Hidradenitis suppurativa: infection, autoimmunity, or both?

Area of Science:

• Dermatology
• Immunology
• Microbiology

Background:

• Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition affecting apocrine gland-rich areas.
• HS presents with painful nodules, abscesses, and fistulas, impacting 0.5-4% of the population, predominantly women.
• The exact pathogenesis remains unclear, but involves genetic factors, skin microbiome alterations, and upregulated inflammatory cytokines like TNF, IL-1, IL-17, and IL-23.

Purpose of the Study:

• To review current evidence on the epidemiological and pathophysiological links between HS, autoimmune diseases, and infectious diseases.
• To explore potential common underlying mechanisms connecting HS with conditions like spondyloarthropathies and metabolic diseases.
• To discuss the role of skin microbiome alterations and keratinocyte activation in HS pathogenesis.

Main Methods:

• Literature review of epidemiological studies and research on HS pathophysiology.
• Analysis of data on inflammatory markers and cytokine profiles in HS patients.
• Examination of studies investigating the skin microbiome in individuals with HS.

Main Results:

• HS shows increased frequency in certain autoimmune rheumatic diseases, such as spondyloarthropathies (SpA).
• Both HS and SpA share associations with metabolic diseases and obesity, suggesting common pathophysiological pathways.
• Alterations in the skin microbiome, including an abundance of biofilm-forming microbes, are reported in HS patients.

Conclusions:

• HS pathogenesis likely involves a complex interplay of genetic predisposition, immune dysregulation, and altered skin microbiome.
• The overlap with autoimmune and metabolic diseases suggests shared inflammatory pathways that warrant further investigation.
• Understanding these links may lead to novel therapeutic strategies for HS, potentially repurposing treatments used for autoimmune conditions.