Atopic dermatitis: a comprehensive updated review of this intriguing disease with futuristic insights

Abstract

Atopic dermatitis (AD) is a paradigmatic prevalent, long-lasting, and inflammatory skin condition with a diverse range of clinical manifestations. The etiology and clinical symptoms of AD are influenced by complex pathophysiological processes, which involve a strong genetic component, epidermal dysfunction, and immunological dysregulation, and a strong influence of other physiological and environmental factors. The FDA has approved targeted and well-tolerated immunomodulators including biologics like dupilumab and crisaborole, and small molecules such as baricitinib, as novel therapies for AD. They effectively treat AD but are too expensive for most patients. The review provides an update on the state of knowledge of AD pathogenesis, discusses the available diagnostic and scoring indices, and provides a scientific foundation for treatment methods for AD. This review also presents data on clinical efficacy of innovative treatments' considering recent guidelines, emphasizing the newest medications and ongoing trials. Finally, the new implication of artificial intelligence (AI) in AD management is explored, where AI can speed up diagnosis and therapy. The PubMed, Google Scholar, and ScienceDirect databases were used for this review.

Keywords: Artificial intelligence; Atopic dermatitis; Biological therapy; ChatGPT; Immune dysfunction; JAK inhibitors; Nanodelivery; Skin.

Figure 1

An outline of atopic dermatitis pathogenesis and mechanism of action of therapeutic agents. Reproduced with permission from Nguyen et al. (2019). CRTH2 chemoattractant receptor homologs molecule expressed on TH2 cells, AhR aryl hydrocarbon receptor, IgE immunoglobulin-E, IL interleukin, and H4R histamine-4 receptor JAK/STAT PDE4 phosphodiesterase 4, R receptor, KOR κ-opioid receptor, NK1R neurokinin-1 receptor, Janus kinase/signal transducer and activator of transcription, and TSLP thymic stromal lymphopoietin

Figure 2

A demonstration of environmental and trigger factors that cause inflammation and the onset and severity of AD clinical course

Figure 3

A diagrammatic representation of AD therapy  based on the severity of the condition