are further informed by the scope of our study, which focused specifically on community hospitals. The exclusion of academic and military institutions—and the tendency of these to exist in more densely populated areas—may have limited how broadly our findings reflect nationwide dermatology access by omitting more established dermatology departments and specialty care. As a result, regional variations in predominant facility type should be considered when interpreting the implications of these results beyond Virginia’s community hospital system.

In response to access limitations and differences in availability, facilities are turning to integrated teledermatology as a valuable tool to expand the reach of specialist care, particularly in rural or resource-limited settings. This modality acts as an important step toward improving equity in care by beginning to bridge geographic gaps; however, along with these logistical advantages, teledermatology also confers diagnostic limitations and clinical trade-offs that should be thoughtfully considered. Our findings highlight the need to expand access in a way that integrates technological advances with in-person care to build a sustainable and effective path forward without compromising the quality of care patients receive. We present these outcomes to emphasize the importance of increasing dermatology involvement in the care of hospitalized patients, which is a promising strategy to improve patient outcomes and reduce existing disparities in Virginia and nationwide.

To the Editor:

It is known that dermatologist evaluation of skin conditions in hospitalized patients confers enhanced diagnostic accuracy, timely and appropriate treatment, and an overall reduction in readmissions compared to assessments by nondermatology hospitalists.¹ Dermatology consultations have been shown to alter diagnoses in up to 50% of cases and lead to changes in management in nearly 75% of cases, even for prevalent dermatologic conditions such as drug rashes, cellulitis, and stasis dermatitis.^1,2 Previous studies have observed a multiday reduction in length of hospital stay, a 10-fold reduction in readmission rate, and lower 30-day mortality, all leading to a reduction in patient morbidity and costs to both the patient and the health care system.^3,4 Despite these benefits, there has been a decrease in the number of dermatologists providing inpatient services and a reduction in medical centers offering dermatology consultations over the past several years.⁵ To better appreciate current trends of declining dermatology inpatient and consultative services within our region, we evaluated the availability of dermatology care at hospitals across Virginia.

A simple telephone survey was conducted across community hospitals in Virginia wherein medical staff administrators were asked to provide details regarding their dermatology staffing. The following figures were collected: number of dermatologists on staff, number of dermatologists with consulting privileges, number of affiliated dermatologists, and number of advanced-practice dermatology providers. Follow-up calls were carried out to elaborate on how dermatologists (when available) were integrated into inpatient care workflow and made accessible to hospitalists and emergency medicine departments. Academic centers, military hospitals, and specialty hospitals were excluded from the survey.

To better appreciate the relationships between hospital and population characteristics and the availability of dermatology care, publicly available data were collected on hospital bed counts and regional population density for each facility.^6-9 Spearman rank correlation analyses were conducted in Microsoft Excel to evaluate the association between the number of dermatologists on staff, number of consulting dermatologists, staffed inpatient beds, and population size.

Sixty-four hospitals—more than 70% of the 90 eligible community hospitals—responded to the survey between May and August 2024 and were included in the study. On-staff dermatologists were present at 8 (12.5%) of the hospitals surveyed; of these, 4 (50.0%) hospitals had between 1 and 5 dermatologists, 3 (37.5%) had between 6 and 10 dermatologists, and 1 (12.5%) had between 11 and 15 dermatologists. An additional 4 (6.3%) hospitals provided consultative dermatology services from outside dermatology clinics. Urban hospitals accounted for 9 of 12 (75%) hospitals offering in-house dermatology services, either through on-staff physicians or consultations with clinic-based providers.

Based on Spearman rank correlation analysis, there was a positive correlation between the number of dermatologists on staff and the number of staffed hospital beds (r=0.61; P <.001). Similarly, there was a positive correlation between the number of dermatologists on staff and the population density of the affiliated region (r=0.58; P <.001). Finally, there was a positive correlation between the number of dermatologists on staff and the number of available consulting dermatologists (r=0.89; P <.001).

At facilities with only consultative dermatology services accessible, there often was no formal dermatology team or department present. Rather, the hospitals relied on a loosely affiliated network of dermatology providers or navigated inpatient dermatology needs almost exclusively via internal medicine hospitalists or emergency medicine physicians. When available, dermatology support from dermatology physicians often was provided through teledermatology platforms. Although teledermatology has a large role in increasing access to care within underserved areas, its reliance on images and second-hand case descriptions can limit the provider’s ability to perform a comprehensive examination and assessment. Moreover, it was noted that few hospital representatives could offer clarity on how dermatologists were integrated into the inpatient setting. It remained unclear whether dermatologists were practically accessible to the inpatient care teams in a structured manner.

The uneven distribution and limited availability of dermatology inpatient care in Virginia reflect national trends and underscore ongoing access issues for patients. Without intentional intervention, these trends are expected to continue, contributing to a glaring gap in hospital services as well as to patient morbidity and mortality. The correlation data obtained in our study further qualify these disparities. The positive correlations between dermatologist availability and hospital size and population density suggest that larger, more urban facilities are more likely to offer inpatient dermatology care, whether through staffing or consultation. This relationship is not unexpected, given the greater financial resources and specialist networks available to facilities with large patient volumes. This suggests that dermatology care is shaped by institutional capacity and geographic leverage rather than clinical need, reinforcing existing disparities.

Importantly, it should be noted that the data may overestimate the true availability of dermatologists to these patients. As revealed via follow-up survey calls, respondent facilities that provided dermatology via consultative services often did not have a defined structure for integrating this care into the inpatient workflow. In some instances, dermatologists were technically affiliated with the hospital but had varying levels of practical interaction with the hospital providers and their patients. Administrative staff's differing awareness regarding dermatology interaction with the hospital facility may reveal systemic underutilization and opportunities to improve coordination to achieve the greatest benefit from dermatology services. These observations are further informed by the scope of our study, which focused specifically on community hospitals. The exclusion of academic and military institutions—and the tendency of these to exist in more densely populated areas—may have limited how broadly our findings reflect nationwide dermatology access by omitting more established dermatology departments and specialty care. As a result, regional variations in predominant facility type should be considered when interpreting the implications of these results beyond Virginia’s community hospital system.

In response to access limitations and differences in availability, facilities are turning to integrated teledermatology as a valuable tool to expand the reach of specialist care, particularly in rural or resource-limited settings. This modality acts as an important step toward improving equity in care by beginning to bridge geographic gaps; however, along with these logistical advantages, teledermatology also confers diagnostic limitations and clinical trade-offs that should be thoughtfully considered. Our findings highlight the need to expand access in a way that integrates technological advances with in-person care to build a sustainable and effective path forward without compromising the quality of care patients receive. We present these outcomes to emphasize the importance of increasing dermatology involvement in the care of hospitalized patients, which is a promising strategy to improve patient outcomes and reduce existing disparities in Virginia and nationwide.

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.