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Sleep disturbances more profound in older adults with atopic dermatitis
especially trouble staying asleep.
Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.
“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”
Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).
The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.
Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.
However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).
“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.
The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.
A version of this article first appeared on Medscape.com.
especially trouble staying asleep.
Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.
“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”
Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).
The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.
Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.
However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).
“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.
The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.
A version of this article first appeared on Medscape.com.
especially trouble staying asleep.
Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.
“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”
Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).
The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.
Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.
However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).
“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.
The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.
A version of this article first appeared on Medscape.com.
FROM REVOLUTIONIZING AD 2021
Atopic Dermatitis in the ED
How does atopic dermatitis present in skin of color?
“We see very heterogenous and broad clinical presentations across the diverse patient populations that we see,” Andrew F. Alexis, MD, MPH, said at the Revolutionizing Atopic Dermatitis symposium. “Some of these differences might be related to population variations in skin barrier function, immunologic factors, genetic factors, and environmental factors, which all interplay to produce variations in the clinical presentation and overall impact of AD. Many nongenetic factors also contribute to differences that we see, including some socioeconomic and other factors that feed into health disparities.”
Dr. Alexis, professor of clinical dermatology at Weill Cornell Medicine, New York, discussed four main clinical features of AD in skin of color.
Erythema is less visible because it is masked by pigment
“There can be some masking of the redness and alteration of that color such that it doesn’t look bright red as it would in the background of lightly pigmented skin,” Dr. Alexis said. “Instead, the [AD lesions] have shades of grayish-red or grayish-brown or reddish-brown. It’s important to recognize this clinical presentation and look carefully and assess the patient – not just visually but with palpation and take into consideration symptomatology so that you don’t fall into the trap of calling an AD lesion postinflammatory hyperpigmentation. It’s also helpful to isolate the islands of normal or nonlesional skin and contrast that with the areas of lesional skin, to get a sense of how active and inflamed the areas are. Palpation really helps to appreciate the elevation of the lesions that are involved.”
Follicular accentuation
Morphological variants common in skin of color include the follicular variant or micropapular variant of AD. “You might just see a collection of papules that are 1-2 mm in size and pruritic and in typical sites of predilection [for] eczema,” he said. Prurigo nodularis–like lesions or prurigo nodularis in association with AD are also seen more frequently in skin of color.
Lichenification
The lichenoid variant of AD is characterized by a violaceous hue and other features that resemble lichen planus and has been reported to be more common in individuals of African descent. A prospective study of about 1,000 patients with AD seen over 2 years at a dermatology clinic in southeastern Nigeria found that 54% of patients had papular lichenoid lesions. In addition, 51% had elevated blood eosinophil counts, especially those with severe disease.
Dr. Alexis added that psoriasiform features have been reported in studies of East Asian populations with AD. These plaques may be more well demarcated and have clinical and histologic features that resemble psoriasis.
Dyspigmentation
One common feature across the spectrum of patients with skin of color “is the risk of longstanding pigmentary sequelae in the form of hyperpigmentation or hypopigmentation,” said Dr. Alexis, who is also vice chair for diversity and inclusion for the department of dermatology at Weill Cornell Medicine. “In very severe longstanding areas with chronic excoriation to the point of breaking of the skin, eroding of the skin, causing permanent damage to the melanocytes, dyspigmentation that resembles vitiligo can be seen. We can also see hypopigmentation as a consequence of topical corticosteroids, particularly those that are class I or class II and are used for prolonged periods of time.”
Dr. Alexis noted that delays in treatment and undertreatment can contribute to a higher risk of pigmentary and other long-term sequelae. “New therapies show promise in improving outcomes in AD patients with skin of color. When it comes to therapeutic responses, there are some post hoc studies that have investigated potential differences in safety and efficacy of the agents that have been recently approved. We clearly need more data to better understand if there are potential racial or ethnic differences.”
Dr. Alexis reported no relevant financial relationships.
Commentary by Lawrence F. Eichenfield, MD
Atopic dermatitis (AD) is highly heterogenous, with tremendous variations in extent, qualities of eczema, symptom complex, and physical presentation. Prior studies have reported disparities of care delivered to racial and ethnic minorities in the United States, as well as higher susceptibility to AD and odds of persistent disease into adulthood from child-onset AD. Recognizing some differences in presentation of AD in patients with skin of color is important as we select our therapeutic interventions, including assessing new treatments being added to our armamentarium. Erythema may be harder to notice in darker skin, but attempting to blanch the skin with pressure can help to assess the color and inflammation. Appreciating lichenoid changes, including papular and “micropapular” AD, and psoriasiform-like thickening in certain patients (reportedly more common in East Asian populations) are important as well. And dyspigmentation is an important aspect of the disease presentation and patient and parental concern, given both hypopigmentaton and hyperpigmentation commonly seen over the course of AD.
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. He disclosed that he has served as an investigator and/or consultant to AbbVie, Lilly, Pfizer, Regeneron, Sanofi-Genzyme, and Verrica.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
“We see very heterogenous and broad clinical presentations across the diverse patient populations that we see,” Andrew F. Alexis, MD, MPH, said at the Revolutionizing Atopic Dermatitis symposium. “Some of these differences might be related to population variations in skin barrier function, immunologic factors, genetic factors, and environmental factors, which all interplay to produce variations in the clinical presentation and overall impact of AD. Many nongenetic factors also contribute to differences that we see, including some socioeconomic and other factors that feed into health disparities.”
Dr. Alexis, professor of clinical dermatology at Weill Cornell Medicine, New York, discussed four main clinical features of AD in skin of color.
Erythema is less visible because it is masked by pigment
“There can be some masking of the redness and alteration of that color such that it doesn’t look bright red as it would in the background of lightly pigmented skin,” Dr. Alexis said. “Instead, the [AD lesions] have shades of grayish-red or grayish-brown or reddish-brown. It’s important to recognize this clinical presentation and look carefully and assess the patient – not just visually but with palpation and take into consideration symptomatology so that you don’t fall into the trap of calling an AD lesion postinflammatory hyperpigmentation. It’s also helpful to isolate the islands of normal or nonlesional skin and contrast that with the areas of lesional skin, to get a sense of how active and inflamed the areas are. Palpation really helps to appreciate the elevation of the lesions that are involved.”
Follicular accentuation
Morphological variants common in skin of color include the follicular variant or micropapular variant of AD. “You might just see a collection of papules that are 1-2 mm in size and pruritic and in typical sites of predilection [for] eczema,” he said. Prurigo nodularis–like lesions or prurigo nodularis in association with AD are also seen more frequently in skin of color.
Lichenification
The lichenoid variant of AD is characterized by a violaceous hue and other features that resemble lichen planus and has been reported to be more common in individuals of African descent. A prospective study of about 1,000 patients with AD seen over 2 years at a dermatology clinic in southeastern Nigeria found that 54% of patients had papular lichenoid lesions. In addition, 51% had elevated blood eosinophil counts, especially those with severe disease.
Dr. Alexis added that psoriasiform features have been reported in studies of East Asian populations with AD. These plaques may be more well demarcated and have clinical and histologic features that resemble psoriasis.
Dyspigmentation
One common feature across the spectrum of patients with skin of color “is the risk of longstanding pigmentary sequelae in the form of hyperpigmentation or hypopigmentation,” said Dr. Alexis, who is also vice chair for diversity and inclusion for the department of dermatology at Weill Cornell Medicine. “In very severe longstanding areas with chronic excoriation to the point of breaking of the skin, eroding of the skin, causing permanent damage to the melanocytes, dyspigmentation that resembles vitiligo can be seen. We can also see hypopigmentation as a consequence of topical corticosteroids, particularly those that are class I or class II and are used for prolonged periods of time.”
Dr. Alexis noted that delays in treatment and undertreatment can contribute to a higher risk of pigmentary and other long-term sequelae. “New therapies show promise in improving outcomes in AD patients with skin of color. When it comes to therapeutic responses, there are some post hoc studies that have investigated potential differences in safety and efficacy of the agents that have been recently approved. We clearly need more data to better understand if there are potential racial or ethnic differences.”
Dr. Alexis reported no relevant financial relationships.
Commentary by Lawrence F. Eichenfield, MD
Atopic dermatitis (AD) is highly heterogenous, with tremendous variations in extent, qualities of eczema, symptom complex, and physical presentation. Prior studies have reported disparities of care delivered to racial and ethnic minorities in the United States, as well as higher susceptibility to AD and odds of persistent disease into adulthood from child-onset AD. Recognizing some differences in presentation of AD in patients with skin of color is important as we select our therapeutic interventions, including assessing new treatments being added to our armamentarium. Erythema may be harder to notice in darker skin, but attempting to blanch the skin with pressure can help to assess the color and inflammation. Appreciating lichenoid changes, including papular and “micropapular” AD, and psoriasiform-like thickening in certain patients (reportedly more common in East Asian populations) are important as well. And dyspigmentation is an important aspect of the disease presentation and patient and parental concern, given both hypopigmentaton and hyperpigmentation commonly seen over the course of AD.
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. He disclosed that he has served as an investigator and/or consultant to AbbVie, Lilly, Pfizer, Regeneron, Sanofi-Genzyme, and Verrica.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
“We see very heterogenous and broad clinical presentations across the diverse patient populations that we see,” Andrew F. Alexis, MD, MPH, said at the Revolutionizing Atopic Dermatitis symposium. “Some of these differences might be related to population variations in skin barrier function, immunologic factors, genetic factors, and environmental factors, which all interplay to produce variations in the clinical presentation and overall impact of AD. Many nongenetic factors also contribute to differences that we see, including some socioeconomic and other factors that feed into health disparities.”
Dr. Alexis, professor of clinical dermatology at Weill Cornell Medicine, New York, discussed four main clinical features of AD in skin of color.
Erythema is less visible because it is masked by pigment
“There can be some masking of the redness and alteration of that color such that it doesn’t look bright red as it would in the background of lightly pigmented skin,” Dr. Alexis said. “Instead, the [AD lesions] have shades of grayish-red or grayish-brown or reddish-brown. It’s important to recognize this clinical presentation and look carefully and assess the patient – not just visually but with palpation and take into consideration symptomatology so that you don’t fall into the trap of calling an AD lesion postinflammatory hyperpigmentation. It’s also helpful to isolate the islands of normal or nonlesional skin and contrast that with the areas of lesional skin, to get a sense of how active and inflamed the areas are. Palpation really helps to appreciate the elevation of the lesions that are involved.”
Follicular accentuation
Morphological variants common in skin of color include the follicular variant or micropapular variant of AD. “You might just see a collection of papules that are 1-2 mm in size and pruritic and in typical sites of predilection [for] eczema,” he said. Prurigo nodularis–like lesions or prurigo nodularis in association with AD are also seen more frequently in skin of color.
Lichenification
The lichenoid variant of AD is characterized by a violaceous hue and other features that resemble lichen planus and has been reported to be more common in individuals of African descent. A prospective study of about 1,000 patients with AD seen over 2 years at a dermatology clinic in southeastern Nigeria found that 54% of patients had papular lichenoid lesions. In addition, 51% had elevated blood eosinophil counts, especially those with severe disease.
Dr. Alexis added that psoriasiform features have been reported in studies of East Asian populations with AD. These plaques may be more well demarcated and have clinical and histologic features that resemble psoriasis.
Dyspigmentation
One common feature across the spectrum of patients with skin of color “is the risk of longstanding pigmentary sequelae in the form of hyperpigmentation or hypopigmentation,” said Dr. Alexis, who is also vice chair for diversity and inclusion for the department of dermatology at Weill Cornell Medicine. “In very severe longstanding areas with chronic excoriation to the point of breaking of the skin, eroding of the skin, causing permanent damage to the melanocytes, dyspigmentation that resembles vitiligo can be seen. We can also see hypopigmentation as a consequence of topical corticosteroids, particularly those that are class I or class II and are used for prolonged periods of time.”
Dr. Alexis noted that delays in treatment and undertreatment can contribute to a higher risk of pigmentary and other long-term sequelae. “New therapies show promise in improving outcomes in AD patients with skin of color. When it comes to therapeutic responses, there are some post hoc studies that have investigated potential differences in safety and efficacy of the agents that have been recently approved. We clearly need more data to better understand if there are potential racial or ethnic differences.”
Dr. Alexis reported no relevant financial relationships.
Commentary by Lawrence F. Eichenfield, MD
Atopic dermatitis (AD) is highly heterogenous, with tremendous variations in extent, qualities of eczema, symptom complex, and physical presentation. Prior studies have reported disparities of care delivered to racial and ethnic minorities in the United States, as well as higher susceptibility to AD and odds of persistent disease into adulthood from child-onset AD. Recognizing some differences in presentation of AD in patients with skin of color is important as we select our therapeutic interventions, including assessing new treatments being added to our armamentarium. Erythema may be harder to notice in darker skin, but attempting to blanch the skin with pressure can help to assess the color and inflammation. Appreciating lichenoid changes, including papular and “micropapular” AD, and psoriasiform-like thickening in certain patients (reportedly more common in East Asian populations) are important as well. And dyspigmentation is an important aspect of the disease presentation and patient and parental concern, given both hypopigmentaton and hyperpigmentation commonly seen over the course of AD.
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. He disclosed that he has served as an investigator and/or consultant to AbbVie, Lilly, Pfizer, Regeneron, Sanofi-Genzyme, and Verrica.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
FROM REVOLUTIONIZING AD 2021
Abrocitinib efficacy dose-dependent, similar across AD age groups
and was comparable in patients aged 51 years and older, results from a post hoc analysis of four trials showed.
Abrocitinib (Cibinqo) is an oral, once-daily, Janus kinase 1 selective inhibitor that has shown good efficacy and safety as monotherapy or combined with topical therapy for treatment of patients with moderate to severe AD. The agent was approved in mid-December in Europe for the treatment of moderate to severe AD in adults who are candidates for systemic therapy and is currently under review by the Food and Drug Administration.
“We know that responses to, and adverse events associated with, systemic therapies may vary among patients of different ages,” Andrew F. Alexis, MD, MPH, said during a late-breaking abstract session at the Revolutionizing Atopic Dermatitis virtual symposium. “The efficacy and safety of abrocitinib monotherapy were previously evaluated in adolescent and adult subpopulations from controlled clinical trials in patients with moderate to severe AD. The objective of the current study was to assess the impact of age on short-term responses to abrocitinib treatment in patients with moderate to severe AD.”
Dr. Alexis, professor of clinical dermatology at Weill Cornell Medicine, New York, and colleagues performed a post hoc analysis across four randomized, double-blind studies that was stratified by age group: 12-17 years, 18-40 years, 41-50 years, and 51 years and older. Efficacy data were assessed separately for patients in the monotherapy pool and in the JADE COMPARE trial. The monotherapy pool included patients from one phase 2b study and two phase 3 studies who received abrocitinib 200 mg, abrocitinib 100 mg, or placebo monotherapy for 12 weeks (JADE-MONO-1 and JADE-MONO-2).
The JADE COMPARE pool included patients who received abrocitinib 200 mg, abrocitinib 100 mg, or placebo, plus medicated topical therapy for 16 weeks. Data from patients in all four trials were pooled for the analysis of treatment-emergent adverse events. Efficacy points analyzed were the Investigator Global Assessment (IGA) score of 0/1 (clear or almost clear), a 75% reduction from baseline in the Eczema Area and Severity Index (EASI-75), or Peak Pruritus Numeric Rating Scale score (PP-NRS4) at week 12 for the monotherapy pool and at week 16 for COMPARE.
In the monotherapy pool, the proportions of patients ages 12-17 years, 18-40 years, 41-50 years, and 51 years and older who achieved an IGA 0/1 response at 12 weeks were 31.3%, 40.2%, 43.8%, and 50.8% (abrocitinib 200 mg); 22%, 23.7%, 22.4%, and 40.8% (abrocitinib 100 mg); and 8.7%, 8%, 3.3%, and 10% (placebo).
In JADE COMPARE, the proportions of patients aged 18-40 years, 41-50 years, and 51 years and older who achieved an IGA 0/1 response were 50%, 53.2%, and 34.8% (abrocitinib 200 mg); 36.9%, 37.1%, and 26.1% (abrocitinib 100 mg); and 12%, 11.8%, and 16.7% (placebo) at 16 weeks. Similar trends were observed for EASI-75 and PP-NRS4 responses at 12 weeks.
Across all age groups, the most common treatment-emergent adverse events were infections/infestations and gastrointestinal effects; most cases were mild or moderate. Nausea was more frequent in the two younger age groups and was dose related: For abrocitinib 200 mg and abrocitinib 100 mg, respectively, the rates of nausea were 18.8% and 7.8% in patients aged 12-17 years; 17.1% and 6.4% in patients aged 18-40 years; and 7.1% and 3.3% in patients aged 51 and older.
“Efficacy responses in patients 51 years of age and older were comparable to those in other age groups,” concluded Dr. Alexis, vice chair for diversity and inclusion in the department of dermatology at Weill Cornell. “The safety profile was consistent across age ranges and was similar to that reported previously.”
The investigators found that treatment response to abrocitinib “in the absence or presence of medicated topical therapy was fairly consistent across age groups, showed similar dose-dependency, and importantly, did not show reduced efficacy in older adults as measured by lesional severity, extent, and itch at 4 months,” said Raj Chovatiya, MD, PhD, assistant professor of dermatology at Northwestern University, Chicago, who was asked to comment on the study.
“Furthermore, the safety profile was consistent across all adults, though notably, nausea was more common among younger age groups, highlighting an area of future investigation,” he added. “Overall, these data show that abrocitinib is associated with similar short-term responses across adulthood and underscore the importance of the JAK-STAT pathway in the underlying pathophysiology of AD in different age groups. It will be interesting to see how these data reflect the real-world setting with both short- and long-term outcomes in a heterogeneous patient population.”
In the interview, Dr. Chovatiya said, “the next frontier in personalized therapy for AD involves deeper clinical phenotyping of our patients and a better understanding of how efficacy and safety vary across patient groups.” For example, he noted, “AD in earlier versus later adulthood may be associated with different clinical signs, symptoms, comorbidities, and other measures of patient burden, and thus, may be associated with different treatment responses to systemic therapy.”
Dr. Alexis disclosed that he has served as an adviser to, or has received consulting fees from, Leo, Galderma, Pfizer, Sanofi-Regeneron, Dermavant, Beiersdorf, Valeant, L’Oréal, BMS, Bausch Health, UCB, Vyne, Arcutis, Janssen, Allergan, Almirall, AbbVie, Sol-Gel, and Amgen.
Dr. Chovatiya disclosed that he is a consultant to, a speaker for, and/or a member of the advisory board for AbbVie, Arena, Arcutis, Incyte, Pfizer, Regeneron, and Sanofi-Genzyme.
A version of this article first appeared on Medscape.com.
and was comparable in patients aged 51 years and older, results from a post hoc analysis of four trials showed.
Abrocitinib (Cibinqo) is an oral, once-daily, Janus kinase 1 selective inhibitor that has shown good efficacy and safety as monotherapy or combined with topical therapy for treatment of patients with moderate to severe AD. The agent was approved in mid-December in Europe for the treatment of moderate to severe AD in adults who are candidates for systemic therapy and is currently under review by the Food and Drug Administration.
“We know that responses to, and adverse events associated with, systemic therapies may vary among patients of different ages,” Andrew F. Alexis, MD, MPH, said during a late-breaking abstract session at the Revolutionizing Atopic Dermatitis virtual symposium. “The efficacy and safety of abrocitinib monotherapy were previously evaluated in adolescent and adult subpopulations from controlled clinical trials in patients with moderate to severe AD. The objective of the current study was to assess the impact of age on short-term responses to abrocitinib treatment in patients with moderate to severe AD.”
Dr. Alexis, professor of clinical dermatology at Weill Cornell Medicine, New York, and colleagues performed a post hoc analysis across four randomized, double-blind studies that was stratified by age group: 12-17 years, 18-40 years, 41-50 years, and 51 years and older. Efficacy data were assessed separately for patients in the monotherapy pool and in the JADE COMPARE trial. The monotherapy pool included patients from one phase 2b study and two phase 3 studies who received abrocitinib 200 mg, abrocitinib 100 mg, or placebo monotherapy for 12 weeks (JADE-MONO-1 and JADE-MONO-2).
The JADE COMPARE pool included patients who received abrocitinib 200 mg, abrocitinib 100 mg, or placebo, plus medicated topical therapy for 16 weeks. Data from patients in all four trials were pooled for the analysis of treatment-emergent adverse events. Efficacy points analyzed were the Investigator Global Assessment (IGA) score of 0/1 (clear or almost clear), a 75% reduction from baseline in the Eczema Area and Severity Index (EASI-75), or Peak Pruritus Numeric Rating Scale score (PP-NRS4) at week 12 for the monotherapy pool and at week 16 for COMPARE.
In the monotherapy pool, the proportions of patients ages 12-17 years, 18-40 years, 41-50 years, and 51 years and older who achieved an IGA 0/1 response at 12 weeks were 31.3%, 40.2%, 43.8%, and 50.8% (abrocitinib 200 mg); 22%, 23.7%, 22.4%, and 40.8% (abrocitinib 100 mg); and 8.7%, 8%, 3.3%, and 10% (placebo).
In JADE COMPARE, the proportions of patients aged 18-40 years, 41-50 years, and 51 years and older who achieved an IGA 0/1 response were 50%, 53.2%, and 34.8% (abrocitinib 200 mg); 36.9%, 37.1%, and 26.1% (abrocitinib 100 mg); and 12%, 11.8%, and 16.7% (placebo) at 16 weeks. Similar trends were observed for EASI-75 and PP-NRS4 responses at 12 weeks.
Across all age groups, the most common treatment-emergent adverse events were infections/infestations and gastrointestinal effects; most cases were mild or moderate. Nausea was more frequent in the two younger age groups and was dose related: For abrocitinib 200 mg and abrocitinib 100 mg, respectively, the rates of nausea were 18.8% and 7.8% in patients aged 12-17 years; 17.1% and 6.4% in patients aged 18-40 years; and 7.1% and 3.3% in patients aged 51 and older.
“Efficacy responses in patients 51 years of age and older were comparable to those in other age groups,” concluded Dr. Alexis, vice chair for diversity and inclusion in the department of dermatology at Weill Cornell. “The safety profile was consistent across age ranges and was similar to that reported previously.”
The investigators found that treatment response to abrocitinib “in the absence or presence of medicated topical therapy was fairly consistent across age groups, showed similar dose-dependency, and importantly, did not show reduced efficacy in older adults as measured by lesional severity, extent, and itch at 4 months,” said Raj Chovatiya, MD, PhD, assistant professor of dermatology at Northwestern University, Chicago, who was asked to comment on the study.
“Furthermore, the safety profile was consistent across all adults, though notably, nausea was more common among younger age groups, highlighting an area of future investigation,” he added. “Overall, these data show that abrocitinib is associated with similar short-term responses across adulthood and underscore the importance of the JAK-STAT pathway in the underlying pathophysiology of AD in different age groups. It will be interesting to see how these data reflect the real-world setting with both short- and long-term outcomes in a heterogeneous patient population.”
In the interview, Dr. Chovatiya said, “the next frontier in personalized therapy for AD involves deeper clinical phenotyping of our patients and a better understanding of how efficacy and safety vary across patient groups.” For example, he noted, “AD in earlier versus later adulthood may be associated with different clinical signs, symptoms, comorbidities, and other measures of patient burden, and thus, may be associated with different treatment responses to systemic therapy.”
Dr. Alexis disclosed that he has served as an adviser to, or has received consulting fees from, Leo, Galderma, Pfizer, Sanofi-Regeneron, Dermavant, Beiersdorf, Valeant, L’Oréal, BMS, Bausch Health, UCB, Vyne, Arcutis, Janssen, Allergan, Almirall, AbbVie, Sol-Gel, and Amgen.
Dr. Chovatiya disclosed that he is a consultant to, a speaker for, and/or a member of the advisory board for AbbVie, Arena, Arcutis, Incyte, Pfizer, Regeneron, and Sanofi-Genzyme.
A version of this article first appeared on Medscape.com.
and was comparable in patients aged 51 years and older, results from a post hoc analysis of four trials showed.
Abrocitinib (Cibinqo) is an oral, once-daily, Janus kinase 1 selective inhibitor that has shown good efficacy and safety as monotherapy or combined with topical therapy for treatment of patients with moderate to severe AD. The agent was approved in mid-December in Europe for the treatment of moderate to severe AD in adults who are candidates for systemic therapy and is currently under review by the Food and Drug Administration.
“We know that responses to, and adverse events associated with, systemic therapies may vary among patients of different ages,” Andrew F. Alexis, MD, MPH, said during a late-breaking abstract session at the Revolutionizing Atopic Dermatitis virtual symposium. “The efficacy and safety of abrocitinib monotherapy were previously evaluated in adolescent and adult subpopulations from controlled clinical trials in patients with moderate to severe AD. The objective of the current study was to assess the impact of age on short-term responses to abrocitinib treatment in patients with moderate to severe AD.”
Dr. Alexis, professor of clinical dermatology at Weill Cornell Medicine, New York, and colleagues performed a post hoc analysis across four randomized, double-blind studies that was stratified by age group: 12-17 years, 18-40 years, 41-50 years, and 51 years and older. Efficacy data were assessed separately for patients in the monotherapy pool and in the JADE COMPARE trial. The monotherapy pool included patients from one phase 2b study and two phase 3 studies who received abrocitinib 200 mg, abrocitinib 100 mg, or placebo monotherapy for 12 weeks (JADE-MONO-1 and JADE-MONO-2).
The JADE COMPARE pool included patients who received abrocitinib 200 mg, abrocitinib 100 mg, or placebo, plus medicated topical therapy for 16 weeks. Data from patients in all four trials were pooled for the analysis of treatment-emergent adverse events. Efficacy points analyzed were the Investigator Global Assessment (IGA) score of 0/1 (clear or almost clear), a 75% reduction from baseline in the Eczema Area and Severity Index (EASI-75), or Peak Pruritus Numeric Rating Scale score (PP-NRS4) at week 12 for the monotherapy pool and at week 16 for COMPARE.
In the monotherapy pool, the proportions of patients ages 12-17 years, 18-40 years, 41-50 years, and 51 years and older who achieved an IGA 0/1 response at 12 weeks were 31.3%, 40.2%, 43.8%, and 50.8% (abrocitinib 200 mg); 22%, 23.7%, 22.4%, and 40.8% (abrocitinib 100 mg); and 8.7%, 8%, 3.3%, and 10% (placebo).
In JADE COMPARE, the proportions of patients aged 18-40 years, 41-50 years, and 51 years and older who achieved an IGA 0/1 response were 50%, 53.2%, and 34.8% (abrocitinib 200 mg); 36.9%, 37.1%, and 26.1% (abrocitinib 100 mg); and 12%, 11.8%, and 16.7% (placebo) at 16 weeks. Similar trends were observed for EASI-75 and PP-NRS4 responses at 12 weeks.
Across all age groups, the most common treatment-emergent adverse events were infections/infestations and gastrointestinal effects; most cases were mild or moderate. Nausea was more frequent in the two younger age groups and was dose related: For abrocitinib 200 mg and abrocitinib 100 mg, respectively, the rates of nausea were 18.8% and 7.8% in patients aged 12-17 years; 17.1% and 6.4% in patients aged 18-40 years; and 7.1% and 3.3% in patients aged 51 and older.
“Efficacy responses in patients 51 years of age and older were comparable to those in other age groups,” concluded Dr. Alexis, vice chair for diversity and inclusion in the department of dermatology at Weill Cornell. “The safety profile was consistent across age ranges and was similar to that reported previously.”
The investigators found that treatment response to abrocitinib “in the absence or presence of medicated topical therapy was fairly consistent across age groups, showed similar dose-dependency, and importantly, did not show reduced efficacy in older adults as measured by lesional severity, extent, and itch at 4 months,” said Raj Chovatiya, MD, PhD, assistant professor of dermatology at Northwestern University, Chicago, who was asked to comment on the study.
“Furthermore, the safety profile was consistent across all adults, though notably, nausea was more common among younger age groups, highlighting an area of future investigation,” he added. “Overall, these data show that abrocitinib is associated with similar short-term responses across adulthood and underscore the importance of the JAK-STAT pathway in the underlying pathophysiology of AD in different age groups. It will be interesting to see how these data reflect the real-world setting with both short- and long-term outcomes in a heterogeneous patient population.”
In the interview, Dr. Chovatiya said, “the next frontier in personalized therapy for AD involves deeper clinical phenotyping of our patients and a better understanding of how efficacy and safety vary across patient groups.” For example, he noted, “AD in earlier versus later adulthood may be associated with different clinical signs, symptoms, comorbidities, and other measures of patient burden, and thus, may be associated with different treatment responses to systemic therapy.”
Dr. Alexis disclosed that he has served as an adviser to, or has received consulting fees from, Leo, Galderma, Pfizer, Sanofi-Regeneron, Dermavant, Beiersdorf, Valeant, L’Oréal, BMS, Bausch Health, UCB, Vyne, Arcutis, Janssen, Allergan, Almirall, AbbVie, Sol-Gel, and Amgen.
Dr. Chovatiya disclosed that he is a consultant to, a speaker for, and/or a member of the advisory board for AbbVie, Arena, Arcutis, Incyte, Pfizer, Regeneron, and Sanofi-Genzyme.
A version of this article first appeared on Medscape.com.
FROM REVOLUTIONIZING AD 2021
CRP elevated in adults with AD and sleep disturbance
and mortality, results from a large cohort analysis showed.
“The implications of these findings are vast,” presenting author Varsha Parthasarathy said during a late-breaking abstract session at the Revolutionizing Atopic Dermatitis virtual symposium. “Poor sleep quality is known to be associated with increased inflammatory markers such as IL-6, IL-17, and CRP, so it is interesting to see this reflected in AD patients with versus without sleep disturbance. Additionally, we know that CRP is a driver of inflammation and is strongly associated with cardiovascular complications such as heart attack and stroke. Therefore, CRP may be a useful prognostic marker in AD patients with sleep disturbances.”
To examine the comorbidity burden of sleep disorders in AD patients and associate findings with inflammatory CRP and cardiovascular comorbidities, Mr. Parthasarathy, a medical student and itch fellow in the department of dermatology at the Johns Hopkins University School of Medicine, Baltimore, and colleagues drew from TriNetX, a health care network of approximately 73 million de-identified medical records in 53 organizations. The years of study were 2015 to 2021. The researchers limited the analysis to adults with at least two instances of International Classification of Diseases, Tenth Revision (ICD-10) code L28 for AD, to capture a population with true AD. Controls were adults without AD who presented for general checkup and were matched to AD patients by age, race, and sex.
The study population consisted of 120,480 AD patients and matched controls. Their mean age was 36 years, 61% were female, and 26% were Black. Compared with controls, AD patients had an increased risk of developing general sleep disorders over the 6-year period (relative risk, 1.10), as well as obstructive sleep apnea (RR, 1.13), insomnia (RR, 1.10), hypersomnia (RR, 1.24), sleep-related movement disorders (RR, 1.36), restless legs syndrome (RR, 1.25), sleep deprivation (RR, 1.36), and unspecified sleep disorders (RR, 1.22).
To examine the association of sleep disturbance with the inflammatory biomarker CRP, the researchers measured CRP levels between these patient groups. They found a substantially higher CRP in AD patients compared with controls (21.2 mg/L vs. 7.6 mg/L, respectively; P < .0001). This finding “is suggestive of a higher level of inflammation in these patients,” Mr. Parthasarathy said. Interestingly, he added, they also found a higher CRP level in AD patients with sleep disturbances compared to AD patients without sleep disturbances (23.3 vs. 20.6 mg/L; P = .02), “also pointing to a higher inflammatory burden in AD patients whose sleep was affected.”
Compared to matched AD patients without sleep disorders, AD patients with sleep disorders were more likely to develop obesity (RR, 2.65), hyperlipidemia (RR, 2.18), type 2 diabetes (RR, 2.45), metabolic syndrome (RR, 4.16), atherosclerosis (RR, 2.42), peripheral vascular disease (RR, 2.47), stroke (RR, 2.37), venous thromboembolism (RR, 2.93), and mortality (hazard ratio, 1.24).
“There is a consequence of not treating patients with atopic dermatitis, especially those patients with sleep disturbance,” the study’s primary author, Shawn G. Kwatra, MD, associate professor of dermatology at Johns Hopkins, told this news organization. “Chronic inflammation can lead to the development of comorbidities, so it is important to offer patients early treatment to reduce their overall inflammation.” He said that he was most surprised by the degree of increased inflammation in the blood of AD as compared to healthy controls. “This likely plays a part in the development of several comorbidities,” he said.
Mr. Parthasarathy acknowledged certain limitations of the study, including the inability to infer causal relationships, as uncontrolled factors may be present. “Additionally, sampling of only patients that have had medical encounters limits the generalizability of the findings,” she said. “However, findings in this large cohort study suggest that clinicians should seek to identify sleep disorders in AD patients and screen for cardiac comorbidities secondary to inflammation in this patient population.”
“There is increased data to suggest that adults with AD, particularly those with more severe disease, may be at an increased risk of cardiovascular disease and the results from [this study] further support the concept of AD as systemic disease,” said Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, who was asked to comment on the study. She cited the large population-based, retrospective design and use of two instances of ICD codes for AD to confirm diagnosis as key strengths of the research. “However, it is unclear if for each patient CRP levels were measured at one single timepoint,” Dr. Chiesa Fuxench said. “For future studies, it would be interesting to see if these levels fluctuate with time and if persistently elevated levels are associated with worse cardiovascular outcomes in this population. More data is needed to better understand the relationship better atopic dermatitis disease severity, impact on sleep, and how this relates to increased systemic inflammation and worse cardiovascular outcomes in this population.”
Dr. Kwatra disclosed support by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award Number K23AR077073-01A1 and previous funding by the Dermatology Foundation and Skin of Color Society. Dr. Kwatra is also an advisory board member/consultant for AbbVie, Celldex Therapeutics, Galderma, Incyte Corporation, Johnson & Johnson, Novartis Pharmaceuticals Corporation, Pfizer, Regeneron Pharmaceuticals, Sanofi, and Kiniksa Pharmaceuticals and has served as an investigator for Galderma, Pfizer, and Sanofi. Dr. Chiesa Fuxench disclosed research grants from several pharmaceutical companies for work related to AD. She has also served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer.
A version of this article first appeared on Medscape.com.
and mortality, results from a large cohort analysis showed.
“The implications of these findings are vast,” presenting author Varsha Parthasarathy said during a late-breaking abstract session at the Revolutionizing Atopic Dermatitis virtual symposium. “Poor sleep quality is known to be associated with increased inflammatory markers such as IL-6, IL-17, and CRP, so it is interesting to see this reflected in AD patients with versus without sleep disturbance. Additionally, we know that CRP is a driver of inflammation and is strongly associated with cardiovascular complications such as heart attack and stroke. Therefore, CRP may be a useful prognostic marker in AD patients with sleep disturbances.”
To examine the comorbidity burden of sleep disorders in AD patients and associate findings with inflammatory CRP and cardiovascular comorbidities, Mr. Parthasarathy, a medical student and itch fellow in the department of dermatology at the Johns Hopkins University School of Medicine, Baltimore, and colleagues drew from TriNetX, a health care network of approximately 73 million de-identified medical records in 53 organizations. The years of study were 2015 to 2021. The researchers limited the analysis to adults with at least two instances of International Classification of Diseases, Tenth Revision (ICD-10) code L28 for AD, to capture a population with true AD. Controls were adults without AD who presented for general checkup and were matched to AD patients by age, race, and sex.
The study population consisted of 120,480 AD patients and matched controls. Their mean age was 36 years, 61% were female, and 26% were Black. Compared with controls, AD patients had an increased risk of developing general sleep disorders over the 6-year period (relative risk, 1.10), as well as obstructive sleep apnea (RR, 1.13), insomnia (RR, 1.10), hypersomnia (RR, 1.24), sleep-related movement disorders (RR, 1.36), restless legs syndrome (RR, 1.25), sleep deprivation (RR, 1.36), and unspecified sleep disorders (RR, 1.22).
To examine the association of sleep disturbance with the inflammatory biomarker CRP, the researchers measured CRP levels between these patient groups. They found a substantially higher CRP in AD patients compared with controls (21.2 mg/L vs. 7.6 mg/L, respectively; P < .0001). This finding “is suggestive of a higher level of inflammation in these patients,” Mr. Parthasarathy said. Interestingly, he added, they also found a higher CRP level in AD patients with sleep disturbances compared to AD patients without sleep disturbances (23.3 vs. 20.6 mg/L; P = .02), “also pointing to a higher inflammatory burden in AD patients whose sleep was affected.”
Compared to matched AD patients without sleep disorders, AD patients with sleep disorders were more likely to develop obesity (RR, 2.65), hyperlipidemia (RR, 2.18), type 2 diabetes (RR, 2.45), metabolic syndrome (RR, 4.16), atherosclerosis (RR, 2.42), peripheral vascular disease (RR, 2.47), stroke (RR, 2.37), venous thromboembolism (RR, 2.93), and mortality (hazard ratio, 1.24).
“There is a consequence of not treating patients with atopic dermatitis, especially those patients with sleep disturbance,” the study’s primary author, Shawn G. Kwatra, MD, associate professor of dermatology at Johns Hopkins, told this news organization. “Chronic inflammation can lead to the development of comorbidities, so it is important to offer patients early treatment to reduce their overall inflammation.” He said that he was most surprised by the degree of increased inflammation in the blood of AD as compared to healthy controls. “This likely plays a part in the development of several comorbidities,” he said.
Mr. Parthasarathy acknowledged certain limitations of the study, including the inability to infer causal relationships, as uncontrolled factors may be present. “Additionally, sampling of only patients that have had medical encounters limits the generalizability of the findings,” she said. “However, findings in this large cohort study suggest that clinicians should seek to identify sleep disorders in AD patients and screen for cardiac comorbidities secondary to inflammation in this patient population.”
“There is increased data to suggest that adults with AD, particularly those with more severe disease, may be at an increased risk of cardiovascular disease and the results from [this study] further support the concept of AD as systemic disease,” said Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, who was asked to comment on the study. She cited the large population-based, retrospective design and use of two instances of ICD codes for AD to confirm diagnosis as key strengths of the research. “However, it is unclear if for each patient CRP levels were measured at one single timepoint,” Dr. Chiesa Fuxench said. “For future studies, it would be interesting to see if these levels fluctuate with time and if persistently elevated levels are associated with worse cardiovascular outcomes in this population. More data is needed to better understand the relationship better atopic dermatitis disease severity, impact on sleep, and how this relates to increased systemic inflammation and worse cardiovascular outcomes in this population.”
Dr. Kwatra disclosed support by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award Number K23AR077073-01A1 and previous funding by the Dermatology Foundation and Skin of Color Society. Dr. Kwatra is also an advisory board member/consultant for AbbVie, Celldex Therapeutics, Galderma, Incyte Corporation, Johnson & Johnson, Novartis Pharmaceuticals Corporation, Pfizer, Regeneron Pharmaceuticals, Sanofi, and Kiniksa Pharmaceuticals and has served as an investigator for Galderma, Pfizer, and Sanofi. Dr. Chiesa Fuxench disclosed research grants from several pharmaceutical companies for work related to AD. She has also served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer.
A version of this article first appeared on Medscape.com.
and mortality, results from a large cohort analysis showed.
“The implications of these findings are vast,” presenting author Varsha Parthasarathy said during a late-breaking abstract session at the Revolutionizing Atopic Dermatitis virtual symposium. “Poor sleep quality is known to be associated with increased inflammatory markers such as IL-6, IL-17, and CRP, so it is interesting to see this reflected in AD patients with versus without sleep disturbance. Additionally, we know that CRP is a driver of inflammation and is strongly associated with cardiovascular complications such as heart attack and stroke. Therefore, CRP may be a useful prognostic marker in AD patients with sleep disturbances.”
To examine the comorbidity burden of sleep disorders in AD patients and associate findings with inflammatory CRP and cardiovascular comorbidities, Mr. Parthasarathy, a medical student and itch fellow in the department of dermatology at the Johns Hopkins University School of Medicine, Baltimore, and colleagues drew from TriNetX, a health care network of approximately 73 million de-identified medical records in 53 organizations. The years of study were 2015 to 2021. The researchers limited the analysis to adults with at least two instances of International Classification of Diseases, Tenth Revision (ICD-10) code L28 for AD, to capture a population with true AD. Controls were adults without AD who presented for general checkup and were matched to AD patients by age, race, and sex.
The study population consisted of 120,480 AD patients and matched controls. Their mean age was 36 years, 61% were female, and 26% were Black. Compared with controls, AD patients had an increased risk of developing general sleep disorders over the 6-year period (relative risk, 1.10), as well as obstructive sleep apnea (RR, 1.13), insomnia (RR, 1.10), hypersomnia (RR, 1.24), sleep-related movement disorders (RR, 1.36), restless legs syndrome (RR, 1.25), sleep deprivation (RR, 1.36), and unspecified sleep disorders (RR, 1.22).
To examine the association of sleep disturbance with the inflammatory biomarker CRP, the researchers measured CRP levels between these patient groups. They found a substantially higher CRP in AD patients compared with controls (21.2 mg/L vs. 7.6 mg/L, respectively; P < .0001). This finding “is suggestive of a higher level of inflammation in these patients,” Mr. Parthasarathy said. Interestingly, he added, they also found a higher CRP level in AD patients with sleep disturbances compared to AD patients without sleep disturbances (23.3 vs. 20.6 mg/L; P = .02), “also pointing to a higher inflammatory burden in AD patients whose sleep was affected.”
Compared to matched AD patients without sleep disorders, AD patients with sleep disorders were more likely to develop obesity (RR, 2.65), hyperlipidemia (RR, 2.18), type 2 diabetes (RR, 2.45), metabolic syndrome (RR, 4.16), atherosclerosis (RR, 2.42), peripheral vascular disease (RR, 2.47), stroke (RR, 2.37), venous thromboembolism (RR, 2.93), and mortality (hazard ratio, 1.24).
“There is a consequence of not treating patients with atopic dermatitis, especially those patients with sleep disturbance,” the study’s primary author, Shawn G. Kwatra, MD, associate professor of dermatology at Johns Hopkins, told this news organization. “Chronic inflammation can lead to the development of comorbidities, so it is important to offer patients early treatment to reduce their overall inflammation.” He said that he was most surprised by the degree of increased inflammation in the blood of AD as compared to healthy controls. “This likely plays a part in the development of several comorbidities,” he said.
Mr. Parthasarathy acknowledged certain limitations of the study, including the inability to infer causal relationships, as uncontrolled factors may be present. “Additionally, sampling of only patients that have had medical encounters limits the generalizability of the findings,” she said. “However, findings in this large cohort study suggest that clinicians should seek to identify sleep disorders in AD patients and screen for cardiac comorbidities secondary to inflammation in this patient population.”
“There is increased data to suggest that adults with AD, particularly those with more severe disease, may be at an increased risk of cardiovascular disease and the results from [this study] further support the concept of AD as systemic disease,” said Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, who was asked to comment on the study. She cited the large population-based, retrospective design and use of two instances of ICD codes for AD to confirm diagnosis as key strengths of the research. “However, it is unclear if for each patient CRP levels were measured at one single timepoint,” Dr. Chiesa Fuxench said. “For future studies, it would be interesting to see if these levels fluctuate with time and if persistently elevated levels are associated with worse cardiovascular outcomes in this population. More data is needed to better understand the relationship better atopic dermatitis disease severity, impact on sleep, and how this relates to increased systemic inflammation and worse cardiovascular outcomes in this population.”
Dr. Kwatra disclosed support by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award Number K23AR077073-01A1 and previous funding by the Dermatology Foundation and Skin of Color Society. Dr. Kwatra is also an advisory board member/consultant for AbbVie, Celldex Therapeutics, Galderma, Incyte Corporation, Johnson & Johnson, Novartis Pharmaceuticals Corporation, Pfizer, Regeneron Pharmaceuticals, Sanofi, and Kiniksa Pharmaceuticals and has served as an investigator for Galderma, Pfizer, and Sanofi. Dr. Chiesa Fuxench disclosed research grants from several pharmaceutical companies for work related to AD. She has also served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer.
A version of this article first appeared on Medscape.com.
Abrocitinib approved for atopic dermatitis in Europe
who are candidates for systemic therapy, the manufacturer announced.
Approval by the European Commission was based on the results of studies that include four phase 3 clinical trials (JADE MONO-1, JADE-MONO-2, JADE COMPARE, JADE REGIMEN) and an ongoing open-label extension study (JADE EXTEND) in over 2,800 patients, according to the Pfizer press release announcing the approval. The approved doses are 100 and 200 mg a day; a 50-mg dose was approved for patients with moderate and severe renal impairment and “ certain patients receiving treatment with inhibitors of cytochrome P450 (CYP) 2C19,” the release said.
The approval follows a positive opinion by the Committee for Medicinal Products for Human Use of the European Medicines Agency supporting marketing authorization for treating AD, issued in October. It will be marketed as Cibinqo.
Abrocitinib is under review at the Food and Drug Administration. It was approved earlier in 2021 for treating AD in the United Kingdom, Japan, and Korea.
emechcatie@mdedge.com
who are candidates for systemic therapy, the manufacturer announced.
Approval by the European Commission was based on the results of studies that include four phase 3 clinical trials (JADE MONO-1, JADE-MONO-2, JADE COMPARE, JADE REGIMEN) and an ongoing open-label extension study (JADE EXTEND) in over 2,800 patients, according to the Pfizer press release announcing the approval. The approved doses are 100 and 200 mg a day; a 50-mg dose was approved for patients with moderate and severe renal impairment and “ certain patients receiving treatment with inhibitors of cytochrome P450 (CYP) 2C19,” the release said.
The approval follows a positive opinion by the Committee for Medicinal Products for Human Use of the European Medicines Agency supporting marketing authorization for treating AD, issued in October. It will be marketed as Cibinqo.
Abrocitinib is under review at the Food and Drug Administration. It was approved earlier in 2021 for treating AD in the United Kingdom, Japan, and Korea.
emechcatie@mdedge.com
who are candidates for systemic therapy, the manufacturer announced.
Approval by the European Commission was based on the results of studies that include four phase 3 clinical trials (JADE MONO-1, JADE-MONO-2, JADE COMPARE, JADE REGIMEN) and an ongoing open-label extension study (JADE EXTEND) in over 2,800 patients, according to the Pfizer press release announcing the approval. The approved doses are 100 and 200 mg a day; a 50-mg dose was approved for patients with moderate and severe renal impairment and “ certain patients receiving treatment with inhibitors of cytochrome P450 (CYP) 2C19,” the release said.
The approval follows a positive opinion by the Committee for Medicinal Products for Human Use of the European Medicines Agency supporting marketing authorization for treating AD, issued in October. It will be marketed as Cibinqo.
Abrocitinib is under review at the Food and Drug Administration. It was approved earlier in 2021 for treating AD in the United Kingdom, Japan, and Korea.
emechcatie@mdedge.com
Dust mite immunotherapy may help some with eczema
, but improvement in the primary outcome was not significant, new data show.
Results of the small, randomized, double-blind, placebo-controlled trial were published recently in The Journal of Allergy and Clinical Immunology: In Practice.
Lead author Sarah Sella Langer, MD, of the department of medicine, Ribeirão Preto (Brazil) Medical School, University of São Paulo, and colleagues said their results suggest HDM SLIT is safe and effective as an add-on treatment.
The dust mite extract therapy had no major side effects after 18 months of treatment, the authors reported.
The researchers included data from 66 patients who completed the study. The participants were at least 3 years old, registered at least 15 on the SCORing Atopic Dermatitis (SCORAD) measure, and had a skin prick test and/or immunoglobulin E (IgE) test for sensitization to dust mites.
Patients were grouped by age (younger than 12 years or 12 years and older) to receive HDM SLIT (n = 35) or placebo (n = 31) 3 days a week for the study period – between May 2018 and June 2020 – at the Clinical Research Unit of Ribeirão Preto Medical School Hospital.
At baseline, the mean SCORAD was 46.9 (range, 17-87).
After 18 months, 74.2% and 58% of patients in HDM SLIT and placebo groups, respectively, showed at least a15-point decrease in SCORAD (relative risk, 1.28; 95% confidence interval, 0.89-1.83). However, those primary outcome results did not reach statistical significance.
On the other hand, some secondary outcomes did show significant results.
At 95% CI, the researchers reported significant objective-SCORAD decreases of 56.8% and 34.9% in HDM SLIT and placebo groups (average difference, 21.3). Significantly more patients had a score of 0 or 1 on the 5-point Investigator’s Global Assessment scale in the intervention group than in the placebo group (14/35 vs. 5/31; RR, 2.63).
There were no significant changes in the Eczema Area and Severity Index, the visual analogue scale for symptoms, the pruritus scale, or the Dermatology Life Quality Index.
Patients in the trial, most of whom had moderate to severe disease, continued to be treated with usual, individualized therapy for AD, in accordance with current guidelines and experts’ recommendations.
Tina Sindher, MD, an allergist with the Sean N. Parker Center for Allergy and Asthma Research at Stanford (Calif.) University, , told this news organization that the results are not robust enough to recommend the immunotherapy widely.
She pointed out that even in the placebo group, more than half the patients met the primary endpoint.
However, she did say HDM SLIT could be considered as an add-on treatment for the right patients, especially since risk for an allergic reaction or other adverse condition is small. The most common adverse effects were headache and abdominal pain, and they were reported in both the treatment and placebo groups.
With AD, she said, “there is no one drug that’s right for everyone,” because genetics and environment make the kind of symptoms and severity and duration different for each patient.
It all comes down to risk and benefits, she said.
She said if she had a patient with an environmental allergy who’s trying to manage nasal congestion and also happened to have eczema, “I think they’re a great candidate for sublingual dust mite therapy because then not only am I treating their nasal congestions, their other symptoms, it may also help their eczema,” Dr. Sindher said.
Without those concurrent conditions, she said, the benefits of dust mite immunotherapy would not outweigh the risks or the potential burden on the patient of having to take the SLIT.
She said she would present the choice to the patient, and if other treatments haven’t been successful and the patient wants to try it, she would be open to a trial period.
The study was supported by the Brazilian National Council for Scientific and Technological Development, the Institute of Investigation in Immunology, the National Institutes of Science and Technology, the Brazilian National Council for Scientific and Technological Development, and the São Paulo Research Foundation. The mite extract for immunotherapy was provided by the laboratory IPI-ASAC Brasil/ASAC Pharma Brasil. Dr. Langer received a doctoral scholarship from the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES). Dr. Sindher reported no relevant financial relationships.
Commentary by Lawrence F. Eichenfield, MD
Environmental triggers of atopic dermatitis (AD) may be difficult to assess, especially as children with AD commonly develop “overlap” conditions of allergic rhinitis, food allergy, and asthma. The place of immunotherapy in treatment of AD has been controversial over the years, with mixed results from studies on its effect on eczema in different subpopulations. However, a holistic view of allergy care makes consideration of environmental allergies reasonable. The study by Dr. Langer and colleagues was a well-designed double-blind placebo-controlled trial of house dust mite sublingual immunotherapy in mite-sensitized AD patients aged 3 and older with at least mild AD, though the mean eczema severity was severe. After 18 months, there was an impressive 74% decrease in eczema score (SCORAD), but also a 58% decrease in the placebo group. While the primary outcome measure wasn’t statistically significant, some secondary ones were. I agree with the commentary in the article that the data doesn’t support immunotherapy being advised to everyone, while its use as an add-on treatment for certain patients in whom the eczema may overlap with other allergic manifestations is reasonable. For several years at Rady Children’s Hospital, San Diego, we have run a multidisciplinary atopic dermatitis program where patients are comanaged by dermatology and allergy. We have learned to appreciate that a broad perspective on managing comorbid conditions in children with AD really helps the patients and families to understand the many effects of inflammatory and allergic conditions, with improved outcomes and quality of life.
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. He disclosed that he has served as an investigator and/or consultant to AbbVie, Lilly, Pfizer, Regeneron, Sanofi-Genzyme, and Verrica.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
, but improvement in the primary outcome was not significant, new data show.
Results of the small, randomized, double-blind, placebo-controlled trial were published recently in The Journal of Allergy and Clinical Immunology: In Practice.
Lead author Sarah Sella Langer, MD, of the department of medicine, Ribeirão Preto (Brazil) Medical School, University of São Paulo, and colleagues said their results suggest HDM SLIT is safe and effective as an add-on treatment.
The dust mite extract therapy had no major side effects after 18 months of treatment, the authors reported.
The researchers included data from 66 patients who completed the study. The participants were at least 3 years old, registered at least 15 on the SCORing Atopic Dermatitis (SCORAD) measure, and had a skin prick test and/or immunoglobulin E (IgE) test for sensitization to dust mites.
Patients were grouped by age (younger than 12 years or 12 years and older) to receive HDM SLIT (n = 35) or placebo (n = 31) 3 days a week for the study period – between May 2018 and June 2020 – at the Clinical Research Unit of Ribeirão Preto Medical School Hospital.
At baseline, the mean SCORAD was 46.9 (range, 17-87).
After 18 months, 74.2% and 58% of patients in HDM SLIT and placebo groups, respectively, showed at least a15-point decrease in SCORAD (relative risk, 1.28; 95% confidence interval, 0.89-1.83). However, those primary outcome results did not reach statistical significance.
On the other hand, some secondary outcomes did show significant results.
At 95% CI, the researchers reported significant objective-SCORAD decreases of 56.8% and 34.9% in HDM SLIT and placebo groups (average difference, 21.3). Significantly more patients had a score of 0 or 1 on the 5-point Investigator’s Global Assessment scale in the intervention group than in the placebo group (14/35 vs. 5/31; RR, 2.63).
There were no significant changes in the Eczema Area and Severity Index, the visual analogue scale for symptoms, the pruritus scale, or the Dermatology Life Quality Index.
Patients in the trial, most of whom had moderate to severe disease, continued to be treated with usual, individualized therapy for AD, in accordance with current guidelines and experts’ recommendations.
Tina Sindher, MD, an allergist with the Sean N. Parker Center for Allergy and Asthma Research at Stanford (Calif.) University, , told this news organization that the results are not robust enough to recommend the immunotherapy widely.
She pointed out that even in the placebo group, more than half the patients met the primary endpoint.
However, she did say HDM SLIT could be considered as an add-on treatment for the right patients, especially since risk for an allergic reaction or other adverse condition is small. The most common adverse effects were headache and abdominal pain, and they were reported in both the treatment and placebo groups.
With AD, she said, “there is no one drug that’s right for everyone,” because genetics and environment make the kind of symptoms and severity and duration different for each patient.
It all comes down to risk and benefits, she said.
She said if she had a patient with an environmental allergy who’s trying to manage nasal congestion and also happened to have eczema, “I think they’re a great candidate for sublingual dust mite therapy because then not only am I treating their nasal congestions, their other symptoms, it may also help their eczema,” Dr. Sindher said.
Without those concurrent conditions, she said, the benefits of dust mite immunotherapy would not outweigh the risks or the potential burden on the patient of having to take the SLIT.
She said she would present the choice to the patient, and if other treatments haven’t been successful and the patient wants to try it, she would be open to a trial period.
The study was supported by the Brazilian National Council for Scientific and Technological Development, the Institute of Investigation in Immunology, the National Institutes of Science and Technology, the Brazilian National Council for Scientific and Technological Development, and the São Paulo Research Foundation. The mite extract for immunotherapy was provided by the laboratory IPI-ASAC Brasil/ASAC Pharma Brasil. Dr. Langer received a doctoral scholarship from the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES). Dr. Sindher reported no relevant financial relationships.
Commentary by Lawrence F. Eichenfield, MD
Environmental triggers of atopic dermatitis (AD) may be difficult to assess, especially as children with AD commonly develop “overlap” conditions of allergic rhinitis, food allergy, and asthma. The place of immunotherapy in treatment of AD has been controversial over the years, with mixed results from studies on its effect on eczema in different subpopulations. However, a holistic view of allergy care makes consideration of environmental allergies reasonable. The study by Dr. Langer and colleagues was a well-designed double-blind placebo-controlled trial of house dust mite sublingual immunotherapy in mite-sensitized AD patients aged 3 and older with at least mild AD, though the mean eczema severity was severe. After 18 months, there was an impressive 74% decrease in eczema score (SCORAD), but also a 58% decrease in the placebo group. While the primary outcome measure wasn’t statistically significant, some secondary ones were. I agree with the commentary in the article that the data doesn’t support immunotherapy being advised to everyone, while its use as an add-on treatment for certain patients in whom the eczema may overlap with other allergic manifestations is reasonable. For several years at Rady Children’s Hospital, San Diego, we have run a multidisciplinary atopic dermatitis program where patients are comanaged by dermatology and allergy. We have learned to appreciate that a broad perspective on managing comorbid conditions in children with AD really helps the patients and families to understand the many effects of inflammatory and allergic conditions, with improved outcomes and quality of life.
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. He disclosed that he has served as an investigator and/or consultant to AbbVie, Lilly, Pfizer, Regeneron, Sanofi-Genzyme, and Verrica.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
, but improvement in the primary outcome was not significant, new data show.
Results of the small, randomized, double-blind, placebo-controlled trial were published recently in The Journal of Allergy and Clinical Immunology: In Practice.
Lead author Sarah Sella Langer, MD, of the department of medicine, Ribeirão Preto (Brazil) Medical School, University of São Paulo, and colleagues said their results suggest HDM SLIT is safe and effective as an add-on treatment.
The dust mite extract therapy had no major side effects after 18 months of treatment, the authors reported.
The researchers included data from 66 patients who completed the study. The participants were at least 3 years old, registered at least 15 on the SCORing Atopic Dermatitis (SCORAD) measure, and had a skin prick test and/or immunoglobulin E (IgE) test for sensitization to dust mites.
Patients were grouped by age (younger than 12 years or 12 years and older) to receive HDM SLIT (n = 35) or placebo (n = 31) 3 days a week for the study period – between May 2018 and June 2020 – at the Clinical Research Unit of Ribeirão Preto Medical School Hospital.
At baseline, the mean SCORAD was 46.9 (range, 17-87).
After 18 months, 74.2% and 58% of patients in HDM SLIT and placebo groups, respectively, showed at least a15-point decrease in SCORAD (relative risk, 1.28; 95% confidence interval, 0.89-1.83). However, those primary outcome results did not reach statistical significance.
On the other hand, some secondary outcomes did show significant results.
At 95% CI, the researchers reported significant objective-SCORAD decreases of 56.8% and 34.9% in HDM SLIT and placebo groups (average difference, 21.3). Significantly more patients had a score of 0 or 1 on the 5-point Investigator’s Global Assessment scale in the intervention group than in the placebo group (14/35 vs. 5/31; RR, 2.63).
There were no significant changes in the Eczema Area and Severity Index, the visual analogue scale for symptoms, the pruritus scale, or the Dermatology Life Quality Index.
Patients in the trial, most of whom had moderate to severe disease, continued to be treated with usual, individualized therapy for AD, in accordance with current guidelines and experts’ recommendations.
Tina Sindher, MD, an allergist with the Sean N. Parker Center for Allergy and Asthma Research at Stanford (Calif.) University, , told this news organization that the results are not robust enough to recommend the immunotherapy widely.
She pointed out that even in the placebo group, more than half the patients met the primary endpoint.
However, she did say HDM SLIT could be considered as an add-on treatment for the right patients, especially since risk for an allergic reaction or other adverse condition is small. The most common adverse effects were headache and abdominal pain, and they were reported in both the treatment and placebo groups.
With AD, she said, “there is no one drug that’s right for everyone,” because genetics and environment make the kind of symptoms and severity and duration different for each patient.
It all comes down to risk and benefits, she said.
She said if she had a patient with an environmental allergy who’s trying to manage nasal congestion and also happened to have eczema, “I think they’re a great candidate for sublingual dust mite therapy because then not only am I treating their nasal congestions, their other symptoms, it may also help their eczema,” Dr. Sindher said.
Without those concurrent conditions, she said, the benefits of dust mite immunotherapy would not outweigh the risks or the potential burden on the patient of having to take the SLIT.
She said she would present the choice to the patient, and if other treatments haven’t been successful and the patient wants to try it, she would be open to a trial period.
The study was supported by the Brazilian National Council for Scientific and Technological Development, the Institute of Investigation in Immunology, the National Institutes of Science and Technology, the Brazilian National Council for Scientific and Technological Development, and the São Paulo Research Foundation. The mite extract for immunotherapy was provided by the laboratory IPI-ASAC Brasil/ASAC Pharma Brasil. Dr. Langer received a doctoral scholarship from the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES). Dr. Sindher reported no relevant financial relationships.
Commentary by Lawrence F. Eichenfield, MD
Environmental triggers of atopic dermatitis (AD) may be difficult to assess, especially as children with AD commonly develop “overlap” conditions of allergic rhinitis, food allergy, and asthma. The place of immunotherapy in treatment of AD has been controversial over the years, with mixed results from studies on its effect on eczema in different subpopulations. However, a holistic view of allergy care makes consideration of environmental allergies reasonable. The study by Dr. Langer and colleagues was a well-designed double-blind placebo-controlled trial of house dust mite sublingual immunotherapy in mite-sensitized AD patients aged 3 and older with at least mild AD, though the mean eczema severity was severe. After 18 months, there was an impressive 74% decrease in eczema score (SCORAD), but also a 58% decrease in the placebo group. While the primary outcome measure wasn’t statistically significant, some secondary ones were. I agree with the commentary in the article that the data doesn’t support immunotherapy being advised to everyone, while its use as an add-on treatment for certain patients in whom the eczema may overlap with other allergic manifestations is reasonable. For several years at Rady Children’s Hospital, San Diego, we have run a multidisciplinary atopic dermatitis program where patients are comanaged by dermatology and allergy. We have learned to appreciate that a broad perspective on managing comorbid conditions in children with AD really helps the patients and families to understand the many effects of inflammatory and allergic conditions, with improved outcomes and quality of life.
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. He disclosed that he has served as an investigator and/or consultant to AbbVie, Lilly, Pfizer, Regeneron, Sanofi-Genzyme, and Verrica.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
DRESS Syndrome Due to Cefdinir Mimicking Superinfected Eczema in a Pediatric Patient
To the Editor:
Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, or drug-induced hypersensitivity syndrome, is a serious and potentially fatal multiorgan drug hypersensitivity reaction. Drug reaction with eosinophilia and systemic symptoms syndrome shares many clinical features with viral exanthems and may be difficult to diagnose in the setting of atopic dermatitis (AD) in which children may have baseline eosinophilia from an atopic diathesis. The cutaneous exanthema also may be variable in presentation, further complicating diagnosis.1,2
A 3-year-old boy with AD since infancy and a history of anaphylaxis to peanuts presented to the emergency department with reported fever, rash, sore throat, and decreased oral intake. Ten days prior, the patient was treated for cellulitis of the left foot with a 7-day course of cefdinir with complete resolution of symptoms. Four days prior to admission, the patient started developing “bumps” on the face and fevers. He was seen at an outside facility, where a rapid test for Streptococcus was negative, and the patient was treated with ibuprofen and fluids for a presumed viral exanthem. The rash subsequently spread to involve the trunk and extremities. On the day of admission, the patient had a positive rapid test for Streptococcus and was referred to the emergency department with concern for superinfected eczema and eczema herpeticum. The patient recently traveled to Puerto Rico, where he had contact with an aunt with active herpes zoster but no other sick contacts. The patient’s immunizations were reported to be up-to-date.
Physical examination revealed the patient was afebrile but irritable and had erythematous crusted papules and patches on the face, arms, and legs, as well as erythematous dry patches on the chest, abdomen, and back (Figure). There were no conjunctival erythematous or oral erosions. The patient was admitted to the hospital for presumed superinfected AD and possible eczema herpeticum. He was started on intravenous clindamycin and acyclovir.
The following day, the patient had new facial edema and fever (temperature, 102.8 °F [39.36 °C]) in addition to palpable mobile cervical, axillary, and inguinal lymphadenopathy. He also was noted to have notably worsening eosinophilia from 1288 (14%) to 2570 (29.2%) cells/µL (reference range, 0%–5%) and new-onset transaminitis. Herpes and varicella-zoster direct fluorescent antibody tests, culture, and serum polymerase chain reaction were all negative, and acyclovir was discontinued. Repeat laboratory tests 12 hours later showed a continued uptrend in transaminitis. Serologies for acute and chronic cytomegalovirus; Epstein-Barr virus; and hepatitis A, B, and C were all nonreactive. The patient was started on intravenous methylprednisolone 1 mg/kg daily for suspected DRESS syndrome likely due to cefdinir.
The patient’s eosinophilia completely resolved (from approximately 2600 to 100 cells/µL) after 1 dose of steroids, and his transaminitis trended down over the next few days. He remained afebrile for the remainder of his admission, and his facial swelling and rash continued to improve. Bacterial culture from the skin grew oxacillin-susceptible Staphylococcus aureus and group A Streptococcus pyogenes. A blood culture was negative. The patient was discharged home to complete a 10-day course of clindamycin and was given topical steroids for the eczema. He continued on oral prednisolone 1 mg/kg daily for 10 days, after which the dose was tapered down for a total 1-month course of systemic corticosteroids. At 1-month follow-up after completing the course of steroids, he was doing well with normal hepatic enzyme levels and no recurrence of fever, facial edema, or rash. He continues to be followed for management of the AD.
Drug reaction with eosinophilia and systemic symptoms syndrome is a serious systemic adverse drug reaction, with high morbidity and even mortality, estimated at 10% in the adult population, though more specific pediatric mortality data are not available.1,2 The exact pathogenesis of DRESS syndrome has not been elucidated. Certain human leukocyte antigen class I alleles are predisposed to the development of DRESS syndrome, but there has not been a human leukocyte antigen subtype identified with beta-lactam–associated DRESS syndrome. Some studies have demonstrated a reactivation of human herpesvirus 6, human herpesvirus 7, and Epstein-Barr virus.3 One study involving 40 patients with DRESS syndrome identified viremia in 76% (29/38) of patients and identified CD8+ T-cell populations directed toward viral epitopes.3 Finally, DRESS syndrome may be related to the slow detoxification and elimination of intermediary products of offending medications that serve as an immunogenic stimulus for the inflammatory cascade.2
In adults, DRESS syndrome was first identified in association with phenytoin, but more recently other drugs have been identified, including other aromatic anticonvulsants (ie, lamotrigine, phenobarbital, carbamazepine), allopurinol, sulfonamides, antiretrovirals (particularly abacavir), and minocycline.2 In a 3-year pediatric prospective study, 11 cases of DRESS syndrome were identified: 4 cases due to lamotrigine, and 3 caused by penicillins.4 The trigger in our patient’s case was the beta-lactam, third-generation cephalosporin cefdinir, and his symptoms developed within 6 days of starting the medication. Many articles report that beta-lactams are a rare cause of DRESS syndrome, with only a handful of cases reported.1,5,6
The diagnosis of DRESS syndrome often can be delayed, as children present acutely febrile and toxic appearing. Unlike many adverse drug reactions, DRESS syndrome does not show rapid resolution with withdrawal of the causative agent, further complicating the diagnosis. The typical onset of DRESS syndrome generally ranges from 2 to 6 weeks after the initiation of the offending drug; however, faster onset of symptoms, similar to our case, has been noted in antibiotic-triggered cases. In the prospective pediatric series by Sasidharanpillai et al,4 the average time to onset among 3 antibiotic-triggered DRESS cases was 5.8 days vs 23.9 days among the 4 cases of lamotrigine-associated DRESS syndrome.
Our patient demonstrated the classic features of DRESS syndrome, including fever, rash, lymphadenopathy, facial edema, peripheral eosinophilia, atypical lymphocytosis, and hepatitis. Based on the proposed RegiSCAR scoring system, our patient was classified as a “definite” case of DRESS syndrome.1,7 Other hematologic findings in DRESS syndrome may include thrombocytopenia and anemia. The liver is the most commonly affected internal organ in DRESS syndrome, with pneumonitis, carditis, and nephritis reported less frequently.1 The pattern of liver injury in our patient was mixed (hepatocellular and cholestatic), the second most common pattern in patients with DRESS syndrome (the cholestatic pattern is most common).8
The exanthem of DRESS syndrome can vary in morphology, with up to 7% of patients reported to have eczemalike lesions in the multinational prospective RegiSCAR study.1 Other entities in the differential diagnosis for our patient included Kawasaki disease, where conjunctivitis and strawberry tongue are classically present, as well as erythrodermic AD, where internal organ involvement is not common.2 Our patient’s exanthem initially was considered to be a flare of AD with superimposed bacterial infection and possible eczema herpeticum. Although bacterial cultures did grow Staphylococcus and Streptococcus, viral studies were all negative, and this alone would not have explained the facial edema, rapidly rising eosinophil count, and transaminitis. The dramatic drop in his eosinophil count and decrease in hepatic enzymes after 1 dose of intravenous methylprednisolone also supported the diagnosis of DRESS syndrome.
Treatment recommendations remain largely anecdotal. Early systemic steroids generally are accepted as the first line of therapy, with a slow taper. Although the average required duration of systemic steroids in 1 series of adults was reported at 50.1 days,9 the duration was shorter (21–35 days) in a series of pediatric patients.4 Our patient’s clinical symptoms and laboratory values normalized after completing a 1-month steroid taper. Other therapies have been tried for recalcitrant cases, including intravenous immunoglobulin, plasmapheresis, rituximab, and valganciclovir.2
Early clinical recognition of the signs and symptoms of DRESS syndrome in the setting of a new medication can decrease morbidity and mortality. Although DRESS syndrome in pediatric patients presents with many similar clinical features as in adults, it may be a greater diagnostic challenge. As in adult cases, timely administration of systemic corticosteroids and tapering based on clinical signs and symptoms can lead to resolution of the hypersensitivity syndrome.
- Kardaun SH, Sekula P, Valeyrie-Allanore L, et al. Drug reaction with eosinophilia and systemic symptoms (DRESS): an original multisystem adverse drug reaction. results from the prospective RegiSCAR study. Br J Dermatol. 2013;169:1071-1080.
- Fernando SL. Drug-reaction eosinophilia and systemic symptoms and drug-induced hypersensitivity syndrome. Australas J Dermatol. 2014;55:15-23.
- Picard D, Janela B, Descamps V, et al. Drug reaction with eosinophilia and systemic symptoms (DRESS): a multiorgan antiviral T cell response. Sci Transl Med. 2010;2:46ra62.
- Sasidharanpillai S, Sabitha S, Riyaz N, et al. Drug reaction with eosinophilia and systemic symptoms in children: a prospective study. Pediatr Dermatol. 2016;33:E162-E165.
- Aouam K, Chaabane A, Toumi A, et al. Drug rash with eosinophilia and systemic symptoms (DRESS) probably induced by cefotaxime: a report of two cases. Clin Med Res. 2012;10:32-35.
- Guleria VS, Dhillon M, Gill S, et al. Ceftriaxone induced drug rash with eosinophilia and systemic symptoms. J Res Pharm Pract. 2014;3:72-74.
- Kardaun SH, Sidoroff A, Valeyrie-Allanore L, et al. Variability in the clinical pattern of cutaneous side-effects of drugs with systemic symptoms: does a DRESS syndrome really exist? Br J Dermatol. 2007;156:609-611.
- Lin IC, Yang HC, Strong C, et al. Liver injury in patients with DRESS: a clinical study of 72 cases. J Am Acad Dermatol. 2015;72:984-991.
- Ang CC, Wang YS, Yoosuff EL, et al. Retrospective analysis of drug-induced hypersensitivity syndrome: a study of 27 patients. J Am Acad Dermatol. 2010;63:219-227.
To the Editor:
Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, or drug-induced hypersensitivity syndrome, is a serious and potentially fatal multiorgan drug hypersensitivity reaction. Drug reaction with eosinophilia and systemic symptoms syndrome shares many clinical features with viral exanthems and may be difficult to diagnose in the setting of atopic dermatitis (AD) in which children may have baseline eosinophilia from an atopic diathesis. The cutaneous exanthema also may be variable in presentation, further complicating diagnosis.1,2
A 3-year-old boy with AD since infancy and a history of anaphylaxis to peanuts presented to the emergency department with reported fever, rash, sore throat, and decreased oral intake. Ten days prior, the patient was treated for cellulitis of the left foot with a 7-day course of cefdinir with complete resolution of symptoms. Four days prior to admission, the patient started developing “bumps” on the face and fevers. He was seen at an outside facility, where a rapid test for Streptococcus was negative, and the patient was treated with ibuprofen and fluids for a presumed viral exanthem. The rash subsequently spread to involve the trunk and extremities. On the day of admission, the patient had a positive rapid test for Streptococcus and was referred to the emergency department with concern for superinfected eczema and eczema herpeticum. The patient recently traveled to Puerto Rico, where he had contact with an aunt with active herpes zoster but no other sick contacts. The patient’s immunizations were reported to be up-to-date.
Physical examination revealed the patient was afebrile but irritable and had erythematous crusted papules and patches on the face, arms, and legs, as well as erythematous dry patches on the chest, abdomen, and back (Figure). There were no conjunctival erythematous or oral erosions. The patient was admitted to the hospital for presumed superinfected AD and possible eczema herpeticum. He was started on intravenous clindamycin and acyclovir.
The following day, the patient had new facial edema and fever (temperature, 102.8 °F [39.36 °C]) in addition to palpable mobile cervical, axillary, and inguinal lymphadenopathy. He also was noted to have notably worsening eosinophilia from 1288 (14%) to 2570 (29.2%) cells/µL (reference range, 0%–5%) and new-onset transaminitis. Herpes and varicella-zoster direct fluorescent antibody tests, culture, and serum polymerase chain reaction were all negative, and acyclovir was discontinued. Repeat laboratory tests 12 hours later showed a continued uptrend in transaminitis. Serologies for acute and chronic cytomegalovirus; Epstein-Barr virus; and hepatitis A, B, and C were all nonreactive. The patient was started on intravenous methylprednisolone 1 mg/kg daily for suspected DRESS syndrome likely due to cefdinir.
The patient’s eosinophilia completely resolved (from approximately 2600 to 100 cells/µL) after 1 dose of steroids, and his transaminitis trended down over the next few days. He remained afebrile for the remainder of his admission, and his facial swelling and rash continued to improve. Bacterial culture from the skin grew oxacillin-susceptible Staphylococcus aureus and group A Streptococcus pyogenes. A blood culture was negative. The patient was discharged home to complete a 10-day course of clindamycin and was given topical steroids for the eczema. He continued on oral prednisolone 1 mg/kg daily for 10 days, after which the dose was tapered down for a total 1-month course of systemic corticosteroids. At 1-month follow-up after completing the course of steroids, he was doing well with normal hepatic enzyme levels and no recurrence of fever, facial edema, or rash. He continues to be followed for management of the AD.
Drug reaction with eosinophilia and systemic symptoms syndrome is a serious systemic adverse drug reaction, with high morbidity and even mortality, estimated at 10% in the adult population, though more specific pediatric mortality data are not available.1,2 The exact pathogenesis of DRESS syndrome has not been elucidated. Certain human leukocyte antigen class I alleles are predisposed to the development of DRESS syndrome, but there has not been a human leukocyte antigen subtype identified with beta-lactam–associated DRESS syndrome. Some studies have demonstrated a reactivation of human herpesvirus 6, human herpesvirus 7, and Epstein-Barr virus.3 One study involving 40 patients with DRESS syndrome identified viremia in 76% (29/38) of patients and identified CD8+ T-cell populations directed toward viral epitopes.3 Finally, DRESS syndrome may be related to the slow detoxification and elimination of intermediary products of offending medications that serve as an immunogenic stimulus for the inflammatory cascade.2
In adults, DRESS syndrome was first identified in association with phenytoin, but more recently other drugs have been identified, including other aromatic anticonvulsants (ie, lamotrigine, phenobarbital, carbamazepine), allopurinol, sulfonamides, antiretrovirals (particularly abacavir), and minocycline.2 In a 3-year pediatric prospective study, 11 cases of DRESS syndrome were identified: 4 cases due to lamotrigine, and 3 caused by penicillins.4 The trigger in our patient’s case was the beta-lactam, third-generation cephalosporin cefdinir, and his symptoms developed within 6 days of starting the medication. Many articles report that beta-lactams are a rare cause of DRESS syndrome, with only a handful of cases reported.1,5,6
The diagnosis of DRESS syndrome often can be delayed, as children present acutely febrile and toxic appearing. Unlike many adverse drug reactions, DRESS syndrome does not show rapid resolution with withdrawal of the causative agent, further complicating the diagnosis. The typical onset of DRESS syndrome generally ranges from 2 to 6 weeks after the initiation of the offending drug; however, faster onset of symptoms, similar to our case, has been noted in antibiotic-triggered cases. In the prospective pediatric series by Sasidharanpillai et al,4 the average time to onset among 3 antibiotic-triggered DRESS cases was 5.8 days vs 23.9 days among the 4 cases of lamotrigine-associated DRESS syndrome.
Our patient demonstrated the classic features of DRESS syndrome, including fever, rash, lymphadenopathy, facial edema, peripheral eosinophilia, atypical lymphocytosis, and hepatitis. Based on the proposed RegiSCAR scoring system, our patient was classified as a “definite” case of DRESS syndrome.1,7 Other hematologic findings in DRESS syndrome may include thrombocytopenia and anemia. The liver is the most commonly affected internal organ in DRESS syndrome, with pneumonitis, carditis, and nephritis reported less frequently.1 The pattern of liver injury in our patient was mixed (hepatocellular and cholestatic), the second most common pattern in patients with DRESS syndrome (the cholestatic pattern is most common).8
The exanthem of DRESS syndrome can vary in morphology, with up to 7% of patients reported to have eczemalike lesions in the multinational prospective RegiSCAR study.1 Other entities in the differential diagnosis for our patient included Kawasaki disease, where conjunctivitis and strawberry tongue are classically present, as well as erythrodermic AD, where internal organ involvement is not common.2 Our patient’s exanthem initially was considered to be a flare of AD with superimposed bacterial infection and possible eczema herpeticum. Although bacterial cultures did grow Staphylococcus and Streptococcus, viral studies were all negative, and this alone would not have explained the facial edema, rapidly rising eosinophil count, and transaminitis. The dramatic drop in his eosinophil count and decrease in hepatic enzymes after 1 dose of intravenous methylprednisolone also supported the diagnosis of DRESS syndrome.
Treatment recommendations remain largely anecdotal. Early systemic steroids generally are accepted as the first line of therapy, with a slow taper. Although the average required duration of systemic steroids in 1 series of adults was reported at 50.1 days,9 the duration was shorter (21–35 days) in a series of pediatric patients.4 Our patient’s clinical symptoms and laboratory values normalized after completing a 1-month steroid taper. Other therapies have been tried for recalcitrant cases, including intravenous immunoglobulin, plasmapheresis, rituximab, and valganciclovir.2
Early clinical recognition of the signs and symptoms of DRESS syndrome in the setting of a new medication can decrease morbidity and mortality. Although DRESS syndrome in pediatric patients presents with many similar clinical features as in adults, it may be a greater diagnostic challenge. As in adult cases, timely administration of systemic corticosteroids and tapering based on clinical signs and symptoms can lead to resolution of the hypersensitivity syndrome.
To the Editor:
Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, or drug-induced hypersensitivity syndrome, is a serious and potentially fatal multiorgan drug hypersensitivity reaction. Drug reaction with eosinophilia and systemic symptoms syndrome shares many clinical features with viral exanthems and may be difficult to diagnose in the setting of atopic dermatitis (AD) in which children may have baseline eosinophilia from an atopic diathesis. The cutaneous exanthema also may be variable in presentation, further complicating diagnosis.1,2
A 3-year-old boy with AD since infancy and a history of anaphylaxis to peanuts presented to the emergency department with reported fever, rash, sore throat, and decreased oral intake. Ten days prior, the patient was treated for cellulitis of the left foot with a 7-day course of cefdinir with complete resolution of symptoms. Four days prior to admission, the patient started developing “bumps” on the face and fevers. He was seen at an outside facility, where a rapid test for Streptococcus was negative, and the patient was treated with ibuprofen and fluids for a presumed viral exanthem. The rash subsequently spread to involve the trunk and extremities. On the day of admission, the patient had a positive rapid test for Streptococcus and was referred to the emergency department with concern for superinfected eczema and eczema herpeticum. The patient recently traveled to Puerto Rico, where he had contact with an aunt with active herpes zoster but no other sick contacts. The patient’s immunizations were reported to be up-to-date.
Physical examination revealed the patient was afebrile but irritable and had erythematous crusted papules and patches on the face, arms, and legs, as well as erythematous dry patches on the chest, abdomen, and back (Figure). There were no conjunctival erythematous or oral erosions. The patient was admitted to the hospital for presumed superinfected AD and possible eczema herpeticum. He was started on intravenous clindamycin and acyclovir.
The following day, the patient had new facial edema and fever (temperature, 102.8 °F [39.36 °C]) in addition to palpable mobile cervical, axillary, and inguinal lymphadenopathy. He also was noted to have notably worsening eosinophilia from 1288 (14%) to 2570 (29.2%) cells/µL (reference range, 0%–5%) and new-onset transaminitis. Herpes and varicella-zoster direct fluorescent antibody tests, culture, and serum polymerase chain reaction were all negative, and acyclovir was discontinued. Repeat laboratory tests 12 hours later showed a continued uptrend in transaminitis. Serologies for acute and chronic cytomegalovirus; Epstein-Barr virus; and hepatitis A, B, and C were all nonreactive. The patient was started on intravenous methylprednisolone 1 mg/kg daily for suspected DRESS syndrome likely due to cefdinir.
The patient’s eosinophilia completely resolved (from approximately 2600 to 100 cells/µL) after 1 dose of steroids, and his transaminitis trended down over the next few days. He remained afebrile for the remainder of his admission, and his facial swelling and rash continued to improve. Bacterial culture from the skin grew oxacillin-susceptible Staphylococcus aureus and group A Streptococcus pyogenes. A blood culture was negative. The patient was discharged home to complete a 10-day course of clindamycin and was given topical steroids for the eczema. He continued on oral prednisolone 1 mg/kg daily for 10 days, after which the dose was tapered down for a total 1-month course of systemic corticosteroids. At 1-month follow-up after completing the course of steroids, he was doing well with normal hepatic enzyme levels and no recurrence of fever, facial edema, or rash. He continues to be followed for management of the AD.
Drug reaction with eosinophilia and systemic symptoms syndrome is a serious systemic adverse drug reaction, with high morbidity and even mortality, estimated at 10% in the adult population, though more specific pediatric mortality data are not available.1,2 The exact pathogenesis of DRESS syndrome has not been elucidated. Certain human leukocyte antigen class I alleles are predisposed to the development of DRESS syndrome, but there has not been a human leukocyte antigen subtype identified with beta-lactam–associated DRESS syndrome. Some studies have demonstrated a reactivation of human herpesvirus 6, human herpesvirus 7, and Epstein-Barr virus.3 One study involving 40 patients with DRESS syndrome identified viremia in 76% (29/38) of patients and identified CD8+ T-cell populations directed toward viral epitopes.3 Finally, DRESS syndrome may be related to the slow detoxification and elimination of intermediary products of offending medications that serve as an immunogenic stimulus for the inflammatory cascade.2
In adults, DRESS syndrome was first identified in association with phenytoin, but more recently other drugs have been identified, including other aromatic anticonvulsants (ie, lamotrigine, phenobarbital, carbamazepine), allopurinol, sulfonamides, antiretrovirals (particularly abacavir), and minocycline.2 In a 3-year pediatric prospective study, 11 cases of DRESS syndrome were identified: 4 cases due to lamotrigine, and 3 caused by penicillins.4 The trigger in our patient’s case was the beta-lactam, third-generation cephalosporin cefdinir, and his symptoms developed within 6 days of starting the medication. Many articles report that beta-lactams are a rare cause of DRESS syndrome, with only a handful of cases reported.1,5,6
The diagnosis of DRESS syndrome often can be delayed, as children present acutely febrile and toxic appearing. Unlike many adverse drug reactions, DRESS syndrome does not show rapid resolution with withdrawal of the causative agent, further complicating the diagnosis. The typical onset of DRESS syndrome generally ranges from 2 to 6 weeks after the initiation of the offending drug; however, faster onset of symptoms, similar to our case, has been noted in antibiotic-triggered cases. In the prospective pediatric series by Sasidharanpillai et al,4 the average time to onset among 3 antibiotic-triggered DRESS cases was 5.8 days vs 23.9 days among the 4 cases of lamotrigine-associated DRESS syndrome.
Our patient demonstrated the classic features of DRESS syndrome, including fever, rash, lymphadenopathy, facial edema, peripheral eosinophilia, atypical lymphocytosis, and hepatitis. Based on the proposed RegiSCAR scoring system, our patient was classified as a “definite” case of DRESS syndrome.1,7 Other hematologic findings in DRESS syndrome may include thrombocytopenia and anemia. The liver is the most commonly affected internal organ in DRESS syndrome, with pneumonitis, carditis, and nephritis reported less frequently.1 The pattern of liver injury in our patient was mixed (hepatocellular and cholestatic), the second most common pattern in patients with DRESS syndrome (the cholestatic pattern is most common).8
The exanthem of DRESS syndrome can vary in morphology, with up to 7% of patients reported to have eczemalike lesions in the multinational prospective RegiSCAR study.1 Other entities in the differential diagnosis for our patient included Kawasaki disease, where conjunctivitis and strawberry tongue are classically present, as well as erythrodermic AD, where internal organ involvement is not common.2 Our patient’s exanthem initially was considered to be a flare of AD with superimposed bacterial infection and possible eczema herpeticum. Although bacterial cultures did grow Staphylococcus and Streptococcus, viral studies were all negative, and this alone would not have explained the facial edema, rapidly rising eosinophil count, and transaminitis. The dramatic drop in his eosinophil count and decrease in hepatic enzymes after 1 dose of intravenous methylprednisolone also supported the diagnosis of DRESS syndrome.
Treatment recommendations remain largely anecdotal. Early systemic steroids generally are accepted as the first line of therapy, with a slow taper. Although the average required duration of systemic steroids in 1 series of adults was reported at 50.1 days,9 the duration was shorter (21–35 days) in a series of pediatric patients.4 Our patient’s clinical symptoms and laboratory values normalized after completing a 1-month steroid taper. Other therapies have been tried for recalcitrant cases, including intravenous immunoglobulin, plasmapheresis, rituximab, and valganciclovir.2
Early clinical recognition of the signs and symptoms of DRESS syndrome in the setting of a new medication can decrease morbidity and mortality. Although DRESS syndrome in pediatric patients presents with many similar clinical features as in adults, it may be a greater diagnostic challenge. As in adult cases, timely administration of systemic corticosteroids and tapering based on clinical signs and symptoms can lead to resolution of the hypersensitivity syndrome.
- Kardaun SH, Sekula P, Valeyrie-Allanore L, et al. Drug reaction with eosinophilia and systemic symptoms (DRESS): an original multisystem adverse drug reaction. results from the prospective RegiSCAR study. Br J Dermatol. 2013;169:1071-1080.
- Fernando SL. Drug-reaction eosinophilia and systemic symptoms and drug-induced hypersensitivity syndrome. Australas J Dermatol. 2014;55:15-23.
- Picard D, Janela B, Descamps V, et al. Drug reaction with eosinophilia and systemic symptoms (DRESS): a multiorgan antiviral T cell response. Sci Transl Med. 2010;2:46ra62.
- Sasidharanpillai S, Sabitha S, Riyaz N, et al. Drug reaction with eosinophilia and systemic symptoms in children: a prospective study. Pediatr Dermatol. 2016;33:E162-E165.
- Aouam K, Chaabane A, Toumi A, et al. Drug rash with eosinophilia and systemic symptoms (DRESS) probably induced by cefotaxime: a report of two cases. Clin Med Res. 2012;10:32-35.
- Guleria VS, Dhillon M, Gill S, et al. Ceftriaxone induced drug rash with eosinophilia and systemic symptoms. J Res Pharm Pract. 2014;3:72-74.
- Kardaun SH, Sidoroff A, Valeyrie-Allanore L, et al. Variability in the clinical pattern of cutaneous side-effects of drugs with systemic symptoms: does a DRESS syndrome really exist? Br J Dermatol. 2007;156:609-611.
- Lin IC, Yang HC, Strong C, et al. Liver injury in patients with DRESS: a clinical study of 72 cases. J Am Acad Dermatol. 2015;72:984-991.
- Ang CC, Wang YS, Yoosuff EL, et al. Retrospective analysis of drug-induced hypersensitivity syndrome: a study of 27 patients. J Am Acad Dermatol. 2010;63:219-227.
- Kardaun SH, Sekula P, Valeyrie-Allanore L, et al. Drug reaction with eosinophilia and systemic symptoms (DRESS): an original multisystem adverse drug reaction. results from the prospective RegiSCAR study. Br J Dermatol. 2013;169:1071-1080.
- Fernando SL. Drug-reaction eosinophilia and systemic symptoms and drug-induced hypersensitivity syndrome. Australas J Dermatol. 2014;55:15-23.
- Picard D, Janela B, Descamps V, et al. Drug reaction with eosinophilia and systemic symptoms (DRESS): a multiorgan antiviral T cell response. Sci Transl Med. 2010;2:46ra62.
- Sasidharanpillai S, Sabitha S, Riyaz N, et al. Drug reaction with eosinophilia and systemic symptoms in children: a prospective study. Pediatr Dermatol. 2016;33:E162-E165.
- Aouam K, Chaabane A, Toumi A, et al. Drug rash with eosinophilia and systemic symptoms (DRESS) probably induced by cefotaxime: a report of two cases. Clin Med Res. 2012;10:32-35.
- Guleria VS, Dhillon M, Gill S, et al. Ceftriaxone induced drug rash with eosinophilia and systemic symptoms. J Res Pharm Pract. 2014;3:72-74.
- Kardaun SH, Sidoroff A, Valeyrie-Allanore L, et al. Variability in the clinical pattern of cutaneous side-effects of drugs with systemic symptoms: does a DRESS syndrome really exist? Br J Dermatol. 2007;156:609-611.
- Lin IC, Yang HC, Strong C, et al. Liver injury in patients with DRESS: a clinical study of 72 cases. J Am Acad Dermatol. 2015;72:984-991.
- Ang CC, Wang YS, Yoosuff EL, et al. Retrospective analysis of drug-induced hypersensitivity syndrome: a study of 27 patients. J Am Acad Dermatol. 2010;63:219-227.
Practice Points
- Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome shares many clinical features with viral exanthems and may be difficult to diagnose in the setting of atopic dermatitis in which children may have baseline eosinophilia from an atopic diathesis.
- Early clinical recognition of the signs and symptoms of DRESS syndrome in the setting of a new medication can decrease morbidity and mortality.
Expert shares top five atopic dermatitis–related questions he fields
Will my child outgrow the eczema?
That is perhaps the No. 1 atopic dermatitis–related question that Lawrence F. Eichenfield, MD, fields from parents in his role as chief of pediatric and adolescent dermatology at Rady’s Children’s Hospital, San Diego.
The answer “is pretty tricky,” he said during MedscapeLive’s annual Las Vegas Dermatology Seminar. “We used to say, ‘yeah, your kid will probably outgrow the disease,’ but we now have good data that show there are variable courses.”
Using data from the birth study cohort known as the Avon Longitudinal Study of Parents and Children, researchers in the United Kingdom investigated the existence of different longitudinal phenotypes of AD among 9,894 children. They found that 58% of the children in the cohort were unaffected or had transient AD, while 12.9% had early-onset/early-resolving AD. The remaining AD phenotypes consisted of 7%-8% patients each (early-onset persistent, early-onset late-resolving, mid-onset resolving, and late-onset resolving).
“There have been several studies that looked at the natural course of AD,” said Dr. Eichenfield, distinguished professor of dermatology and pediatrics at the University of California, San Diego. “A cohort study from Thailand showed that 50% of patients with childhood AD lost their AD diagnosis about 5 years into it, while there was an increase in allergic rhino-conjunctivitis and asthma, similar to what’s been seen in atopic march studies,” he noted.
A separate group of investigators analyzed records from The Health Improvement Network in the UK to determine the prevalence of AD among more than 8 million patients seen in primary care between 1994 and 2013. They found that the cumulative lifetime prevalence of atopic eczema was 9.9% and the highest rates of active disease were among children and older adults. “The takeaway was markedly inconsistent in terms of whether AD went away over time or increased over time, so it’s really not especially helpful prevalence data,” Dr. Eichenfield said. “Overall, you have a high prevalence in the first years of life, it decreases, and it may increase again when people are 60 years and older. Whether that’s truly AD or xerotic eczema isn’t known in this data set.”
A separate meta-analysis of 17 studies reported that 26% of adults with AD said they had adult-onset disease, which is characterized by more atopy, more foot dermatitis, and less flexural involvement.
Dr. Eichenfield tells parents, “there’s a really good chance (depending on disease severity) that 60% to 70% of children will outgrow their eczema or most of it,” he said. “If you ask me when, I won’t tell you. The important thing is to treat it to minimize its impact. We want minimal rash, minimal itch, and minimal sleep disturbance. Sometimes I say, ‘that might improve the chance of the eczema getting better over time.’ ”
Following are four other common questions parents and patients ask him:
Can we figure out the allergies causing the eczema? “This is probably one of the most unnerving questions I get asked,” he said. “It’s a loaded question. My answer is that allergies are intertwined with AD. Searching for the secret allergy causing the atopic dermatitis is rarely successful.” Sensitization is much more common with AD, he added, meaning specific IgE testing, whether it be blood testing or skin prick testing. “The more severe your eczema is, the more chance you’ll have of real food allergy,” he said. “About 15% of milder eczema patients will have at least one food allergy, but when you get to the more moderate to severe cases, about 40% will have a true food allergy.”
Food reactions may not cause eczema, though. Food reactions can cause urticaria, angioedema, eczematous dermatitis, allergic contact dermatitis, contact urticaria, and respiratory findings. According to National Institutes of Health guidelines for food allergy, skin prick tests and serum IgE tests are recommended to assist in identification of foods that may be provoking IgE-mediated food reactions, but are not diagnostic of food allergy.
“There’s a huge literature showing that there’s a lot of food allergy testing that’s just not helpful,” he said. In one study, 89% of food challenges administered in patients who were listed as being allergic based on skin prick tests or serum IgE tests did not have a true food allergy.
“Empiric elimination diets aren’t especially useful. However, we occasionally see children who do have AD exacerbated by food allergies in the first year of life,” he said. NIH guidelines suggest that children younger than 5 years of age with moderate to severe AD be considered for food allergy evaluation for milk, egg, peanut, wheat, and soy, if at least one of the following conditions is met: the child has persistent AD in spite of optimized management and topical therapy, and/or the child has a reliable history of an immediate reaction after ingestion of a specific food.
“We do know that there are high rates of comorbid allergic processes, besides food allergy, associated with atopic dermatitis, including allergic rhinitis and asthma both in children and adults,” Dr. Eichenfield said. “I do discuss allergy triggers and their importance in the life of the individual, though not necessarily as factors in AD. There are a variety of environmental allergens and/or environmental triggers that can significantly impact AD. Recently, we have seen studies discussing air pollution and wildfires as exacerbators of AD.”
How should I bathe and moisturize? There are no standard guidelines for the frequency, type, or duration of bathing in patients with AD, he said, though in more severe disease, frequent bathing can be helpful along with standard anti-inflammatory topical medicines. “I keep my general recommendations vague,” Dr. Eichenfield said. “I do explain that we don’t want to use harsh soaps; we want to be gentle in our washing. I usually recommend daily to every other day bathing. It’s important to pat the skin dry and then apply a moisturizer. Applying a moisturizer 2-3 minutes after bathing is important and limited significant cleanser use can be helpful.”
Moisturizers and emollients are a standard of care in U.S. guidelines published in 2013 and 2014, and international guidelines, and are steroid-sparing and useful for both prevention and maintenance. “I tell parents and patients that there is no reason to avoid bathing because of AD as long as you moisturize after,” he said.
Do I have to use topical [name of drug]? “I try to explain that there is skin barrier dysfunction that stimulates the inflammatory milieu, and that inflammation in the skin or blood in AD negatively impacts skin barrier function,” Dr. Eichenfield said. “I explain that if inflammation doesn’t get better with good skin care, moisturizers, and avoidance of triggers, we need anti-inflammatory medication. Then we discuss what the options are, the significant variation in strengths of topical corticosteroids, and topical nonsteroid options.”
When he counsels parents and patients on the use of topical corticosteroids, he tells them that cortisone is a naturally-occurring metabolite, and that “we can work together to let you know how much medicine to use, and how a safe amount is a powerful tool to fix the eczema.” He often says that topical steroids “are like hammers. We have tiny hammers, like over-the-counter hydrocortisone, and sledgehammers like clobetasol. We also have ‘screwdrivers’ and ‘pliers’ with nonsteroidal topical calcineurin and PDE-4 inhibitors, which are especially useful for maintenance therapy. Topical ruxolitinib is a new medicine that we may use for patients as well. The label includes discussion of side effects from oral JAK inhibitors as well as from the drug development program, so it takes some time to talk through.”
Is it time for a stronger systemic medicine? Any conversation about this topic should support the concept that the AD is multifactorial. “We have the rash of eczema,” he said. “We have the itch. We have impact on sleep disturbance. We have the comorbidities. We have other physical changes, which can happen with bacterial infections and other immune system or cardiovascular changes. We have the impact on quality of life and impact on school and work. When we recognize that if patients have significant enough disease that it is not getting better with topicals and is having a negative impact on their lives, we can move our discussion to systemic therapy.”
When counseling patients about systemic therapy, Dr. Eichenfield will conduct a body surface area assessment and document how bad the itch is. “But I’m not just recording the information; I’m bringing it out in the room,” he said. “I’ll do a BSA assessment and say, for example, ‘oh, you have 32% of your body involved with eczema.’ I ask about sleep disturbance, to get the answer ‘out in the room.’ ” He also asks questions such as: “When was the last time your skin was last totally clear? Are there activities that you or your family don’t do because of your eczema, or that you’re living your life around it? Is there anxiety or depression?” Documenting both the impact on quality of life and the severity of disease “makes it easier to discuss systemic therapy,” Dr. Eichenfield said. “Meanwhile, as the provider, I am trying to figure out if the patient should ‘go into the topical therapy bucket’ or into the ‘systemic therapy bucket.’ ”
Counseling about systemic therapy includes shared decision-making regarding the choice of biologics versus oral JAK inhibitors versus traditional systemic agent or phototherapy. Factors to consider in the decision making include patient age, sex, severity, comorbidities, prior therapy, risk aversion, duration, medication access, and desired efficacy. “Evolving therapies can change the conversation, the questions, and the outcomes, but the overarching desired outcome is long-term disease control, minimal eczematous rash, minimal pruritus, and minimal sleep disturbance,” he said.
Dr. Eichenfield disclosed that he has served as a consultant to or investigator for AbbVie; Almirall; Arcutis; Arena; Asana; Termagant; Dermira; Forte Biosciences; Galderma Laboratories; Glenmark/Chinos; Incyte; Kyowa Kirin; Leo Pharma; Eli Lilly and Company; Novartis; Ortho Dermatology; Otsuka; Pfizer; Freestone; Regeneron, and Sanofi Genzyme.
MedscapeLive and this news organization are owned by the same parent company.
Will my child outgrow the eczema?
That is perhaps the No. 1 atopic dermatitis–related question that Lawrence F. Eichenfield, MD, fields from parents in his role as chief of pediatric and adolescent dermatology at Rady’s Children’s Hospital, San Diego.
The answer “is pretty tricky,” he said during MedscapeLive’s annual Las Vegas Dermatology Seminar. “We used to say, ‘yeah, your kid will probably outgrow the disease,’ but we now have good data that show there are variable courses.”
Using data from the birth study cohort known as the Avon Longitudinal Study of Parents and Children, researchers in the United Kingdom investigated the existence of different longitudinal phenotypes of AD among 9,894 children. They found that 58% of the children in the cohort were unaffected or had transient AD, while 12.9% had early-onset/early-resolving AD. The remaining AD phenotypes consisted of 7%-8% patients each (early-onset persistent, early-onset late-resolving, mid-onset resolving, and late-onset resolving).
“There have been several studies that looked at the natural course of AD,” said Dr. Eichenfield, distinguished professor of dermatology and pediatrics at the University of California, San Diego. “A cohort study from Thailand showed that 50% of patients with childhood AD lost their AD diagnosis about 5 years into it, while there was an increase in allergic rhino-conjunctivitis and asthma, similar to what’s been seen in atopic march studies,” he noted.
A separate group of investigators analyzed records from The Health Improvement Network in the UK to determine the prevalence of AD among more than 8 million patients seen in primary care between 1994 and 2013. They found that the cumulative lifetime prevalence of atopic eczema was 9.9% and the highest rates of active disease were among children and older adults. “The takeaway was markedly inconsistent in terms of whether AD went away over time or increased over time, so it’s really not especially helpful prevalence data,” Dr. Eichenfield said. “Overall, you have a high prevalence in the first years of life, it decreases, and it may increase again when people are 60 years and older. Whether that’s truly AD or xerotic eczema isn’t known in this data set.”
A separate meta-analysis of 17 studies reported that 26% of adults with AD said they had adult-onset disease, which is characterized by more atopy, more foot dermatitis, and less flexural involvement.
Dr. Eichenfield tells parents, “there’s a really good chance (depending on disease severity) that 60% to 70% of children will outgrow their eczema or most of it,” he said. “If you ask me when, I won’t tell you. The important thing is to treat it to minimize its impact. We want minimal rash, minimal itch, and minimal sleep disturbance. Sometimes I say, ‘that might improve the chance of the eczema getting better over time.’ ”
Following are four other common questions parents and patients ask him:
Can we figure out the allergies causing the eczema? “This is probably one of the most unnerving questions I get asked,” he said. “It’s a loaded question. My answer is that allergies are intertwined with AD. Searching for the secret allergy causing the atopic dermatitis is rarely successful.” Sensitization is much more common with AD, he added, meaning specific IgE testing, whether it be blood testing or skin prick testing. “The more severe your eczema is, the more chance you’ll have of real food allergy,” he said. “About 15% of milder eczema patients will have at least one food allergy, but when you get to the more moderate to severe cases, about 40% will have a true food allergy.”
Food reactions may not cause eczema, though. Food reactions can cause urticaria, angioedema, eczematous dermatitis, allergic contact dermatitis, contact urticaria, and respiratory findings. According to National Institutes of Health guidelines for food allergy, skin prick tests and serum IgE tests are recommended to assist in identification of foods that may be provoking IgE-mediated food reactions, but are not diagnostic of food allergy.
“There’s a huge literature showing that there’s a lot of food allergy testing that’s just not helpful,” he said. In one study, 89% of food challenges administered in patients who were listed as being allergic based on skin prick tests or serum IgE tests did not have a true food allergy.
“Empiric elimination diets aren’t especially useful. However, we occasionally see children who do have AD exacerbated by food allergies in the first year of life,” he said. NIH guidelines suggest that children younger than 5 years of age with moderate to severe AD be considered for food allergy evaluation for milk, egg, peanut, wheat, and soy, if at least one of the following conditions is met: the child has persistent AD in spite of optimized management and topical therapy, and/or the child has a reliable history of an immediate reaction after ingestion of a specific food.
“We do know that there are high rates of comorbid allergic processes, besides food allergy, associated with atopic dermatitis, including allergic rhinitis and asthma both in children and adults,” Dr. Eichenfield said. “I do discuss allergy triggers and their importance in the life of the individual, though not necessarily as factors in AD. There are a variety of environmental allergens and/or environmental triggers that can significantly impact AD. Recently, we have seen studies discussing air pollution and wildfires as exacerbators of AD.”
How should I bathe and moisturize? There are no standard guidelines for the frequency, type, or duration of bathing in patients with AD, he said, though in more severe disease, frequent bathing can be helpful along with standard anti-inflammatory topical medicines. “I keep my general recommendations vague,” Dr. Eichenfield said. “I do explain that we don’t want to use harsh soaps; we want to be gentle in our washing. I usually recommend daily to every other day bathing. It’s important to pat the skin dry and then apply a moisturizer. Applying a moisturizer 2-3 minutes after bathing is important and limited significant cleanser use can be helpful.”
Moisturizers and emollients are a standard of care in U.S. guidelines published in 2013 and 2014, and international guidelines, and are steroid-sparing and useful for both prevention and maintenance. “I tell parents and patients that there is no reason to avoid bathing because of AD as long as you moisturize after,” he said.
Do I have to use topical [name of drug]? “I try to explain that there is skin barrier dysfunction that stimulates the inflammatory milieu, and that inflammation in the skin or blood in AD negatively impacts skin barrier function,” Dr. Eichenfield said. “I explain that if inflammation doesn’t get better with good skin care, moisturizers, and avoidance of triggers, we need anti-inflammatory medication. Then we discuss what the options are, the significant variation in strengths of topical corticosteroids, and topical nonsteroid options.”
When he counsels parents and patients on the use of topical corticosteroids, he tells them that cortisone is a naturally-occurring metabolite, and that “we can work together to let you know how much medicine to use, and how a safe amount is a powerful tool to fix the eczema.” He often says that topical steroids “are like hammers. We have tiny hammers, like over-the-counter hydrocortisone, and sledgehammers like clobetasol. We also have ‘screwdrivers’ and ‘pliers’ with nonsteroidal topical calcineurin and PDE-4 inhibitors, which are especially useful for maintenance therapy. Topical ruxolitinib is a new medicine that we may use for patients as well. The label includes discussion of side effects from oral JAK inhibitors as well as from the drug development program, so it takes some time to talk through.”
Is it time for a stronger systemic medicine? Any conversation about this topic should support the concept that the AD is multifactorial. “We have the rash of eczema,” he said. “We have the itch. We have impact on sleep disturbance. We have the comorbidities. We have other physical changes, which can happen with bacterial infections and other immune system or cardiovascular changes. We have the impact on quality of life and impact on school and work. When we recognize that if patients have significant enough disease that it is not getting better with topicals and is having a negative impact on their lives, we can move our discussion to systemic therapy.”
When counseling patients about systemic therapy, Dr. Eichenfield will conduct a body surface area assessment and document how bad the itch is. “But I’m not just recording the information; I’m bringing it out in the room,” he said. “I’ll do a BSA assessment and say, for example, ‘oh, you have 32% of your body involved with eczema.’ I ask about sleep disturbance, to get the answer ‘out in the room.’ ” He also asks questions such as: “When was the last time your skin was last totally clear? Are there activities that you or your family don’t do because of your eczema, or that you’re living your life around it? Is there anxiety or depression?” Documenting both the impact on quality of life and the severity of disease “makes it easier to discuss systemic therapy,” Dr. Eichenfield said. “Meanwhile, as the provider, I am trying to figure out if the patient should ‘go into the topical therapy bucket’ or into the ‘systemic therapy bucket.’ ”
Counseling about systemic therapy includes shared decision-making regarding the choice of biologics versus oral JAK inhibitors versus traditional systemic agent or phototherapy. Factors to consider in the decision making include patient age, sex, severity, comorbidities, prior therapy, risk aversion, duration, medication access, and desired efficacy. “Evolving therapies can change the conversation, the questions, and the outcomes, but the overarching desired outcome is long-term disease control, minimal eczematous rash, minimal pruritus, and minimal sleep disturbance,” he said.
Dr. Eichenfield disclosed that he has served as a consultant to or investigator for AbbVie; Almirall; Arcutis; Arena; Asana; Termagant; Dermira; Forte Biosciences; Galderma Laboratories; Glenmark/Chinos; Incyte; Kyowa Kirin; Leo Pharma; Eli Lilly and Company; Novartis; Ortho Dermatology; Otsuka; Pfizer; Freestone; Regeneron, and Sanofi Genzyme.
MedscapeLive and this news organization are owned by the same parent company.
Will my child outgrow the eczema?
That is perhaps the No. 1 atopic dermatitis–related question that Lawrence F. Eichenfield, MD, fields from parents in his role as chief of pediatric and adolescent dermatology at Rady’s Children’s Hospital, San Diego.
The answer “is pretty tricky,” he said during MedscapeLive’s annual Las Vegas Dermatology Seminar. “We used to say, ‘yeah, your kid will probably outgrow the disease,’ but we now have good data that show there are variable courses.”
Using data from the birth study cohort known as the Avon Longitudinal Study of Parents and Children, researchers in the United Kingdom investigated the existence of different longitudinal phenotypes of AD among 9,894 children. They found that 58% of the children in the cohort were unaffected or had transient AD, while 12.9% had early-onset/early-resolving AD. The remaining AD phenotypes consisted of 7%-8% patients each (early-onset persistent, early-onset late-resolving, mid-onset resolving, and late-onset resolving).
“There have been several studies that looked at the natural course of AD,” said Dr. Eichenfield, distinguished professor of dermatology and pediatrics at the University of California, San Diego. “A cohort study from Thailand showed that 50% of patients with childhood AD lost their AD diagnosis about 5 years into it, while there was an increase in allergic rhino-conjunctivitis and asthma, similar to what’s been seen in atopic march studies,” he noted.
A separate group of investigators analyzed records from The Health Improvement Network in the UK to determine the prevalence of AD among more than 8 million patients seen in primary care between 1994 and 2013. They found that the cumulative lifetime prevalence of atopic eczema was 9.9% and the highest rates of active disease were among children and older adults. “The takeaway was markedly inconsistent in terms of whether AD went away over time or increased over time, so it’s really not especially helpful prevalence data,” Dr. Eichenfield said. “Overall, you have a high prevalence in the first years of life, it decreases, and it may increase again when people are 60 years and older. Whether that’s truly AD or xerotic eczema isn’t known in this data set.”
A separate meta-analysis of 17 studies reported that 26% of adults with AD said they had adult-onset disease, which is characterized by more atopy, more foot dermatitis, and less flexural involvement.
Dr. Eichenfield tells parents, “there’s a really good chance (depending on disease severity) that 60% to 70% of children will outgrow their eczema or most of it,” he said. “If you ask me when, I won’t tell you. The important thing is to treat it to minimize its impact. We want minimal rash, minimal itch, and minimal sleep disturbance. Sometimes I say, ‘that might improve the chance of the eczema getting better over time.’ ”
Following are four other common questions parents and patients ask him:
Can we figure out the allergies causing the eczema? “This is probably one of the most unnerving questions I get asked,” he said. “It’s a loaded question. My answer is that allergies are intertwined with AD. Searching for the secret allergy causing the atopic dermatitis is rarely successful.” Sensitization is much more common with AD, he added, meaning specific IgE testing, whether it be blood testing or skin prick testing. “The more severe your eczema is, the more chance you’ll have of real food allergy,” he said. “About 15% of milder eczema patients will have at least one food allergy, but when you get to the more moderate to severe cases, about 40% will have a true food allergy.”
Food reactions may not cause eczema, though. Food reactions can cause urticaria, angioedema, eczematous dermatitis, allergic contact dermatitis, contact urticaria, and respiratory findings. According to National Institutes of Health guidelines for food allergy, skin prick tests and serum IgE tests are recommended to assist in identification of foods that may be provoking IgE-mediated food reactions, but are not diagnostic of food allergy.
“There’s a huge literature showing that there’s a lot of food allergy testing that’s just not helpful,” he said. In one study, 89% of food challenges administered in patients who were listed as being allergic based on skin prick tests or serum IgE tests did not have a true food allergy.
“Empiric elimination diets aren’t especially useful. However, we occasionally see children who do have AD exacerbated by food allergies in the first year of life,” he said. NIH guidelines suggest that children younger than 5 years of age with moderate to severe AD be considered for food allergy evaluation for milk, egg, peanut, wheat, and soy, if at least one of the following conditions is met: the child has persistent AD in spite of optimized management and topical therapy, and/or the child has a reliable history of an immediate reaction after ingestion of a specific food.
“We do know that there are high rates of comorbid allergic processes, besides food allergy, associated with atopic dermatitis, including allergic rhinitis and asthma both in children and adults,” Dr. Eichenfield said. “I do discuss allergy triggers and their importance in the life of the individual, though not necessarily as factors in AD. There are a variety of environmental allergens and/or environmental triggers that can significantly impact AD. Recently, we have seen studies discussing air pollution and wildfires as exacerbators of AD.”
How should I bathe and moisturize? There are no standard guidelines for the frequency, type, or duration of bathing in patients with AD, he said, though in more severe disease, frequent bathing can be helpful along with standard anti-inflammatory topical medicines. “I keep my general recommendations vague,” Dr. Eichenfield said. “I do explain that we don’t want to use harsh soaps; we want to be gentle in our washing. I usually recommend daily to every other day bathing. It’s important to pat the skin dry and then apply a moisturizer. Applying a moisturizer 2-3 minutes after bathing is important and limited significant cleanser use can be helpful.”
Moisturizers and emollients are a standard of care in U.S. guidelines published in 2013 and 2014, and international guidelines, and are steroid-sparing and useful for both prevention and maintenance. “I tell parents and patients that there is no reason to avoid bathing because of AD as long as you moisturize after,” he said.
Do I have to use topical [name of drug]? “I try to explain that there is skin barrier dysfunction that stimulates the inflammatory milieu, and that inflammation in the skin or blood in AD negatively impacts skin barrier function,” Dr. Eichenfield said. “I explain that if inflammation doesn’t get better with good skin care, moisturizers, and avoidance of triggers, we need anti-inflammatory medication. Then we discuss what the options are, the significant variation in strengths of topical corticosteroids, and topical nonsteroid options.”
When he counsels parents and patients on the use of topical corticosteroids, he tells them that cortisone is a naturally-occurring metabolite, and that “we can work together to let you know how much medicine to use, and how a safe amount is a powerful tool to fix the eczema.” He often says that topical steroids “are like hammers. We have tiny hammers, like over-the-counter hydrocortisone, and sledgehammers like clobetasol. We also have ‘screwdrivers’ and ‘pliers’ with nonsteroidal topical calcineurin and PDE-4 inhibitors, which are especially useful for maintenance therapy. Topical ruxolitinib is a new medicine that we may use for patients as well. The label includes discussion of side effects from oral JAK inhibitors as well as from the drug development program, so it takes some time to talk through.”
Is it time for a stronger systemic medicine? Any conversation about this topic should support the concept that the AD is multifactorial. “We have the rash of eczema,” he said. “We have the itch. We have impact on sleep disturbance. We have the comorbidities. We have other physical changes, which can happen with bacterial infections and other immune system or cardiovascular changes. We have the impact on quality of life and impact on school and work. When we recognize that if patients have significant enough disease that it is not getting better with topicals and is having a negative impact on their lives, we can move our discussion to systemic therapy.”
When counseling patients about systemic therapy, Dr. Eichenfield will conduct a body surface area assessment and document how bad the itch is. “But I’m not just recording the information; I’m bringing it out in the room,” he said. “I’ll do a BSA assessment and say, for example, ‘oh, you have 32% of your body involved with eczema.’ I ask about sleep disturbance, to get the answer ‘out in the room.’ ” He also asks questions such as: “When was the last time your skin was last totally clear? Are there activities that you or your family don’t do because of your eczema, or that you’re living your life around it? Is there anxiety or depression?” Documenting both the impact on quality of life and the severity of disease “makes it easier to discuss systemic therapy,” Dr. Eichenfield said. “Meanwhile, as the provider, I am trying to figure out if the patient should ‘go into the topical therapy bucket’ or into the ‘systemic therapy bucket.’ ”
Counseling about systemic therapy includes shared decision-making regarding the choice of biologics versus oral JAK inhibitors versus traditional systemic agent or phototherapy. Factors to consider in the decision making include patient age, sex, severity, comorbidities, prior therapy, risk aversion, duration, medication access, and desired efficacy. “Evolving therapies can change the conversation, the questions, and the outcomes, but the overarching desired outcome is long-term disease control, minimal eczematous rash, minimal pruritus, and minimal sleep disturbance,” he said.
Dr. Eichenfield disclosed that he has served as a consultant to or investigator for AbbVie; Almirall; Arcutis; Arena; Asana; Termagant; Dermira; Forte Biosciences; Galderma Laboratories; Glenmark/Chinos; Incyte; Kyowa Kirin; Leo Pharma; Eli Lilly and Company; Novartis; Ortho Dermatology; Otsuka; Pfizer; Freestone; Regeneron, and Sanofi Genzyme.
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FROM THE MEDSCAPELIVE LAS VEGAS DERMATOLOGY SEMINAR
Association of height, BMI, and AD in young children may be transient
The , according to a large cohort study published online in JAMA Dermatology.
“The potential for ‘catch up’ in height for children with atopic dermatitis observed in our study may be explained with resolution of atopic dermatitis or successful treatment,” write senior author Aaron M. Drucker, MD, ScM, from the division of dermatology, University of Toronto, and Women’s College Hospital in Toronto, and colleagues. They postulated that, while the association between AD and shorter height is “is likely multifactorial,” it may be driven in part by sleep loss caused by AD, or corticosteroid treatment of AD, both of which can result in growth retardation and subsequent increased BMI.
The researchers used data from TARGet Kids!, a prospective, longitudinal cohort study designed to study multiple health conditions in children from general pediatric and family practices across Toronto. Their study included 10,611 children for whom there was data on height, weight, BMI, and standardized z scores, which account for age and sex differences in anthropometric characteristics. Clinically relevant covariates that were collected included child age, sex, birth weight, history of asthma, family income, maternal and paternal ethnicity, and maternal height and BMI.
The mean age of the children in the study at cohort entry was 23 months, and they were followed for a median of 28.5 months, during which time they had a median of two visits. At baseline, 947 (8.9%) children had parent-reported AD, with this number rising to 1,834 (17.3%) during follow-up.
After adjusting for covariates, AD was associated with lower mean z-height (P < .001), higher mean z-BMI (P = .008), but lower mean z-weight (P < .001), compared with children without AD. Using World Health Organization growth tables, the researchers estimated that “children with atopic dermatitis were, on average, approximately 0.5 cm shorter at age 2 years and 0.6 cm shorter at age 5 years than children without atopic dermatitis” after adjusting for covariates. They also estimated that children with AD were “on average, approximately 0.2 more BMI units at age 2 years” than children without AD. The associations between AD and height diminished by age 14 years, as did the association between AD and BMI by age 5.5 years.
“Given that we found children with atopic dermatitis to be somewhat less heavy, as measured by z-weight, than children without atopic dermatitis and that this association did not attenuate with age, it is possible that our findings for BMI, and perhaps those of previous studies, are explained mainly by differences in height,” the authors write. “This distinction has obvious clinical importance – rather than a focus on obesity and obesogenic behaviors being problematic in children with atopic dermatitis, research might be better directed at understanding the association between atopic dermatitis and initially shorter stature.”
Asked to comment on the study results, Jonathan Silverberg, MD, PhD, MPH, associate professor of dermatology, George Washington University, Washington, told this news organization he would have preferred using the wording “in addition to focusing on obesity,” rather than “focus on obesity.”
“We should not ignore diet and sedentary activity as important factors,” he said, pointing to another recent study that found higher rates of eating disorders associated with AD.
Dr. Silverberg said that he was not familiar enough with the cohort sample to comment on how representative it is of the Canadian population, or on how generalizable the results are to other regions and populations. Generalizability, he added, “is an important issue, as we previously found regional differences with respect to the association between AD and obesity.”
In addition, he noted that in the study AD was defined as an “ever history” of disease rather than “in the past year or currently,” so, even though it is a longitudinal study, “it is really looking at how AD at any point in patients’ lives is related to weight or stature,” he explained. But, he added, “many cases of childhood AD ‘burn out’ or become milder/clear as the children get older. So, if the AD clears, then one would expect to see attenuation of associations as the children get older. However, this doesn’t tell us about how persistent AD into later childhood or adolescence is related to height or weight.”
Previous studies found that short stature and obesity were particularly associated with moderate – and even more to severe – atopic dermatitis, Dr. Silverberg said. It is likely that most patients in this primary care cohort had mild disease, he noted, so the effect sizes are likely diluted by mostly mild disease “and not relevant to the more persistent and severe AD patients encountered in the dermatology practice setting.”
The study was supported by the department of medicine, Women’s College Hospital, and the Canadian Institutes of Health Research.
One author reported receiving compensation from the British Journal of Dermatology, the American Academy of Dermatology, and the National Eczema Association and has served as a paid consultant for the Canadian Agency for Drugs and Technologies in Health outside the submitted work. No other disclosures were reported. Dr. Silverberg has disclosed no relevant financial relationships.
Commentary by Robert Sidbury, MD, MPH
Among the more puzzling “associations” to emerge in recent literature has been the association between atopic dermatitis (AD) and obesity. I see many children with severe AD every day and my gestalt “association” is a thinner, shorter child rather than an overweight one. Dr. Drucker and colleagues’ data has helped me understand this dissonance. Children with AD do in fact, on average, weigh less but they are also shorter, possibly explaining their higher body mass index (BMI). More important, these findings are transient, with height differences dissipating by 14 years of age, and BMI differences by kindergarten. This information should train providers’ sights on optimal AD treatment and optimal nutritional and lifestyle support without undue concern for obesity or obesogenic behaviors.
Dr. Sidbury is chief of dermatology at Seattle Children's Hospital and professor, department of pediatrics, University of Washington, Seattle. He is a site principal investigator for dupilumab trials, for which the hospital has a contract with Regeneron.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
The , according to a large cohort study published online in JAMA Dermatology.
“The potential for ‘catch up’ in height for children with atopic dermatitis observed in our study may be explained with resolution of atopic dermatitis or successful treatment,” write senior author Aaron M. Drucker, MD, ScM, from the division of dermatology, University of Toronto, and Women’s College Hospital in Toronto, and colleagues. They postulated that, while the association between AD and shorter height is “is likely multifactorial,” it may be driven in part by sleep loss caused by AD, or corticosteroid treatment of AD, both of which can result in growth retardation and subsequent increased BMI.
The researchers used data from TARGet Kids!, a prospective, longitudinal cohort study designed to study multiple health conditions in children from general pediatric and family practices across Toronto. Their study included 10,611 children for whom there was data on height, weight, BMI, and standardized z scores, which account for age and sex differences in anthropometric characteristics. Clinically relevant covariates that were collected included child age, sex, birth weight, history of asthma, family income, maternal and paternal ethnicity, and maternal height and BMI.
The mean age of the children in the study at cohort entry was 23 months, and they were followed for a median of 28.5 months, during which time they had a median of two visits. At baseline, 947 (8.9%) children had parent-reported AD, with this number rising to 1,834 (17.3%) during follow-up.
After adjusting for covariates, AD was associated with lower mean z-height (P < .001), higher mean z-BMI (P = .008), but lower mean z-weight (P < .001), compared with children without AD. Using World Health Organization growth tables, the researchers estimated that “children with atopic dermatitis were, on average, approximately 0.5 cm shorter at age 2 years and 0.6 cm shorter at age 5 years than children without atopic dermatitis” after adjusting for covariates. They also estimated that children with AD were “on average, approximately 0.2 more BMI units at age 2 years” than children without AD. The associations between AD and height diminished by age 14 years, as did the association between AD and BMI by age 5.5 years.
“Given that we found children with atopic dermatitis to be somewhat less heavy, as measured by z-weight, than children without atopic dermatitis and that this association did not attenuate with age, it is possible that our findings for BMI, and perhaps those of previous studies, are explained mainly by differences in height,” the authors write. “This distinction has obvious clinical importance – rather than a focus on obesity and obesogenic behaviors being problematic in children with atopic dermatitis, research might be better directed at understanding the association between atopic dermatitis and initially shorter stature.”
Asked to comment on the study results, Jonathan Silverberg, MD, PhD, MPH, associate professor of dermatology, George Washington University, Washington, told this news organization he would have preferred using the wording “in addition to focusing on obesity,” rather than “focus on obesity.”
“We should not ignore diet and sedentary activity as important factors,” he said, pointing to another recent study that found higher rates of eating disorders associated with AD.
Dr. Silverberg said that he was not familiar enough with the cohort sample to comment on how representative it is of the Canadian population, or on how generalizable the results are to other regions and populations. Generalizability, he added, “is an important issue, as we previously found regional differences with respect to the association between AD and obesity.”
In addition, he noted that in the study AD was defined as an “ever history” of disease rather than “in the past year or currently,” so, even though it is a longitudinal study, “it is really looking at how AD at any point in patients’ lives is related to weight or stature,” he explained. But, he added, “many cases of childhood AD ‘burn out’ or become milder/clear as the children get older. So, if the AD clears, then one would expect to see attenuation of associations as the children get older. However, this doesn’t tell us about how persistent AD into later childhood or adolescence is related to height or weight.”
Previous studies found that short stature and obesity were particularly associated with moderate – and even more to severe – atopic dermatitis, Dr. Silverberg said. It is likely that most patients in this primary care cohort had mild disease, he noted, so the effect sizes are likely diluted by mostly mild disease “and not relevant to the more persistent and severe AD patients encountered in the dermatology practice setting.”
The study was supported by the department of medicine, Women’s College Hospital, and the Canadian Institutes of Health Research.
One author reported receiving compensation from the British Journal of Dermatology, the American Academy of Dermatology, and the National Eczema Association and has served as a paid consultant for the Canadian Agency for Drugs and Technologies in Health outside the submitted work. No other disclosures were reported. Dr. Silverberg has disclosed no relevant financial relationships.
Commentary by Robert Sidbury, MD, MPH
Among the more puzzling “associations” to emerge in recent literature has been the association between atopic dermatitis (AD) and obesity. I see many children with severe AD every day and my gestalt “association” is a thinner, shorter child rather than an overweight one. Dr. Drucker and colleagues’ data has helped me understand this dissonance. Children with AD do in fact, on average, weigh less but they are also shorter, possibly explaining their higher body mass index (BMI). More important, these findings are transient, with height differences dissipating by 14 years of age, and BMI differences by kindergarten. This information should train providers’ sights on optimal AD treatment and optimal nutritional and lifestyle support without undue concern for obesity or obesogenic behaviors.
Dr. Sidbury is chief of dermatology at Seattle Children's Hospital and professor, department of pediatrics, University of Washington, Seattle. He is a site principal investigator for dupilumab trials, for which the hospital has a contract with Regeneron.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
The , according to a large cohort study published online in JAMA Dermatology.
“The potential for ‘catch up’ in height for children with atopic dermatitis observed in our study may be explained with resolution of atopic dermatitis or successful treatment,” write senior author Aaron M. Drucker, MD, ScM, from the division of dermatology, University of Toronto, and Women’s College Hospital in Toronto, and colleagues. They postulated that, while the association between AD and shorter height is “is likely multifactorial,” it may be driven in part by sleep loss caused by AD, or corticosteroid treatment of AD, both of which can result in growth retardation and subsequent increased BMI.
The researchers used data from TARGet Kids!, a prospective, longitudinal cohort study designed to study multiple health conditions in children from general pediatric and family practices across Toronto. Their study included 10,611 children for whom there was data on height, weight, BMI, and standardized z scores, which account for age and sex differences in anthropometric characteristics. Clinically relevant covariates that were collected included child age, sex, birth weight, history of asthma, family income, maternal and paternal ethnicity, and maternal height and BMI.
The mean age of the children in the study at cohort entry was 23 months, and they were followed for a median of 28.5 months, during which time they had a median of two visits. At baseline, 947 (8.9%) children had parent-reported AD, with this number rising to 1,834 (17.3%) during follow-up.
After adjusting for covariates, AD was associated with lower mean z-height (P < .001), higher mean z-BMI (P = .008), but lower mean z-weight (P < .001), compared with children without AD. Using World Health Organization growth tables, the researchers estimated that “children with atopic dermatitis were, on average, approximately 0.5 cm shorter at age 2 years and 0.6 cm shorter at age 5 years than children without atopic dermatitis” after adjusting for covariates. They also estimated that children with AD were “on average, approximately 0.2 more BMI units at age 2 years” than children without AD. The associations between AD and height diminished by age 14 years, as did the association between AD and BMI by age 5.5 years.
“Given that we found children with atopic dermatitis to be somewhat less heavy, as measured by z-weight, than children without atopic dermatitis and that this association did not attenuate with age, it is possible that our findings for BMI, and perhaps those of previous studies, are explained mainly by differences in height,” the authors write. “This distinction has obvious clinical importance – rather than a focus on obesity and obesogenic behaviors being problematic in children with atopic dermatitis, research might be better directed at understanding the association between atopic dermatitis and initially shorter stature.”
Asked to comment on the study results, Jonathan Silverberg, MD, PhD, MPH, associate professor of dermatology, George Washington University, Washington, told this news organization he would have preferred using the wording “in addition to focusing on obesity,” rather than “focus on obesity.”
“We should not ignore diet and sedentary activity as important factors,” he said, pointing to another recent study that found higher rates of eating disorders associated with AD.
Dr. Silverberg said that he was not familiar enough with the cohort sample to comment on how representative it is of the Canadian population, or on how generalizable the results are to other regions and populations. Generalizability, he added, “is an important issue, as we previously found regional differences with respect to the association between AD and obesity.”
In addition, he noted that in the study AD was defined as an “ever history” of disease rather than “in the past year or currently,” so, even though it is a longitudinal study, “it is really looking at how AD at any point in patients’ lives is related to weight or stature,” he explained. But, he added, “many cases of childhood AD ‘burn out’ or become milder/clear as the children get older. So, if the AD clears, then one would expect to see attenuation of associations as the children get older. However, this doesn’t tell us about how persistent AD into later childhood or adolescence is related to height or weight.”
Previous studies found that short stature and obesity were particularly associated with moderate – and even more to severe – atopic dermatitis, Dr. Silverberg said. It is likely that most patients in this primary care cohort had mild disease, he noted, so the effect sizes are likely diluted by mostly mild disease “and not relevant to the more persistent and severe AD patients encountered in the dermatology practice setting.”
The study was supported by the department of medicine, Women’s College Hospital, and the Canadian Institutes of Health Research.
One author reported receiving compensation from the British Journal of Dermatology, the American Academy of Dermatology, and the National Eczema Association and has served as a paid consultant for the Canadian Agency for Drugs and Technologies in Health outside the submitted work. No other disclosures were reported. Dr. Silverberg has disclosed no relevant financial relationships.
Commentary by Robert Sidbury, MD, MPH
Among the more puzzling “associations” to emerge in recent literature has been the association between atopic dermatitis (AD) and obesity. I see many children with severe AD every day and my gestalt “association” is a thinner, shorter child rather than an overweight one. Dr. Drucker and colleagues’ data has helped me understand this dissonance. Children with AD do in fact, on average, weigh less but they are also shorter, possibly explaining their higher body mass index (BMI). More important, these findings are transient, with height differences dissipating by 14 years of age, and BMI differences by kindergarten. This information should train providers’ sights on optimal AD treatment and optimal nutritional and lifestyle support without undue concern for obesity or obesogenic behaviors.
Dr. Sidbury is chief of dermatology at Seattle Children's Hospital and professor, department of pediatrics, University of Washington, Seattle. He is a site principal investigator for dupilumab trials, for which the hospital has a contract with Regeneron.
A version of this article first appeared on Medscape.com.
This article was updated 6/18/22.
FROM JAMA DERMATOLOGY