M. Grace Hren

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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.