Essential Site Maintenance: Authorea-powered sites will be updated circa 15:00-17:00 Eastern on Tuesday 5 November.
There should be no interruption to normal services, but please contact us at [email protected] in case you face any issues.

M. Grace Hren

and 4 more

Algorithms in allergy: Diagnosis and management of atopic dermatitis in adulthoodM. Grace Hren1,2, Ester Del Duca1, Helen He1, Andrew L. Ji1,2, Emma Guttman-Yassky1*1Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA2Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA*Correspondence:Emma Guttman-Yassky, MD, PhDAtopic dermatitis (AD) is a chronic inflammatory skin disease characterized by significant pruritus, eczematous lesions, and a relapsing course.1,2 Once mainly considered a pediatric disease that diminishes with age, current epidemiologic studies suggest a prevalence of ~7% among adults in the United States.3 Associated with atopic (e.g. asthma, rhinitis, food allergy) and non-atopic (e.g. psychiatric, autoimmune, infectious) comorbidities, as well as diminished life quality, appropriate treatment of AD is crucial.4,5 This algorithm offers a practical guide for management of AD in adults.As a purely clinical diagnosis, there are no biomarkers or confirmatory laboratory tests for AD, and with a highly heterogenous presentation, the differential for AD is extensive.2,3 Lacking specific diagnostic criteria, a combination of history, morphology/distribution of lesions, and exclusion of differentials reinforces diagnosis.1,2,3 Several groups have proposed criteria for AD (Hanifin and Rajka (1980), United Kingdom Working Party (1994), among others).3 More recently, the American Academy of Dermatology released an updated set of criteria with essential (must be present), important (support diagnosis), and associated (suggest diagnosis) features of AD (Figure 1 ).6 If diagnosis remains unclear, a skin biopsy or patch test can exclude alternative diagnoses or determine underlying triggers, respectively.3,6After establishing diagnosis, stratification of AD as mild, moderate, or severe may assist in management. Scoring Atopic Dermatitis (SCORAD), Eczema Area and Severity Index (EASI), and Patient-Oriented Eczema Measure (POEM) are AD severity scores validated for clinical trials, but these scores are not routinely utilized in clinical practice.6 Rather, physician assessment of cutaneous involvement, plus patient-reported frequency of itching and impact on daily living, psychosocial well-being, and sleep can direct stratification (Figure 1 ).7At any severity, general management of AD consists of patient education and encouragement of proactive measures. Instruct patients to apply emollients and moisturizers multiple times per day, maintain healthy bathing routines, and avoid exacerbating factors (Figure 2 ).8Among patients with mild AD, use of low-to-medium potency topical corticosteroids (TCS) 1-2 times daily for maximum of two weeks is first-line management. Due to potential risk of skin atrophy, consistent use of TCS for greater than two weeks is not recommended.8If low-to-medium potency TCS use leads to disease resolution, commence maintenance treatment, employing frequent use of moisturizers plus intermittent use of low-to-medium potency TCS to reduce flares and relapse.8 If unresolved, consider topical calcineurin inhibitors (TCI), crisaborole ointment, or ruxolitinib cream. Allow 2-4 weeks to elapse before reassessing response.8 Consider other potential etiologies, such as non-adherence (assess for fear of TCS side effects impeding use), contact allergy (conduct patch testing), infection (consider antibiotics or 0.005% diluted bleach baths), or misdiagnosis (consider biopsy).8For those lacking in response to above therapies, along with patients presenting with moderate-to-severe AD, commence treatment with medium-to-high potency TCS daily for two weeks.8 Low potency TCS, TCI, or crisaborole ointment can be utilized for areas with increased risk for skin atrophy.8Consider systemic therapies for patients with moderate-to-severe AD nonresponsive to topicals, or as first-line therapy for patients with severe/extensive skin involvement. First-line systemic agents include dupilumab and tralokinumab, two monoclonal antibodies that target the Th2 pathway with excellent safety profiles.9 Other systemic options include oral Janus kinase inhibitors (e.g. upadacitinib, abrocitinib) or conventional immunosuppressants (e.g. methotrexate, azathioprine, cyclosporine, mycophenolate mofetil). However, these therapeutics possess their own respective safety concerns, warranting increased caution and monitoring.9 Narrow-band ultraviolet B (NB-UVB) phototherapy can be considered, but the commitment (2-3x/week in office) may be prohibitive for patients.9 Systemic corticosteroids are not recommended due to risk of rebound flare.9 Once moderate-to-severe AD is controlled, proceed with long-term maintenance therapy, consisting of a systemic agent plus TCS or other topical therapies to prevent flares and relapse.

Benjamin Ungar

and 13 more

Background: In the SARS-CoV-2/COVID-19 pandemic, we need to understand the impact of immunomodulatory medications on COVID-19 symptom severity in patients with inflammatory diseases, including the Type 2/Th2 polarized skin disease, atopic dermatitis/AD. Since it is believed that Type 1/Th1immunity controls viral infections, and that there is a Th1/Th2 counter-regulation, we hypothesized that Th2 targeting with the IL-4Rα-antagonist, dupilumab, in patients with moderate-to-severe AD rebalances Th1/Th2 axis, potentially leading to attenuated COVID-19 symptoms. Methods: 1,237 moderate-to-severe AD patients in the Icahn School of Medicine at Mount Sinai Department of Dermatology were enrolled in a registry. Patients were screened for COVID-19-related symptoms and assigned a severity score (asymptomatic[0]-fatal[5]). Scores were compared among 3 treatment groups: dupilumab (n=632), other systemic treatments (n=107), and limited/no treatment (n=498). Demographic and comorbid covariates were adjusted by multivariate logistic regression models. Results: The dupilumab-treated group showed reduced incidence and severity of COVID-19 symptoms versus other treatment groups. Dupilumab-treated patients were less likely to experience moderate-to-severe symptoms versus patients on other systemics (p=0.01) and on limited/no treatment (p=0.04), and less likely to experience any symptoms versus patients on other systemics (p=0.01). This effect was seen in our entire cohort and in the subgroup of patients with verified COVID-19 or high-risk exposure. Conclusions: Patients on dupilumab experienced less severe COVID-19 manifestations and lesser symptoms compared to patients on other systemics and on limited/no treatment. These results suggest that Th2 modulation with dupilumab may have a protective effect on anti-viral immune response in AD patients.