Is there a link between cholesterol-lowering medications and atopic dermatitis?

Cholesterol-lowering medications (CLMs) are used globally. Cholesterol is a key stratum corneum lipid that helps maintain epidermal barrier integrity. Barrier dysfunction contribute to pathogenesis of atopic dermatitis (AD). Clarifying whether CLMs impact AD has implications for dermatology and cardiology.

We synthesized evidence from experimental, clinical, and genetic epidemiology through targeted literature searches and expert selections. It focuses on 1) skin barrier biology and epidermal cholesterol metabolism, and 2) potential effect of CLMs on AD. We discuss findings from experimental studies comparing topical versus systemic statins; population-based observations of AD among CLM users; and Mendelian randomization analyses of CLMs.

Effect of CLMs on AD is biologically plausible but clinically unproven. Signals of concern are most consistent for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and Niemann-Pick C1-Like 1 (NPC1L1) inhibition, whereas Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition appears protective in some populations. Current studies are limited by confounding, heterogeneous outcomes and sparse ancestry-specific analyses. Until robust causal and pharmacoepidemiologic studies across ancestries are available, clinicians should prioritize established cardiovascular benefit of lipid reduction while monitoring for new or worsening dermatitis after therapy initiation. Future work should triangulate Mendelian randomization with pharmacoepidemiology designs in large, diverse datasets to deliver definitive guidance.