Atopic dermatitis (AD) is a highly pruritic, chronic inflammatory skin disease. The diagnosis is made using evaluated clinical criteria. Disease activity and burden are best measured with a composite score, assessing both objective and subjective symptoms, such as SCORing Atopic Dermatitis (SCORAD). AD management must take into account clinical and pathogenic variabilities, the patient's age and also target flare prevention. Basic therapy includes hydrating and barrierstabilizing topical treatment universally applied, as well as avoiding specific and unspecific provocation factors. Visible skin lesions are treated with anti-inflammatory topical agents such as corticosteroids and calcineurin inhibitors (tacrolimus and pimecrolimus), which are preferred in sensitive locations. Topical tacrolimus and some mid-potency corticosteroids are proven agents for proactive therapy, which is defined as the long-term intermittent anti-inflammatory therapy of frequently relapsing skin areas. Systemic anti-inflammatory or immunosuppressive treatment is a rapidly changing † See Appendix section.

Summary Background Food allergy is a common problem in patients with atopic dermatitis (AD), particularly in children. While immediate reactions to food are well characterized, the importance of food as a provocation factor for late eczematous reactions has been a subject of debate for several decades. Objective To investigate the importance of food for the induction of late eczematous reactions in children with AD and to correlate the clinical outcome to the results of specific IgE determinations and atopy patch tests (APTs). Methods One hundred and six double‐blind placebo‐controlled food challenges (DBPCFCs) to cow's milk, hen's egg, wheat and soy in 64 children with AD (median age 2 years) were analysed retrospectively. Total and food‐specific IgE were determined by CAP RAST FEIA and APTs with native foodstuff were performed. The diagnostic values of specific IgE and APT results were calculated. Results Forty‐nine (46%) of the challenges were related to a clinical reaction. An exacerbation of AD (late eczematous reaction) commonly occurred 24 h after the ingestion of food. Isolated late eczematous reactions were seen in 12% of all positive challenges. Forty‐five percent of the positive challenges were associated with late eczematous responses, which followed immediate‐type reactions. The sensitivity of food‐specific IgE and the APT was 76% and 70%, respectively. Specific IgE and APT were often false positive, which resulted in low positive predictive values (64% and 45%, respectively). Conclusions Late eczematous reactions may often be observed upon food challenge in children with AD. Due to the poor reliability of food‐specific IgE and APT results DBPCFCs have still to be regarded as the gold standard for the appropriate diagnosis of food responsive eczema in children with AD.

Atopic dermatitis (AD) is a complex disease with elevated risk of respiratory comorbidities. 1,2 Severely affected patients are often treated with immune-modulating systemic drugs. 3,4 On 11 March 2020, the World Health Organization declared the 2019 novel coronavirus severe acute respiratory syndrome (SARS-Cov-2) epidemic to be a pandemic. The number of cases worldwide is increasing exponentially and poses a major health threat, especially for those who are elderly and immunocompromised, or have comorbidities. This also applies to AD patients on systemic immune-modulating treatment. In these days of uncertainty, reallocation of medical resources, curfew, hoarding and shutdown of normal social life, patients, caregivers and doctors ask questions regarding the continuation of systemic immunemodulating treatment of AD patients. The ETFAD decided to address some of these questions here: What do we recommend for AD patients treated with immune-modulating therapy at times of SARS-Cov-2 pandemic?

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This study demonstrates that controlled exposure to airborne allergens of patients with a so-called extrinsic IgE-mediated form of AD induced a worsening of cutaneous symptoms.

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Summary This guideline is an update from August 2020 the S2k‐guideline “Atopic dermatitis” published in 2015. The reason for updating this chapter of the guideline were the current developments in the field of systemic therapy of atopic dermatitis. The agreed recommendations for systemic treatment in atopic dermatitis of the present guideline are based on current scientific data. Due to the approval of dupilumab for the treatment of moderate to severe atopic dermatitis, which cannot be treated sufficiently with topical drugs alone, this part of the guideline has now been adapted and newly consented. The indication for systemic therapy and the therapeutic response to topical and systemic treatment should be recorded and documented in a suitable form in clinic and practice. A standardized documentation of the indication for system therapy in atopic dermatitis can be recommended and is also part of the updated chapter of this guideline.

Background As an evidence resource for the currently planned European Academy of Allergy and Clinical Immunology (EAACI) clinical practice guideline “systemic treatment of atopic dermatitis (AD),” we critically appraised evidence on systemic treatments for moderate‐to‐severe AD. Methods We systematically identified randomized controlled trials (RCTs) investigating the safety and efficacy of systemic treatments for AD up to February 2020. Primary efficacy outcomes were clinical signs, AD symptoms and health‐related quality of life. Primary safety outcomes included cumulative incidence rates for (serious) adverse events. Trial quality was assessed applying the Cochrane Risk of Bias Tool 2.0. Meta‐analyses were conducted where appropriate. Results 50 RCTs totalling 6681 patients were included. Trial evidence was identified for apremilast, azathioprine (AZA), baricitinib, ciclosporin A (CSA), corticosteroids, dupilumab, interferon‐gamma, intravenous immunoglobulins (IVIG), mepolizumab, methotrexate (MTX), omalizumab, upadacitinib and ustekinumab. Meta‐analyses were indicated for the efficacy of baricitinib [EASI75 RD 0.16, 95% CI (0.10;0.23)] and dupilumab [EASI75, RD 0.37, 95% CI (0.32;0.42)] indicating short‐term (ie 16‐week treatment) superiority over placebo. Furthermore, efficacy analyses of AZA and CSA indicated short‐term superiority over placebo; however, nonvalidated scores were used and can therefore not be compared to EASI. Conclusion The most robust, replicated high‐quality trial evidence is present for the efficacy and safety of dupilumab for up to 1 year in adults. Robust trial evidence was further revealed for AZA, baricitinib and CSA. Methodological restrictions led to limited evidence‐based conclusions for all other systemic treatments. Head‐to‐head trials with novel systemic treatments are required to clarify the future role of conventional therapies.