Dermatology

At the hospital, the physicians noted that there were no lesions on the mucous membranes of the patient’s eyes, ears, nose, mouth or anus and his vital signs were within normal limits. He was empirically treated with 1 dose of methylprednisolone (125 mg intravenous [IV]) and started on IV piperacillin-tazobactam and vancomycin. The patient subsequently revealed that he’d had a similar experience a year earlier after being treated with TMP-SMX for cellulitis. During the previous episode, he said the lesions were located on the exact same areas of his glans penis and chin. Based on the morphologic characteristics of the eruption and the history of similar lesions that appeared following previous treatment with TMP-SMX, the physician diagnosed disseminated fixed-drug eruption in this patient.

A fixed-drug eruption is an adverse cutaneous reaction to a drug that is defined by a dusky red or violaceous macule, which evolves into a patch, and eventually, an edematous plaque. Fixed-drug eruptions are typically solitary, but may be generalized (as was the case with this patient). The pathophysiology of the disease involves resident intra-epidermal CD8+ T-cells resembling effector memory T-cells. These T-cells are increased in number at the dermoepidermal junction of normal appearing skin; their aberrant activation leads to an inflammatory response, stimulating tissue destruction and formation of the classic fixed-drug lesion.

This diagnosis usually is made based on a history of similar lesions recurring at the same location in response to a specific drug and the classic physical exam findings of well-demarcated, edematous, and violaceous plaques. A skin biopsy may be performed to confirm a fixed-drug eruption in the case of clinical equipoise.

Fixed-drug eruptions occasionally exhibit bullae and erosions and must be differentiated from more serious generalized bullous diseases, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The differential diagnosis also includes erythema multiforme, early bullous drug eruption, and bullous arthropod assault, which may leave similar hyperpigmented patches.

Management of a disseminated fixed-drug eruption requires a thorough history to identify the causative agent (including over-the-counter drugs, herbals, topicals, and eye drops). Most patients are asymptomatic, but some (like this patient) are symptomatic and experience generalized pruritus, cutaneous burning, and/or pain. Symptomatic therapy includes oral antihistamines and potent topical glucocorticoid ointment for non-eroded lesions. Additionally, if not medically contraindicated, oral steroids may be used for generalized or extremely painful mucosal lesions at a dose of 0.5 mg/kg daily for 3 to 5 days.

Local wound care of eroded lesions includes keeping the site moist with a bland emollient and bandaging. The inciting agent must be added to the patient’s allergy list and avoided in the future. In equivocal cases, it is prudent to admit the patient for observation to ensure that the eruption is not a nascent SJS or TEN eruption.

In this case, the patient was admitted to the observation unit overnight to monitor for the appearance of systemic symptoms and to assess the evolution of the rash for further mucosal involvement that could have indicated SJS. Upon reassessment the next day, his older lesions had evolved into vesiculated and necrotic areas as per the natural history of severe fixed-drug eruption. He was prescribed prednisone 40 mg/d for 3 days to help with local inflammation, pain, and itching. TMP-SMX was added to his allergy list and he was given local wound care instructions. He was told to return if he developed any systemic symptoms.

‌

This case was adapted from: Bucher J, Rahnama-Moghadam S, Osswald S. Generalized rash follows ankle ulceration. J Fam Pract. 2016;65:489-491.

At the hospital, the physicians noted that there were no lesions on the mucous membranes of the patient’s eyes, ears, nose, mouth or anus and his vital signs were within normal limits. He was empirically treated with 1 dose of methylprednisolone (125 mg intravenous [IV]) and started on IV piperacillin-tazobactam and vancomycin. The patient subsequently revealed that he’d had a similar experience a year earlier after being treated with TMP-SMX for cellulitis. During the previous episode, he said the lesions were located on the exact same areas of his glans penis and chin. Based on the morphologic characteristics of the eruption and the history of similar lesions that appeared following previous treatment with TMP-SMX, the physician diagnosed disseminated fixed-drug eruption in this patient.

A fixed-drug eruption is an adverse cutaneous reaction to a drug that is defined by a dusky red or violaceous macule, which evolves into a patch, and eventually, an edematous plaque. Fixed-drug eruptions are typically solitary, but may be generalized (as was the case with this patient). The pathophysiology of the disease involves resident intra-epidermal CD8+ T-cells resembling effector memory T-cells. These T-cells are increased in number at the dermoepidermal junction of normal appearing skin; their aberrant activation leads to an inflammatory response, stimulating tissue destruction and formation of the classic fixed-drug lesion.

This diagnosis usually is made based on a history of similar lesions recurring at the same location in response to a specific drug and the classic physical exam findings of well-demarcated, edematous, and violaceous plaques. A skin biopsy may be performed to confirm a fixed-drug eruption in the case of clinical equipoise.

Fixed-drug eruptions occasionally exhibit bullae and erosions and must be differentiated from more serious generalized bullous diseases, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The differential diagnosis also includes erythema multiforme, early bullous drug eruption, and bullous arthropod assault, which may leave similar hyperpigmented patches.

Management of a disseminated fixed-drug eruption requires a thorough history to identify the causative agent (including over-the-counter drugs, herbals, topicals, and eye drops). Most patients are asymptomatic, but some (like this patient) are symptomatic and experience generalized pruritus, cutaneous burning, and/or pain. Symptomatic therapy includes oral antihistamines and potent topical glucocorticoid ointment for non-eroded lesions. Additionally, if not medically contraindicated, oral steroids may be used for generalized or extremely painful mucosal lesions at a dose of 0.5 mg/kg daily for 3 to 5 days.

Local wound care of eroded lesions includes keeping the site moist with a bland emollient and bandaging. The inciting agent must be added to the patient’s allergy list and avoided in the future. In equivocal cases, it is prudent to admit the patient for observation to ensure that the eruption is not a nascent SJS or TEN eruption.

In this case, the patient was admitted to the observation unit overnight to monitor for the appearance of systemic symptoms and to assess the evolution of the rash for further mucosal involvement that could have indicated SJS. Upon reassessment the next day, his older lesions had evolved into vesiculated and necrotic areas as per the natural history of severe fixed-drug eruption. He was prescribed prednisone 40 mg/d for 3 days to help with local inflammation, pain, and itching. TMP-SMX was added to his allergy list and he was given local wound care instructions. He was told to return if he developed any systemic symptoms.

‌

This case was adapted from: Bucher J, Rahnama-Moghadam S, Osswald S. Generalized rash follows ankle ulceration. J Fam Pract. 2016;65:489-491.

At the hospital, the physicians noted that there were no lesions on the mucous membranes of the patient’s eyes, ears, nose, mouth or anus and his vital signs were within normal limits. He was empirically treated with 1 dose of methylprednisolone (125 mg intravenous [IV]) and started on IV piperacillin-tazobactam and vancomycin. The patient subsequently revealed that he’d had a similar experience a year earlier after being treated with TMP-SMX for cellulitis. During the previous episode, he said the lesions were located on the exact same areas of his glans penis and chin. Based on the morphologic characteristics of the eruption and the history of similar lesions that appeared following previous treatment with TMP-SMX, the physician diagnosed disseminated fixed-drug eruption in this patient.

A fixed-drug eruption is an adverse cutaneous reaction to a drug that is defined by a dusky red or violaceous macule, which evolves into a patch, and eventually, an edematous plaque. Fixed-drug eruptions are typically solitary, but may be generalized (as was the case with this patient). The pathophysiology of the disease involves resident intra-epidermal CD8+ T-cells resembling effector memory T-cells. These T-cells are increased in number at the dermoepidermal junction of normal appearing skin; their aberrant activation leads to an inflammatory response, stimulating tissue destruction and formation of the classic fixed-drug lesion.

This diagnosis usually is made based on a history of similar lesions recurring at the same location in response to a specific drug and the classic physical exam findings of well-demarcated, edematous, and violaceous plaques. A skin biopsy may be performed to confirm a fixed-drug eruption in the case of clinical equipoise.

Fixed-drug eruptions occasionally exhibit bullae and erosions and must be differentiated from more serious generalized bullous diseases, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The differential diagnosis also includes erythema multiforme, early bullous drug eruption, and bullous arthropod assault, which may leave similar hyperpigmented patches.

Management of a disseminated fixed-drug eruption requires a thorough history to identify the causative agent (including over-the-counter drugs, herbals, topicals, and eye drops). Most patients are asymptomatic, but some (like this patient) are symptomatic and experience generalized pruritus, cutaneous burning, and/or pain. Symptomatic therapy includes oral antihistamines and potent topical glucocorticoid ointment for non-eroded lesions. Additionally, if not medically contraindicated, oral steroids may be used for generalized or extremely painful mucosal lesions at a dose of 0.5 mg/kg daily for 3 to 5 days.

Local wound care of eroded lesions includes keeping the site moist with a bland emollient and bandaging. The inciting agent must be added to the patient’s allergy list and avoided in the future. In equivocal cases, it is prudent to admit the patient for observation to ensure that the eruption is not a nascent SJS or TEN eruption.

In this case, the patient was admitted to the observation unit overnight to monitor for the appearance of systemic symptoms and to assess the evolution of the rash for further mucosal involvement that could have indicated SJS. Upon reassessment the next day, his older lesions had evolved into vesiculated and necrotic areas as per the natural history of severe fixed-drug eruption. He was prescribed prednisone 40 mg/d for 3 days to help with local inflammation, pain, and itching. TMP-SMX was added to his allergy list and he was given local wound care instructions. He was told to return if he developed any systemic symptoms.

‌

This case was adapted from: Bucher J, Rahnama-Moghadam S, Osswald S. Generalized rash follows ankle ulceration. J Fam Pract. 2016;65:489-491.

Trimethoprim-sulfamethoxazole (TMP-SMX) was linked to severe acute respiratory distress syndrome (ARDS) in five previously healthy teens, two of whom died.

TMP-SMX, a frequently prescribed antibiotic, has been associated with “idiosyncratic adverse drug reactions, including cutaneous reactions and hypersensitivity syndromes,” but pulmonary complications are rare, especially in children, wrote Jenna O. Miller, MD, of the University of Missouri–Kansas City and colleagues.

In a case series published in Pediatrics, the researchers described the patients, who were aged 13-18 years; the 18-year-old was male, the others were female. Four of the patients (three females, one male) were taking TMP-SMX for acne vulgaris. One of these patients, a 13-year-old girl, underwent a bilateral lung and heart transplant after developing interstitial lung disease and died as a result of solid organ transplant complications. The other death occurred in a 15-year-old girl who was taking TMP-SMX to treat a urinary tract infection. This patient developed interstitial lung disease and died of complications from the disease while awaiting a lung transplant.

“In all cases, patients were transferred to academic medical facilities, and pediatric pulmonologists and infectious diseases specialists performed extensive evaluations,” the researchers wrote. The patients did not improve when the drug was discontinued, and four of the five were considered or listed for organ transplants. The spectrum of disease was varied among the patients, and the pathophysiology remains poorly understood.

Although no clinical test could confirm causality between TMP-SMX and ARDS in the five teens, “the extensive negative workup, paired with recent TMP-SMX exposure and similarity among these cases, raises the possibility that the observed ARDS was TMP-SMX triggered,” they wrote.

The researchers had no financial conflicts to disclose.

SOURCE: Miller JO et al. Pediatrics. 2019 May 29. doi: 10.1542/peds.2018.3242.

Trimethoprim-sulfamethoxazole (TMP-SMX) was linked to severe acute respiratory distress syndrome (ARDS) in five previously healthy teens, two of whom died.

TMP-SMX, a frequently prescribed antibiotic, has been associated with “idiosyncratic adverse drug reactions, including cutaneous reactions and hypersensitivity syndromes,” but pulmonary complications are rare, especially in children, wrote Jenna O. Miller, MD, of the University of Missouri–Kansas City and colleagues.

In a case series published in Pediatrics, the researchers described the patients, who were aged 13-18 years; the 18-year-old was male, the others were female. Four of the patients (three females, one male) were taking TMP-SMX for acne vulgaris. One of these patients, a 13-year-old girl, underwent a bilateral lung and heart transplant after developing interstitial lung disease and died as a result of solid organ transplant complications. The other death occurred in a 15-year-old girl who was taking TMP-SMX to treat a urinary tract infection. This patient developed interstitial lung disease and died of complications from the disease while awaiting a lung transplant.

“In all cases, patients were transferred to academic medical facilities, and pediatric pulmonologists and infectious diseases specialists performed extensive evaluations,” the researchers wrote. The patients did not improve when the drug was discontinued, and four of the five were considered or listed for organ transplants. The spectrum of disease was varied among the patients, and the pathophysiology remains poorly understood.

Although no clinical test could confirm causality between TMP-SMX and ARDS in the five teens, “the extensive negative workup, paired with recent TMP-SMX exposure and similarity among these cases, raises the possibility that the observed ARDS was TMP-SMX triggered,” they wrote.

The researchers had no financial conflicts to disclose.

SOURCE: Miller JO et al. Pediatrics. 2019 May 29. doi: 10.1542/peds.2018.3242.

Trimethoprim-sulfamethoxazole (TMP-SMX) was linked to severe acute respiratory distress syndrome (ARDS) in five previously healthy teens, two of whom died.

TMP-SMX, a frequently prescribed antibiotic, has been associated with “idiosyncratic adverse drug reactions, including cutaneous reactions and hypersensitivity syndromes,” but pulmonary complications are rare, especially in children, wrote Jenna O. Miller, MD, of the University of Missouri–Kansas City and colleagues.

In a case series published in Pediatrics, the researchers described the patients, who were aged 13-18 years; the 18-year-old was male, the others were female. Four of the patients (three females, one male) were taking TMP-SMX for acne vulgaris. One of these patients, a 13-year-old girl, underwent a bilateral lung and heart transplant after developing interstitial lung disease and died as a result of solid organ transplant complications. The other death occurred in a 15-year-old girl who was taking TMP-SMX to treat a urinary tract infection. This patient developed interstitial lung disease and died of complications from the disease while awaiting a lung transplant.

“In all cases, patients were transferred to academic medical facilities, and pediatric pulmonologists and infectious diseases specialists performed extensive evaluations,” the researchers wrote. The patients did not improve when the drug was discontinued, and four of the five were considered or listed for organ transplants. The spectrum of disease was varied among the patients, and the pathophysiology remains poorly understood.

Although no clinical test could confirm causality between TMP-SMX and ARDS in the five teens, “the extensive negative workup, paired with recent TMP-SMX exposure and similarity among these cases, raises the possibility that the observed ARDS was TMP-SMX triggered,” they wrote.

The researchers had no financial conflicts to disclose.

SOURCE: Miller JO et al. Pediatrics. 2019 May 29. doi: 10.1542/peds.2018.3242.

Use of aspirin or nonaspirin NSAIDs was not associated with a reduced risk of basal cell carcinoma (BCC) or squamous cell carcinoma (SCC), in a large, prospective cohort study of Australian residents.

Fuse/Thinkstock

“Overall, we observed weak and inconsistent inverse associations between use of these medications and incidence of either BCC or SCC,” wrote Nirmala Pandeya, PhD, of the University of Queensland (Australia) and coauthors. “While we did observe a modest reduction in risk of BCC associated with NSAID use among people with high risk of skin cancer ... no statistically significant associations were seen with aspirin use,” they added. The study was published in the British Journal of Dermatology.

While reviews of observational studies have suggested that NSAIDs may have “a potential benefit” in reducing the incidence of BCC and SCC, the results have varied, they noted.

To investigate the potential chemopreventive effects of NSAID use on skin cancer, the investigators used data from the QSkin Sun and Health Study, a prospective cohort of 43,764 residents of Queensland, Australia. Those eligible for the study had a white ethnic background and no history of melanoma; 34,630 participants were available for analysis, their median age was 57 years, and 55% were women

Almost 15,600 (45%) were classified as “high risk” because they had had at least one skin cancer excision or more than five actinic lesions treated; 18,828 participants were classified as “average to low risk;” and data were unavailable for 206 participants. One‐third of the participants in the high-risk group (5,398) used aspirin; of these individuals, 39% (2,132) used aspirin more than once a week (defined as “frequent” users). Also, 60% (9,236) used NSAIDs, and of those, 24% (2,229) were frequent users.

During a median follow-up of 3 years, 3,421 of those in the study (10%) developed one or more BCC, and 1,470 (4%) developed one or more SCC.


Compared with never users, frequent NSAID use in the high-risk group was modestly associated with a reduced risk of BCC (hazard ratio, 0.84; 95% confidence interval, 0.71-0.99), but not with SCC. Aspirin use was weakly associated with a reduced risk of SCC (HR, 0.77; 95% CI, 0.64-0.93) but only among infrequent users and was not associated with BCC risk. In the average- to low-risk group, there was no association with either NSAIDs or aspirin and BCC or SCC occurrence.

The authors noted limitations of their study, including its reliance on self-reported NSAID use and a lack of detail in regard to usage dose and duration. In addition, though the investigators controlled for all likely confounders, “the possibility of some residual confounding cannot be excluded.”

The QSkin Study was funded by a grant from the National Health and Medical Research Council of Australia (NHMRC). The authors declared no conflicts of interest.

SOURCE: Pandeya N et al. Br J Dermatol. 2019 Mar 28. doi: 10.1111/bjd.17938.

Use of aspirin or nonaspirin NSAIDs was not associated with a reduced risk of basal cell carcinoma (BCC) or squamous cell carcinoma (SCC), in a large, prospective cohort study of Australian residents.

Fuse/Thinkstock

“Overall, we observed weak and inconsistent inverse associations between use of these medications and incidence of either BCC or SCC,” wrote Nirmala Pandeya, PhD, of the University of Queensland (Australia) and coauthors. “While we did observe a modest reduction in risk of BCC associated with NSAID use among people with high risk of skin cancer ... no statistically significant associations were seen with aspirin use,” they added. The study was published in the British Journal of Dermatology.

While reviews of observational studies have suggested that NSAIDs may have “a potential benefit” in reducing the incidence of BCC and SCC, the results have varied, they noted.

To investigate the potential chemopreventive effects of NSAID use on skin cancer, the investigators used data from the QSkin Sun and Health Study, a prospective cohort of 43,764 residents of Queensland, Australia. Those eligible for the study had a white ethnic background and no history of melanoma; 34,630 participants were available for analysis, their median age was 57 years, and 55% were women

Almost 15,600 (45%) were classified as “high risk” because they had had at least one skin cancer excision or more than five actinic lesions treated; 18,828 participants were classified as “average to low risk;” and data were unavailable for 206 participants. One‐third of the participants in the high-risk group (5,398) used aspirin; of these individuals, 39% (2,132) used aspirin more than once a week (defined as “frequent” users). Also, 60% (9,236) used NSAIDs, and of those, 24% (2,229) were frequent users.

During a median follow-up of 3 years, 3,421 of those in the study (10%) developed one or more BCC, and 1,470 (4%) developed one or more SCC.


Compared with never users, frequent NSAID use in the high-risk group was modestly associated with a reduced risk of BCC (hazard ratio, 0.84; 95% confidence interval, 0.71-0.99), but not with SCC. Aspirin use was weakly associated with a reduced risk of SCC (HR, 0.77; 95% CI, 0.64-0.93) but only among infrequent users and was not associated with BCC risk. In the average- to low-risk group, there was no association with either NSAIDs or aspirin and BCC or SCC occurrence.

The authors noted limitations of their study, including its reliance on self-reported NSAID use and a lack of detail in regard to usage dose and duration. In addition, though the investigators controlled for all likely confounders, “the possibility of some residual confounding cannot be excluded.”

The QSkin Study was funded by a grant from the National Health and Medical Research Council of Australia (NHMRC). The authors declared no conflicts of interest.

SOURCE: Pandeya N et al. Br J Dermatol. 2019 Mar 28. doi: 10.1111/bjd.17938.

Use of aspirin or nonaspirin NSAIDs was not associated with a reduced risk of basal cell carcinoma (BCC) or squamous cell carcinoma (SCC), in a large, prospective cohort study of Australian residents.

Fuse/Thinkstock

“Overall, we observed weak and inconsistent inverse associations between use of these medications and incidence of either BCC or SCC,” wrote Nirmala Pandeya, PhD, of the University of Queensland (Australia) and coauthors. “While we did observe a modest reduction in risk of BCC associated with NSAID use among people with high risk of skin cancer ... no statistically significant associations were seen with aspirin use,” they added. The study was published in the British Journal of Dermatology.

While reviews of observational studies have suggested that NSAIDs may have “a potential benefit” in reducing the incidence of BCC and SCC, the results have varied, they noted.

To investigate the potential chemopreventive effects of NSAID use on skin cancer, the investigators used data from the QSkin Sun and Health Study, a prospective cohort of 43,764 residents of Queensland, Australia. Those eligible for the study had a white ethnic background and no history of melanoma; 34,630 participants were available for analysis, their median age was 57 years, and 55% were women

Almost 15,600 (45%) were classified as “high risk” because they had had at least one skin cancer excision or more than five actinic lesions treated; 18,828 participants were classified as “average to low risk;” and data were unavailable for 206 participants. One‐third of the participants in the high-risk group (5,398) used aspirin; of these individuals, 39% (2,132) used aspirin more than once a week (defined as “frequent” users). Also, 60% (9,236) used NSAIDs, and of those, 24% (2,229) were frequent users.

During a median follow-up of 3 years, 3,421 of those in the study (10%) developed one or more BCC, and 1,470 (4%) developed one or more SCC.


Compared with never users, frequent NSAID use in the high-risk group was modestly associated with a reduced risk of BCC (hazard ratio, 0.84; 95% confidence interval, 0.71-0.99), but not with SCC. Aspirin use was weakly associated with a reduced risk of SCC (HR, 0.77; 95% CI, 0.64-0.93) but only among infrequent users and was not associated with BCC risk. In the average- to low-risk group, there was no association with either NSAIDs or aspirin and BCC or SCC occurrence.

The authors noted limitations of their study, including its reliance on self-reported NSAID use and a lack of detail in regard to usage dose and duration. In addition, though the investigators controlled for all likely confounders, “the possibility of some residual confounding cannot be excluded.”

The QSkin Study was funded by a grant from the National Health and Medical Research Council of Australia (NHMRC). The authors declared no conflicts of interest.

SOURCE: Pandeya N et al. Br J Dermatol. 2019 Mar 28. doi: 10.1111/bjd.17938.

Almost 10% of patients hospitalized with a dermatologic diagnosis are readmitted within 30 days, based on a national sample of 3.6 million skin-related hospitalizations.

Data from the Nationwide Readmissions Database also showed that the same-cause readmission rate was 3.3% after 30 days and 7.8% within the calendar year (CY) over the 5-year study period of 2010-2014, Myron Zhang, MD, of the department of dermatology at Weill Cornell Medicine, New York, and his associates reported in the Journal of the American Academy of Dermatology.

The total cost of the CY readmissions was $2.54 billion, which works out to $508 million per year or $8,995 per visit. The most common dermatologic diagnosis – cellulitis made up 83.6% of all hospitalizations – was also the most expensive in terms of readmissions, resulting in $1.9 billion in CY costs, Dr. Zhang and associates wrote.

Overall readmission rates for cellulitis were not provided, but annual rates ranged from 9.1% to 9.3% (30-day all cause), from 7.7% to 8.1% (CY same cause), and from 3.1% to 3.3% (30-day same cause), they wrote.

The dermatologic diagnosis with the highest 30-day same-cause readmission rate was vascular hamartomas at 21.1%, followed by dermatomyositis (18.3%) and thrombotic microangiopathy (13.7%). Dermatomyositis had the highest CY same-cause readmission rate (30.8%) and mycosis fungoides had the highest 30-day all-cause rate (32.3%), according to the investigators.

“Diseases, characteristics, and comorbidities associated with high readmission rates should trigger hospitals to consider dermatology consultation, coordinate outpatient follow-up, and support underinsured outpatient access. These measures have been shown to reduce readmissions or hospital visits in general dermatologic settings, but outcomes in individual diseases are not well studied,” Dr. Zhang and associates wrote. They noted that there have been “very few prior studies of readmissions for skin diseases.”

rfranki@mdedge.com

SOURCE: Zhang M et al. J Am Acad. Dermatol. 2019. doi: 10.1016/j.jaad.2019.05.023. .

Almost 10% of patients hospitalized with a dermatologic diagnosis are readmitted within 30 days, based on a national sample of 3.6 million skin-related hospitalizations.

Data from the Nationwide Readmissions Database also showed that the same-cause readmission rate was 3.3% after 30 days and 7.8% within the calendar year (CY) over the 5-year study period of 2010-2014, Myron Zhang, MD, of the department of dermatology at Weill Cornell Medicine, New York, and his associates reported in the Journal of the American Academy of Dermatology.

The total cost of the CY readmissions was $2.54 billion, which works out to $508 million per year or $8,995 per visit. The most common dermatologic diagnosis – cellulitis made up 83.6% of all hospitalizations – was also the most expensive in terms of readmissions, resulting in $1.9 billion in CY costs, Dr. Zhang and associates wrote.

Overall readmission rates for cellulitis were not provided, but annual rates ranged from 9.1% to 9.3% (30-day all cause), from 7.7% to 8.1% (CY same cause), and from 3.1% to 3.3% (30-day same cause), they wrote.

The dermatologic diagnosis with the highest 30-day same-cause readmission rate was vascular hamartomas at 21.1%, followed by dermatomyositis (18.3%) and thrombotic microangiopathy (13.7%). Dermatomyositis had the highest CY same-cause readmission rate (30.8%) and mycosis fungoides had the highest 30-day all-cause rate (32.3%), according to the investigators.

“Diseases, characteristics, and comorbidities associated with high readmission rates should trigger hospitals to consider dermatology consultation, coordinate outpatient follow-up, and support underinsured outpatient access. These measures have been shown to reduce readmissions or hospital visits in general dermatologic settings, but outcomes in individual diseases are not well studied,” Dr. Zhang and associates wrote. They noted that there have been “very few prior studies of readmissions for skin diseases.”

rfranki@mdedge.com

SOURCE: Zhang M et al. J Am Acad. Dermatol. 2019. doi: 10.1016/j.jaad.2019.05.023. .

Almost 10% of patients hospitalized with a dermatologic diagnosis are readmitted within 30 days, based on a national sample of 3.6 million skin-related hospitalizations.

Data from the Nationwide Readmissions Database also showed that the same-cause readmission rate was 3.3% after 30 days and 7.8% within the calendar year (CY) over the 5-year study period of 2010-2014, Myron Zhang, MD, of the department of dermatology at Weill Cornell Medicine, New York, and his associates reported in the Journal of the American Academy of Dermatology.

The total cost of the CY readmissions was $2.54 billion, which works out to $508 million per year or $8,995 per visit. The most common dermatologic diagnosis – cellulitis made up 83.6% of all hospitalizations – was also the most expensive in terms of readmissions, resulting in $1.9 billion in CY costs, Dr. Zhang and associates wrote.

Overall readmission rates for cellulitis were not provided, but annual rates ranged from 9.1% to 9.3% (30-day all cause), from 7.7% to 8.1% (CY same cause), and from 3.1% to 3.3% (30-day same cause), they wrote.

The dermatologic diagnosis with the highest 30-day same-cause readmission rate was vascular hamartomas at 21.1%, followed by dermatomyositis (18.3%) and thrombotic microangiopathy (13.7%). Dermatomyositis had the highest CY same-cause readmission rate (30.8%) and mycosis fungoides had the highest 30-day all-cause rate (32.3%), according to the investigators.

“Diseases, characteristics, and comorbidities associated with high readmission rates should trigger hospitals to consider dermatology consultation, coordinate outpatient follow-up, and support underinsured outpatient access. These measures have been shown to reduce readmissions or hospital visits in general dermatologic settings, but outcomes in individual diseases are not well studied,” Dr. Zhang and associates wrote. They noted that there have been “very few prior studies of readmissions for skin diseases.”

rfranki@mdedge.com

SOURCE: Zhang M et al. J Am Acad. Dermatol. 2019. doi: 10.1016/j.jaad.2019.05.023. .

A 52-year-old man self-refers to dermatology for evaluation of an irritated lesion on the posterolateral aspect of his neck. It’s been there for years, waxing and waning but always being irritated by his shirt collar or seat belt.

He has shown the lesion to his primary care provider on several occasions. Various topical preparations, including steroid and antifungal creams, have been prescribed—to no avail.

The patient owns a landscaping business. He has worked outdoors since he was in his teens and acknowledges that in his younger years, he was not careful about sun protection. For the past 20 years or so, however, he has worn a wide-brimmed hat and long-sleeved shirt while working.

His health is good in all other respects.

EXAMINATION
The lesion is a pink, scaly, 2-cm ovoid patch on the left side of the patient’s neck. Several areas of scabbing are seen within the bounds of the lesion, the margins of which are very well defined.

There is much evidence of sun damage on his neck and arms, with prominent pilosebaceous units and rhomboidal lining of the neck skin. Elsewhere, on sun-exposed skin, there are numerous actinic keratoses, telangiectasias, and poikilodermatous changes.

The lesion is biopsied by shave technique and the sample submitted to pathology.

What’s the diagnosis?

DISCUSSION
The biopsy results confirmed the impression of superficial squamous cell carcinoma (SSC) with focal areas of invasion.

One thinks of skin cancer as being “a thing,” a papule or nodule, and that’s usually true. But there are several types of skin cancer that manifest as a fixed rash—meaning it stays in the same place year after year, unlike other rashes (eg, psoriasis, eczema, or fungal infection). Common examples, besides superficial SCC (also known as Bowen disease), include superficial basal cell carcinoma (BCC), Paget disease (mammary and extramammary), cutaneous T-cell lymphoma, and even local recurrence of breast cancer.

This patient’s occupation and history of (abundantly evident) sun damage put him at risk for a sun-caused skin cancer. As so often happens, the problem was initially misdiagnosed by a provider who was only looking at the lesion instead of factoring in the context in which it appeared. Who has the lesion is almost as important as the lesion itself.

Without a biopsy, Bowen disease is often indistinguishable from superficial BCC; the latter can take on a variety of appearances, from scar-like (cicatricial) to pigmented (especially in patients with darker skin) to the most common, nodular/noduloulcerative. Another item in the differential is discoid lupus erythematosus, particularly when the lesion manifests in a highly sun-exposed area.

Treatment of this patient’s lesion entailed full excision with 3-mm margins. This option was chosen based on the focal areas of invasion and theoretical potential for metastasis.

TAKE-HOME LEARNING POINTS

• Intraepidermal squamous cell carcinoma (Bowen disease) presents as a red, scaly rash with a rounded, well-demarcated border, almost always on skin directly overexposed to the sun.
• These cancers grow slowly, are fixed in location, never heal, and—given enough time—often become focally invasive.
• They will often be misdiagnosed as fungal infection, psoriasis, or eczema, because of the misperception that skin cancers are always papular or nodular.
• A history of sun exposure and resulting markers of dermatoheliosis serve to corroborate the putative diagnosis.

A 52-year-old man self-refers to dermatology for evaluation of an irritated lesion on the posterolateral aspect of his neck. It’s been there for years, waxing and waning but always being irritated by his shirt collar or seat belt.

He has shown the lesion to his primary care provider on several occasions. Various topical preparations, including steroid and antifungal creams, have been prescribed—to no avail.

The patient owns a landscaping business. He has worked outdoors since he was in his teens and acknowledges that in his younger years, he was not careful about sun protection. For the past 20 years or so, however, he has worn a wide-brimmed hat and long-sleeved shirt while working.

His health is good in all other respects.

EXAMINATION
The lesion is a pink, scaly, 2-cm ovoid patch on the left side of the patient’s neck. Several areas of scabbing are seen within the bounds of the lesion, the margins of which are very well defined.

There is much evidence of sun damage on his neck and arms, with prominent pilosebaceous units and rhomboidal lining of the neck skin. Elsewhere, on sun-exposed skin, there are numerous actinic keratoses, telangiectasias, and poikilodermatous changes.

The lesion is biopsied by shave technique and the sample submitted to pathology.

What’s the diagnosis?

DISCUSSION
The biopsy results confirmed the impression of superficial squamous cell carcinoma (SSC) with focal areas of invasion.

One thinks of skin cancer as being “a thing,” a papule or nodule, and that’s usually true. But there are several types of skin cancer that manifest as a fixed rash—meaning it stays in the same place year after year, unlike other rashes (eg, psoriasis, eczema, or fungal infection). Common examples, besides superficial SCC (also known as Bowen disease), include superficial basal cell carcinoma (BCC), Paget disease (mammary and extramammary), cutaneous T-cell lymphoma, and even local recurrence of breast cancer.

This patient’s occupation and history of (abundantly evident) sun damage put him at risk for a sun-caused skin cancer. As so often happens, the problem was initially misdiagnosed by a provider who was only looking at the lesion instead of factoring in the context in which it appeared. Who has the lesion is almost as important as the lesion itself.

Without a biopsy, Bowen disease is often indistinguishable from superficial BCC; the latter can take on a variety of appearances, from scar-like (cicatricial) to pigmented (especially in patients with darker skin) to the most common, nodular/noduloulcerative. Another item in the differential is discoid lupus erythematosus, particularly when the lesion manifests in a highly sun-exposed area.

Treatment of this patient’s lesion entailed full excision with 3-mm margins. This option was chosen based on the focal areas of invasion and theoretical potential for metastasis.

TAKE-HOME LEARNING POINTS

• Intraepidermal squamous cell carcinoma (Bowen disease) presents as a red, scaly rash with a rounded, well-demarcated border, almost always on skin directly overexposed to the sun.
• These cancers grow slowly, are fixed in location, never heal, and—given enough time—often become focally invasive.
• They will often be misdiagnosed as fungal infection, psoriasis, or eczema, because of the misperception that skin cancers are always papular or nodular.
• A history of sun exposure and resulting markers of dermatoheliosis serve to corroborate the putative diagnosis.

A 52-year-old man self-refers to dermatology for evaluation of an irritated lesion on the posterolateral aspect of his neck. It’s been there for years, waxing and waning but always being irritated by his shirt collar or seat belt.

He has shown the lesion to his primary care provider on several occasions. Various topical preparations, including steroid and antifungal creams, have been prescribed—to no avail.

The patient owns a landscaping business. He has worked outdoors since he was in his teens and acknowledges that in his younger years, he was not careful about sun protection. For the past 20 years or so, however, he has worn a wide-brimmed hat and long-sleeved shirt while working.

His health is good in all other respects.

EXAMINATION
The lesion is a pink, scaly, 2-cm ovoid patch on the left side of the patient’s neck. Several areas of scabbing are seen within the bounds of the lesion, the margins of which are very well defined.

There is much evidence of sun damage on his neck and arms, with prominent pilosebaceous units and rhomboidal lining of the neck skin. Elsewhere, on sun-exposed skin, there are numerous actinic keratoses, telangiectasias, and poikilodermatous changes.

The lesion is biopsied by shave technique and the sample submitted to pathology.

What’s the diagnosis?

DISCUSSION
The biopsy results confirmed the impression of superficial squamous cell carcinoma (SSC) with focal areas of invasion.

One thinks of skin cancer as being “a thing,” a papule or nodule, and that’s usually true. But there are several types of skin cancer that manifest as a fixed rash—meaning it stays in the same place year after year, unlike other rashes (eg, psoriasis, eczema, or fungal infection). Common examples, besides superficial SCC (also known as Bowen disease), include superficial basal cell carcinoma (BCC), Paget disease (mammary and extramammary), cutaneous T-cell lymphoma, and even local recurrence of breast cancer.

This patient’s occupation and history of (abundantly evident) sun damage put him at risk for a sun-caused skin cancer. As so often happens, the problem was initially misdiagnosed by a provider who was only looking at the lesion instead of factoring in the context in which it appeared. Who has the lesion is almost as important as the lesion itself.

Without a biopsy, Bowen disease is often indistinguishable from superficial BCC; the latter can take on a variety of appearances, from scar-like (cicatricial) to pigmented (especially in patients with darker skin) to the most common, nodular/noduloulcerative. Another item in the differential is discoid lupus erythematosus, particularly when the lesion manifests in a highly sun-exposed area.

Treatment of this patient’s lesion entailed full excision with 3-mm margins. This option was chosen based on the focal areas of invasion and theoretical potential for metastasis.

TAKE-HOME LEARNING POINTS

• Intraepidermal squamous cell carcinoma (Bowen disease) presents as a red, scaly rash with a rounded, well-demarcated border, almost always on skin directly overexposed to the sun.
• These cancers grow slowly, are fixed in location, never heal, and—given enough time—often become focally invasive.
• They will often be misdiagnosed as fungal infection, psoriasis, or eczema, because of the misperception that skin cancers are always papular or nodular.
• A history of sun exposure and resulting markers of dermatoheliosis serve to corroborate the putative diagnosis.

The FP thought this looked like granuloma annulare (GA) but had never seen so many lesions on a patient. Some lesions were not round (more oval or elongated), while others were not completely enclosed geometric shapes (with breaks in the multiple ring patterns). However, all of the lesions were slightly raised with erythema and no scale. (The FP also considered tinea corporis, but ruled it out because there was no scale.)

He consulted some Internet resources and was convinced that this was disseminated GA. The greatest risk factor for this somewhat mysterious disease of unknown origin is female gender. It is also often associated with diabetes, but diabetes is not the cause.

Although intralesional steroids work when treating disseminated GA, this approach is not realistic for widespread disease. A number of options have been studied and reported in small series or case reports. The FP presented various options to the patient, and together they decided to try pentoxifylline 400 mg 3 times daily for systemic treatment. Pentoxifylline is approved for claudication and has few adverse effects or risks. While this treatment is off-label for GA, there are no FDA approved treatments.

During a follow-up visit 1 month later, the number of lesions had been reduced by half. The FP continued treating the patient with pentoxifylline with the hope of achieving full resolution.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mauskar M, Usatine R. Granuloma annulare. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1141-1146.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com

The FP thought this looked like granuloma annulare (GA) but had never seen so many lesions on a patient. Some lesions were not round (more oval or elongated), while others were not completely enclosed geometric shapes (with breaks in the multiple ring patterns). However, all of the lesions were slightly raised with erythema and no scale. (The FP also considered tinea corporis, but ruled it out because there was no scale.)

He consulted some Internet resources and was convinced that this was disseminated GA. The greatest risk factor for this somewhat mysterious disease of unknown origin is female gender. It is also often associated with diabetes, but diabetes is not the cause.

Although intralesional steroids work when treating disseminated GA, this approach is not realistic for widespread disease. A number of options have been studied and reported in small series or case reports. The FP presented various options to the patient, and together they decided to try pentoxifylline 400 mg 3 times daily for systemic treatment. Pentoxifylline is approved for claudication and has few adverse effects or risks. While this treatment is off-label for GA, there are no FDA approved treatments.

During a follow-up visit 1 month later, the number of lesions had been reduced by half. The FP continued treating the patient with pentoxifylline with the hope of achieving full resolution.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mauskar M, Usatine R. Granuloma annulare. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1141-1146.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com

The FP thought this looked like granuloma annulare (GA) but had never seen so many lesions on a patient. Some lesions were not round (more oval or elongated), while others were not completely enclosed geometric shapes (with breaks in the multiple ring patterns). However, all of the lesions were slightly raised with erythema and no scale. (The FP also considered tinea corporis, but ruled it out because there was no scale.)

He consulted some Internet resources and was convinced that this was disseminated GA. The greatest risk factor for this somewhat mysterious disease of unknown origin is female gender. It is also often associated with diabetes, but diabetes is not the cause.

Although intralesional steroids work when treating disseminated GA, this approach is not realistic for widespread disease. A number of options have been studied and reported in small series or case reports. The FP presented various options to the patient, and together they decided to try pentoxifylline 400 mg 3 times daily for systemic treatment. Pentoxifylline is approved for claudication and has few adverse effects or risks. While this treatment is off-label for GA, there are no FDA approved treatments.

During a follow-up visit 1 month later, the number of lesions had been reduced by half. The FP continued treating the patient with pentoxifylline with the hope of achieving full resolution.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mauskar M, Usatine R. Granuloma annulare. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1141-1146.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com

Gender-affirming hormone use was significantly associated with reports of androgenetic alopecia in transgender men, based on data from a survey of 991 individuals.

Given the importance of hair in body image and gender identity, hair concerns are important to the quality of life of gender-minority individuals, wrote Dustin Marks, of Massachusetts General Hospital, Boston, and colleagues.

To explore the impact of hormone use on hair loss in gender-minority patients, the researchers conducted a web-based survey of transgender individuals aged 18 years and older, who self-identified as gender minority. Participants were invited based on profiles on Facebook, YouTube, and Instagram. The findings were published in a research letter in the British Journal of Dermatology.

The 991 survey respondents included 59% transmen, 31% transwomen, and 9% gender nonbinary or gender queer. The average age of the participants was 33 years; 79% were white, 89% had medical insurance, and 91% reported using gender-affirming hormones.

Overall, 65% of transwomen, 43% of transmen, and 35% of nonbinary individuals reported scalp hair loss or thinning. Scalp hair loss was significantly more common among transmen on masculinizing hormones compared to transmen not on hormones (45% vs. 17%). Scalp hair loss was not significantly different between transwomen on feminizing hormones and those not on hormones.

The transwomen who reported scalp hair loss and were on hormones reported significantly less severe Sinclair grades, compared with transwomen with scalp hair loss and were not on hormones. By contrast, transmen and nonbinary individuals on testosterone reported significantly more hair loss (using Hamilton-Norwood and Sinclair scores) between a baseline before hormone use and their present state of hormone use.

The findings support the impact of testosterone use on androgenic alopecia (AGA) in gender-minority patients similar to the established role of testosterone in male pattern hair loss overall, the researchers wrote.

“Some transmen, moreover, may view AGA as a wanted masculine trait, while others seek dermatologic evaluation and treatment for their hair loss,” they noted. By contrast, some transwomen may find AGA especially distressing. In this study, AGA scores were stable for transwomen, which suggests that feminizing hormones may be enough to stabilize hair loss in these patients.

The study was limited by several factors including use of a convenience sample study population without cisgender controls, lack of data on the duration of hormone use, and specific focus on AGE, the researchers noted.

“Mindful of these limitations, clinicians should appreciate the impact of gender-affirming hormones on androgenetic alopecia severity and continue to address the hair concerns of each patient individually,” they wrote.

The researchers had no financial conflicts to disclose, and no sources of study funding were reported.

SOURCE: Marks D et al. Br J Dermatol. 2019 May 3. doi: 10.1111/bjd.18099.

Gender-affirming hormone use was significantly associated with reports of androgenetic alopecia in transgender men, based on data from a survey of 991 individuals.

Given the importance of hair in body image and gender identity, hair concerns are important to the quality of life of gender-minority individuals, wrote Dustin Marks, of Massachusetts General Hospital, Boston, and colleagues.

To explore the impact of hormone use on hair loss in gender-minority patients, the researchers conducted a web-based survey of transgender individuals aged 18 years and older, who self-identified as gender minority. Participants were invited based on profiles on Facebook, YouTube, and Instagram. The findings were published in a research letter in the British Journal of Dermatology.

The 991 survey respondents included 59% transmen, 31% transwomen, and 9% gender nonbinary or gender queer. The average age of the participants was 33 years; 79% were white, 89% had medical insurance, and 91% reported using gender-affirming hormones.

Overall, 65% of transwomen, 43% of transmen, and 35% of nonbinary individuals reported scalp hair loss or thinning. Scalp hair loss was significantly more common among transmen on masculinizing hormones compared to transmen not on hormones (45% vs. 17%). Scalp hair loss was not significantly different between transwomen on feminizing hormones and those not on hormones.

The transwomen who reported scalp hair loss and were on hormones reported significantly less severe Sinclair grades, compared with transwomen with scalp hair loss and were not on hormones. By contrast, transmen and nonbinary individuals on testosterone reported significantly more hair loss (using Hamilton-Norwood and Sinclair scores) between a baseline before hormone use and their present state of hormone use.

The findings support the impact of testosterone use on androgenic alopecia (AGA) in gender-minority patients similar to the established role of testosterone in male pattern hair loss overall, the researchers wrote.

“Some transmen, moreover, may view AGA as a wanted masculine trait, while others seek dermatologic evaluation and treatment for their hair loss,” they noted. By contrast, some transwomen may find AGA especially distressing. In this study, AGA scores were stable for transwomen, which suggests that feminizing hormones may be enough to stabilize hair loss in these patients.

The study was limited by several factors including use of a convenience sample study population without cisgender controls, lack of data on the duration of hormone use, and specific focus on AGE, the researchers noted.

“Mindful of these limitations, clinicians should appreciate the impact of gender-affirming hormones on androgenetic alopecia severity and continue to address the hair concerns of each patient individually,” they wrote.

The researchers had no financial conflicts to disclose, and no sources of study funding were reported.

SOURCE: Marks D et al. Br J Dermatol. 2019 May 3. doi: 10.1111/bjd.18099.

Gender-affirming hormone use was significantly associated with reports of androgenetic alopecia in transgender men, based on data from a survey of 991 individuals.

Given the importance of hair in body image and gender identity, hair concerns are important to the quality of life of gender-minority individuals, wrote Dustin Marks, of Massachusetts General Hospital, Boston, and colleagues.

To explore the impact of hormone use on hair loss in gender-minority patients, the researchers conducted a web-based survey of transgender individuals aged 18 years and older, who self-identified as gender minority. Participants were invited based on profiles on Facebook, YouTube, and Instagram. The findings were published in a research letter in the British Journal of Dermatology.

The 991 survey respondents included 59% transmen, 31% transwomen, and 9% gender nonbinary or gender queer. The average age of the participants was 33 years; 79% were white, 89% had medical insurance, and 91% reported using gender-affirming hormones.

Overall, 65% of transwomen, 43% of transmen, and 35% of nonbinary individuals reported scalp hair loss or thinning. Scalp hair loss was significantly more common among transmen on masculinizing hormones compared to transmen not on hormones (45% vs. 17%). Scalp hair loss was not significantly different between transwomen on feminizing hormones and those not on hormones.

The transwomen who reported scalp hair loss and were on hormones reported significantly less severe Sinclair grades, compared with transwomen with scalp hair loss and were not on hormones. By contrast, transmen and nonbinary individuals on testosterone reported significantly more hair loss (using Hamilton-Norwood and Sinclair scores) between a baseline before hormone use and their present state of hormone use.

The findings support the impact of testosterone use on androgenic alopecia (AGA) in gender-minority patients similar to the established role of testosterone in male pattern hair loss overall, the researchers wrote.

“Some transmen, moreover, may view AGA as a wanted masculine trait, while others seek dermatologic evaluation and treatment for their hair loss,” they noted. By contrast, some transwomen may find AGA especially distressing. In this study, AGA scores were stable for transwomen, which suggests that feminizing hormones may be enough to stabilize hair loss in these patients.

The study was limited by several factors including use of a convenience sample study population without cisgender controls, lack of data on the duration of hormone use, and specific focus on AGE, the researchers noted.

“Mindful of these limitations, clinicians should appreciate the impact of gender-affirming hormones on androgenetic alopecia severity and continue to address the hair concerns of each patient individually,” they wrote.

The researchers had no financial conflicts to disclose, and no sources of study funding were reported.

SOURCE: Marks D et al. Br J Dermatol. 2019 May 3. doi: 10.1111/bjd.18099.

Lichen striatus (LS) is a common benign skin condition that presents in children between the ages of 5 and 15 years.¹ The rash is typically unilateral and most frequently on the extremities, although it may appear on the face, trunk, or buttocks. The lesions start as pink or skin-colored asymptomatic papules in a linear orientation following the lines of Blaschko. Lesions usually evolve over several weeks, and typically resolve in 6-12 months. There may be residual postinflammatory hypo- or hyperpigmentation which often improves within a few years.

Of note, there are subsets of lichen striatus: Hypopigmented lichen striatus with minimal papules has been termed “lichen striatus albus.” Nail lichen striatus may present as onycholysis or fissuring of nails, present as an isolated finding, or more commonly in association with concurrent affected skin. Nail lichen striatus typically resolves on its own, however there are case reports of improvement with intralesional steroids.²

There is no established etiology for LS. Autoimmune disease, viruses, immunizations, medications, and hypersensitivity reactions have been associated with triggering LS in various case reports, although strength of the associations is low. Children have been reported to have LS following scarlet fever and Candida vulvitis.³ Diagnosis usually is clinical, although biopsy may be helpful for histopathologic confirmation. No work-up for associated infections or conditions is warranted.

The differential for linear papular lesions includes inflammatory linear verrucous epidermal nevus (ILVEN), blaschkitis, or linear morphea. ILVEN is a hamartoma that usually is congenital or presents in early childhood; presents with linear or whorled, hyperkeratotic papules and plaque in similar linear “line of Blaschko” patterns; and represents cutaneous mosaicism. It is often difficult to differentiate between lichen striatus and ILVEN, however lichen striatus is not congenital, and is a self-limited condition. Under dermoscopy (polarized light systems) findings of LS more frequently demonstrate gray granular pigmentation. ILVEN is more frequently associated with cerebriform pattern.⁴ Blaschkitis is a term for a blaschkoid inflammation of the skin that presents with more eczematous findings and histology of spongiosis, unlike the lichenoid findings of LS. It is typically accompanied by noticeable pruritus and broader bands of involved area, and has older age of onset than LS. Linear morphea is a deeper inflammatory process of the dermis or subcutaneous fat, presenting with sclerotic skin, and typically has associated atrophy.

Treatment need not be pursued for lichen striatus because it is a benign condition. The lesions typically self-resolve without any residual scarring. If patients have associated pruritus then low- to midpotency topical steroids can be used for symptomatic relief.
 

Dr. Kaushik is with the division of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego, and Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Dr. Kaushik or Dr. Eichenfield. Email them at pdnews@mdedge.com.

References

1. Gupta D, Mathes E. Lichen Striatus. (Levy ML ed.) 2019: UpToDate.

2. Dermatol Ther. 2018 Nov;31(6):e12713.

3. Int J Dermatol. 2018 Sep;57(9):1118-9.

4. J Dermatol. 2017 Dec;44(12):e355-6.

Lichen striatus (LS) is a common benign skin condition that presents in children between the ages of 5 and 15 years.¹ The rash is typically unilateral and most frequently on the extremities, although it may appear on the face, trunk, or buttocks. The lesions start as pink or skin-colored asymptomatic papules in a linear orientation following the lines of Blaschko. Lesions usually evolve over several weeks, and typically resolve in 6-12 months. There may be residual postinflammatory hypo- or hyperpigmentation which often improves within a few years.

Of note, there are subsets of lichen striatus: Hypopigmented lichen striatus with minimal papules has been termed “lichen striatus albus.” Nail lichen striatus may present as onycholysis or fissuring of nails, present as an isolated finding, or more commonly in association with concurrent affected skin. Nail lichen striatus typically resolves on its own, however there are case reports of improvement with intralesional steroids.²

There is no established etiology for LS. Autoimmune disease, viruses, immunizations, medications, and hypersensitivity reactions have been associated with triggering LS in various case reports, although strength of the associations is low. Children have been reported to have LS following scarlet fever and Candida vulvitis.³ Diagnosis usually is clinical, although biopsy may be helpful for histopathologic confirmation. No work-up for associated infections or conditions is warranted.

The differential for linear papular lesions includes inflammatory linear verrucous epidermal nevus (ILVEN), blaschkitis, or linear morphea. ILVEN is a hamartoma that usually is congenital or presents in early childhood; presents with linear or whorled, hyperkeratotic papules and plaque in similar linear “line of Blaschko” patterns; and represents cutaneous mosaicism. It is often difficult to differentiate between lichen striatus and ILVEN, however lichen striatus is not congenital, and is a self-limited condition. Under dermoscopy (polarized light systems) findings of LS more frequently demonstrate gray granular pigmentation. ILVEN is more frequently associated with cerebriform pattern.⁴ Blaschkitis is a term for a blaschkoid inflammation of the skin that presents with more eczematous findings and histology of spongiosis, unlike the lichenoid findings of LS. It is typically accompanied by noticeable pruritus and broader bands of involved area, and has older age of onset than LS. Linear morphea is a deeper inflammatory process of the dermis or subcutaneous fat, presenting with sclerotic skin, and typically has associated atrophy.

Treatment need not be pursued for lichen striatus because it is a benign condition. The lesions typically self-resolve without any residual scarring. If patients have associated pruritus then low- to midpotency topical steroids can be used for symptomatic relief.
 

Dr. Kaushik is with the division of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego, and Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Dr. Kaushik or Dr. Eichenfield. Email them at pdnews@mdedge.com.

References

1. Gupta D, Mathes E. Lichen Striatus. (Levy ML ed.) 2019: UpToDate.

2. Dermatol Ther. 2018 Nov;31(6):e12713.

3. Int J Dermatol. 2018 Sep;57(9):1118-9.

4. J Dermatol. 2017 Dec;44(12):e355-6.

Lichen striatus (LS) is a common benign skin condition that presents in children between the ages of 5 and 15 years.¹ The rash is typically unilateral and most frequently on the extremities, although it may appear on the face, trunk, or buttocks. The lesions start as pink or skin-colored asymptomatic papules in a linear orientation following the lines of Blaschko. Lesions usually evolve over several weeks, and typically resolve in 6-12 months. There may be residual postinflammatory hypo- or hyperpigmentation which often improves within a few years.

Of note, there are subsets of lichen striatus: Hypopigmented lichen striatus with minimal papules has been termed “lichen striatus albus.” Nail lichen striatus may present as onycholysis or fissuring of nails, present as an isolated finding, or more commonly in association with concurrent affected skin. Nail lichen striatus typically resolves on its own, however there are case reports of improvement with intralesional steroids.²

There is no established etiology for LS. Autoimmune disease, viruses, immunizations, medications, and hypersensitivity reactions have been associated with triggering LS in various case reports, although strength of the associations is low. Children have been reported to have LS following scarlet fever and Candida vulvitis.³ Diagnosis usually is clinical, although biopsy may be helpful for histopathologic confirmation. No work-up for associated infections or conditions is warranted.

The differential for linear papular lesions includes inflammatory linear verrucous epidermal nevus (ILVEN), blaschkitis, or linear morphea. ILVEN is a hamartoma that usually is congenital or presents in early childhood; presents with linear or whorled, hyperkeratotic papules and plaque in similar linear “line of Blaschko” patterns; and represents cutaneous mosaicism. It is often difficult to differentiate between lichen striatus and ILVEN, however lichen striatus is not congenital, and is a self-limited condition. Under dermoscopy (polarized light systems) findings of LS more frequently demonstrate gray granular pigmentation. ILVEN is more frequently associated with cerebriform pattern.⁴ Blaschkitis is a term for a blaschkoid inflammation of the skin that presents with more eczematous findings and histology of spongiosis, unlike the lichenoid findings of LS. It is typically accompanied by noticeable pruritus and broader bands of involved area, and has older age of onset than LS. Linear morphea is a deeper inflammatory process of the dermis or subcutaneous fat, presenting with sclerotic skin, and typically has associated atrophy.

Treatment need not be pursued for lichen striatus because it is a benign condition. The lesions typically self-resolve without any residual scarring. If patients have associated pruritus then low- to midpotency topical steroids can be used for symptomatic relief.
 

Dr. Kaushik is with the division of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego, and Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Dr. Kaushik or Dr. Eichenfield. Email them at pdnews@mdedge.com.

References

1. Gupta D, Mathes E. Lichen Striatus. (Levy ML ed.) 2019: UpToDate.

2. Dermatol Ther. 2018 Nov;31(6):e12713.

3. Int J Dermatol. 2018 Sep;57(9):1118-9.

4. J Dermatol. 2017 Dec;44(12):e355-6.

CHICAGO – Atopic dermatitis in adulthood was associated with a twofold increase in the risk of developing dementia late in life, based on results from a large longitudinal cohort study presented at the annual meeting of the Society for Investigative Dermatology.

Ted Bosworth/MDedge News

“After adjusting for potential mediators such as smoking status, depression, cardiovascular disease, and asthma or rhinitis, the effect was decreased slightly but still remained strongly statistically significant,” reported Katrina Abuabara, MD, of the University of California, San Francisco.

Atopic dermatitis is the latest in growing list of chronic inflammatory conditions that have been associated with an increased risk of dementia, according to Dr. Abuabara, who cited a body of evidence suggesting that inflammation triggers or exacerbates the processes that drive risk of developing dementia late in life.

Interest in the potential association of atopic dermatitis and dementia has been triggered “by a paradigm shift in which we now think of atopic dermatitis as a systemic inflammatory condition.” Dr. Abuabara reported.

In a primary care database of more than 1 million patients, both atopic dermatitis and dementia were common in those aged 60 years or older. The two disorders were identified in 6.75% and 6.49% of patients, respectively.

Cox proportional hazard ratios were employed to determine the relationship between the presence of atopic dermatitis and subsequent development of dementia. The median follow-up was 8 years. Atopic dermatitis was classified as mild, moderate, or severe involvement based on treatment records.

Patients with dementia associated with infectious diseases such as HIV, alcoholism, and other exogenous toxins were excluded from the analysis.

For those with atopic dermatitis relative to those without, the unadjusted hazard ratios were 1.91 for dementia of any type, 2.14 for Alzheimer’s dementia, and 2.25 for vascular-related dementia. After adjustment for confounders such as age, sex, and socioeconomic status, these hazard ratios, respectively, were only somewhat lower and remained statistically significant.

There was a trend for greater dementia risk with greater atopic dermatitis severity, rising from 2.07 in those with mild atopic dermatitis to 2.72 to those with severe disease, according to Dr. Abuabara.

“The important next step is to determine if better control of atopic dermatitis results in a lower risk of dementia,” she said.

According to Dr. Abuabara, some experimental studies have supported the hypothesis that downregulation of systemic markers of inflammation may be protective.

“Even if you reduced risk by a small amount, it would translate into a large health impact because of the large and growing prevalence of dementia,” she said.

Dr. Abuabara is a consultant for the TARGET-DERM study, sponsored by Target PharmaSolutions.

CHICAGO – Atopic dermatitis in adulthood was associated with a twofold increase in the risk of developing dementia late in life, based on results from a large longitudinal cohort study presented at the annual meeting of the Society for Investigative Dermatology.

Ted Bosworth/MDedge News

“After adjusting for potential mediators such as smoking status, depression, cardiovascular disease, and asthma or rhinitis, the effect was decreased slightly but still remained strongly statistically significant,” reported Katrina Abuabara, MD, of the University of California, San Francisco.

Atopic dermatitis is the latest in growing list of chronic inflammatory conditions that have been associated with an increased risk of dementia, according to Dr. Abuabara, who cited a body of evidence suggesting that inflammation triggers or exacerbates the processes that drive risk of developing dementia late in life.

Interest in the potential association of atopic dermatitis and dementia has been triggered “by a paradigm shift in which we now think of atopic dermatitis as a systemic inflammatory condition.” Dr. Abuabara reported.

In a primary care database of more than 1 million patients, both atopic dermatitis and dementia were common in those aged 60 years or older. The two disorders were identified in 6.75% and 6.49% of patients, respectively.

Cox proportional hazard ratios were employed to determine the relationship between the presence of atopic dermatitis and subsequent development of dementia. The median follow-up was 8 years. Atopic dermatitis was classified as mild, moderate, or severe involvement based on treatment records.

Patients with dementia associated with infectious diseases such as HIV, alcoholism, and other exogenous toxins were excluded from the analysis.

For those with atopic dermatitis relative to those without, the unadjusted hazard ratios were 1.91 for dementia of any type, 2.14 for Alzheimer’s dementia, and 2.25 for vascular-related dementia. After adjustment for confounders such as age, sex, and socioeconomic status, these hazard ratios, respectively, were only somewhat lower and remained statistically significant.

There was a trend for greater dementia risk with greater atopic dermatitis severity, rising from 2.07 in those with mild atopic dermatitis to 2.72 to those with severe disease, according to Dr. Abuabara.

“The important next step is to determine if better control of atopic dermatitis results in a lower risk of dementia,” she said.

According to Dr. Abuabara, some experimental studies have supported the hypothesis that downregulation of systemic markers of inflammation may be protective.

“Even if you reduced risk by a small amount, it would translate into a large health impact because of the large and growing prevalence of dementia,” she said.

Dr. Abuabara is a consultant for the TARGET-DERM study, sponsored by Target PharmaSolutions.

CHICAGO – Atopic dermatitis in adulthood was associated with a twofold increase in the risk of developing dementia late in life, based on results from a large longitudinal cohort study presented at the annual meeting of the Society for Investigative Dermatology.

Ted Bosworth/MDedge News

“After adjusting for potential mediators such as smoking status, depression, cardiovascular disease, and asthma or rhinitis, the effect was decreased slightly but still remained strongly statistically significant,” reported Katrina Abuabara, MD, of the University of California, San Francisco.

Atopic dermatitis is the latest in growing list of chronic inflammatory conditions that have been associated with an increased risk of dementia, according to Dr. Abuabara, who cited a body of evidence suggesting that inflammation triggers or exacerbates the processes that drive risk of developing dementia late in life.

Interest in the potential association of atopic dermatitis and dementia has been triggered “by a paradigm shift in which we now think of atopic dermatitis as a systemic inflammatory condition.” Dr. Abuabara reported.

In a primary care database of more than 1 million patients, both atopic dermatitis and dementia were common in those aged 60 years or older. The two disorders were identified in 6.75% and 6.49% of patients, respectively.

Cox proportional hazard ratios were employed to determine the relationship between the presence of atopic dermatitis and subsequent development of dementia. The median follow-up was 8 years. Atopic dermatitis was classified as mild, moderate, or severe involvement based on treatment records.

Patients with dementia associated with infectious diseases such as HIV, alcoholism, and other exogenous toxins were excluded from the analysis.

For those with atopic dermatitis relative to those without, the unadjusted hazard ratios were 1.91 for dementia of any type, 2.14 for Alzheimer’s dementia, and 2.25 for vascular-related dementia. After adjustment for confounders such as age, sex, and socioeconomic status, these hazard ratios, respectively, were only somewhat lower and remained statistically significant.

There was a trend for greater dementia risk with greater atopic dermatitis severity, rising from 2.07 in those with mild atopic dermatitis to 2.72 to those with severe disease, according to Dr. Abuabara.

“The important next step is to determine if better control of atopic dermatitis results in a lower risk of dementia,” she said.

According to Dr. Abuabara, some experimental studies have supported the hypothesis that downregulation of systemic markers of inflammation may be protective.

“Even if you reduced risk by a small amount, it would translate into a large health impact because of the large and growing prevalence of dementia,” she said.

Dr. Abuabara is a consultant for the TARGET-DERM study, sponsored by Target PharmaSolutions.

The FP diagnosed granuloma annulare (GA) in this patient, based on the typical clinical appearance of a raised ring on the back of the hand with no scale.

GA is a common benign cutaneous, inflammatory disorder of unknown origin. It affects twice as many women as men. It features annular lesions that have raised borders and are skin-colored to erythematous. The rings may become hyperpigmented and often feature a central depression. These lesions are typically 1 to 5 cm wide. Although the classical appearance of GA is annular, the rings may not always be complete. Most importantly, there is no scaling, which one would expect to see in tinea infections, also known as “ringworm.”

The most common form of granuloma annulare is localized, as it was in this case. It typically presents on the dorsal surfaces of extremities, especially of the hands and feet. When the presentation is classic, there is no need for a biopsy to confirm the diagnosis.

The most effective treatment for local disease is intralesional triamcinolone (5mg/mL). (See Watch & Learn: Intralesional injections.) The FP offered this treatment to the patient, and she tolerated the procedure well. The GA resolved over the weeks that followed with some faint hypopigmentation that lasted for several months. The patient was happy with the results.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mauskar M, Usatine R. Granuloma annulare. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1141-1146.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com

The FP diagnosed granuloma annulare (GA) in this patient, based on the typical clinical appearance of a raised ring on the back of the hand with no scale.

GA is a common benign cutaneous, inflammatory disorder of unknown origin. It affects twice as many women as men. It features annular lesions that have raised borders and are skin-colored to erythematous. The rings may become hyperpigmented and often feature a central depression. These lesions are typically 1 to 5 cm wide. Although the classical appearance of GA is annular, the rings may not always be complete. Most importantly, there is no scaling, which one would expect to see in tinea infections, also known as “ringworm.”

The most common form of granuloma annulare is localized, as it was in this case. It typically presents on the dorsal surfaces of extremities, especially of the hands and feet. When the presentation is classic, there is no need for a biopsy to confirm the diagnosis.

The most effective treatment for local disease is intralesional triamcinolone (5mg/mL). (See Watch & Learn: Intralesional injections.) The FP offered this treatment to the patient, and she tolerated the procedure well. The GA resolved over the weeks that followed with some faint hypopigmentation that lasted for several months. The patient was happy with the results.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mauskar M, Usatine R. Granuloma annulare. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1141-1146.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com

The FP diagnosed granuloma annulare (GA) in this patient, based on the typical clinical appearance of a raised ring on the back of the hand with no scale.

GA is a common benign cutaneous, inflammatory disorder of unknown origin. It affects twice as many women as men. It features annular lesions that have raised borders and are skin-colored to erythematous. The rings may become hyperpigmented and often feature a central depression. These lesions are typically 1 to 5 cm wide. Although the classical appearance of GA is annular, the rings may not always be complete. Most importantly, there is no scaling, which one would expect to see in tinea infections, also known as “ringworm.”

The most common form of granuloma annulare is localized, as it was in this case. It typically presents on the dorsal surfaces of extremities, especially of the hands and feet. When the presentation is classic, there is no need for a biopsy to confirm the diagnosis.

The most effective treatment for local disease is intralesional triamcinolone (5mg/mL). (See Watch & Learn: Intralesional injections.) The FP offered this treatment to the patient, and she tolerated the procedure well. The GA resolved over the weeks that followed with some faint hypopigmentation that lasted for several months. The patient was happy with the results.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mauskar M, Usatine R. Granuloma annulare. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1141-1146.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com