Researchers have identified apocrine gland damage and the release of specific keratins, KRT18 and KRT19, according to a recent study.

In the study, published in the Journal of Investigative Dermatology, the researchers suggested a potential role for apocrine gland (AG) damage in the early pathogenesis of hidradenitis suppurativa (HS). They analyzed lesional (LS), nonlesional (NLS), and healthy skin samples from 12 patients with HS and 8 healthy controls using histological analysis and single-cell RNA sequencing.

The findings indicated that AG size was significantly reduced in LS and NLS compared with healthy controls. The mean AG area in LS was only 28% of that in controls (65,182 μm² vs 234,270 μm², P = .0008). Histologic analysis showed that 54.6% of AGs in LS and 48.7% in NLS exhibited cellular degeneration, including ballooning, cytolysis, and epithelial discontinuity, compared with just 9% in controls (P < .01). Damaged AGs released keratins KRT18 and KRT19, with elevated levels observed on the skin surface of patients with HS. KRT19 was also identified in the dermis of LS and NLS, surrounded by inflammatory cells such as neutrophils and macrophages. Serum KRT19 levels were negatively correlated with age at disease onset (Spearman’s r = –0.522, P = .018), indicating an association that may warrant further investigation into its role in early disease detection.

Additionally, AGs in LS demonstrated upregulation of neutrophil recruitment pathways, including CXCL-CXCR and SAA1-FPR2 signaling, which were absent or minimally active in healthy controls. These findings suggested that AG dysfunction and keratin release may contribute to early inflammatory processes in HS. While KRT18 and KRT19 hold promise as potential biomarkers for HS severity and progression, further research is needed to validate their clinical utility. 

Full disclosures can be found in the published study.