Infectious complications of atopic dermatitis: An update.

Background: Infectious complications are a major co-morbidity of atopic dermatitis (AD). Since our last review, multiple medications have been approved for AD. In this update, we reviewed the role of these medications in the infectious complications of AD. In addition, new findings in the pathophysiology, clinical management and therapy are updated.

Objective: To summarize recent advances in skin barrier lipid dysregulation, and various aspects of innate and adaptive immunity that contribute to the pathogenesis of infectious complications of atopic dermatitis (AD), to present practical guidance in the management and prevention of infections in AD, and to discuss the role of current AD therapy in infection in detail.

Methods: Data sources include published literature obtained through PubMed searches. Study selection entailed studies relevant to the mechanisms of infection in AD, clinical implications, treatments, prevention, and future therapy.

Results: A decrease in lipids with long-chain fatty acids and omega-esterified ceramides renders the skin barrier of AD more hydrophobic and susceptible to Staphylococcus aureus. Self-DNA and RNase inhibitors interfere with the activity of host antimicrobial peptides/proteins against S aureus. CD1a-restricted T cells against S aureus lipid antigen may play a pathogenic role in AD. Meta-analyses reported that dupilumab, which targets interleukin-4 and interleukin-13, decreases the frequency of infections in AD, whereas oral Janus kinase inhibitors, which have a broader immunosuppressing effect, are associated with an increased risk of herpes zoster and herpes-related infections.

Conclusion: Infectious complications remain a major comorbidity in uncontrolled AD. Clinicians will continue to face these challenges in routine practice. Successful prevention and treatment will depend on our understanding of AD pathophysiology.