Hidradenitis suppurativa: infection, autoimmunity, or both?

Abstract

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease mainly affecting areas rich in apocrine glands. Clinically, is characterized by painful subcutaneous nodules and if left untreated to pus secretion, abscess and fistula formation. Its frequency is estimated to be 0.5–4% of the general population, affecting women more often. Pathogenesis of HS is still not clearly defined. It seems to be a combination of genetic factors with alterations in the skin microbiome. Furthermore, at tissue (i.e. skin) as well as at serum level, several inflammatory cytokines are upregulated. The most important of the latter are tumor necrosis factor (TNF), interleukin (IL)-1, IL-17, and IL-23. Adding another level of complexity, it has been suggested that keratinocytes might be intrinsically activated, contributing also to the observed inflammation. Interestingly, it has been noted that frequency of HS is increased in some autoimmune rheumatic diseases, such as spondyloarthropathies (SpA). Of note, both HS and SpA have relatively strong association with metabolic diseases and obesity implying that there are indeed some common underlying pathophysiological pathways. Although no specific microbe has been identified, alterations in the microbiome of the skin of these patients have been reported. Of note, microbes with a capability for biofilm formation are abundant. Treatment of HS among others, include antibiotics as well as biologic drugs targeting TNF and other cytokines and used for autoimmune rheumatic diseases. Herein, we review the current evidence on links between HS and autoimmune diseases and infectious diseases with a focus on epidemiology and pathophysiology.