Abstract

Objectives To assess inflammatory serum markers including serum proinflammatory cytokines, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) according to the clinical inflammatory activity of patients with hidradenitis suppurativa (HS). Patients and Methods Seventy-four patients with HS were studied based on the Hidradenitis Suppurativa-Physician Global Assessment (HS-PGA) score and Hurley staging system. Proinflammatory cytokines were measured using a multiplex cytokine assay. Twenty-two healthy volunteers were recruited. Results Serum interleukin- (IL-) 6, IL-23, soluble tumour necrosis factor alpha (TNF-α) receptor I (sTNF-RI), CRP, and ESR were different in the patients with HS compared with those in the healthy controls (P < 0.05). The levels of IL-1β, IL-6, IL-8, IL-10, IL-12p70, IL-17A, sTNF-RII, CRP, and ESR were significantly elevated according to inflammatory activity based on HS-PGA scores (r > 0.25, P < 0.05). The levels of IL-6 (r = 0.53, P < 0.001), CRP (r = 0.54, P < 0.001), and ESR (r = 0.60, P < 0.001) were especially well correlated with clinical inflammatory activity based on HS-PGA scores. The levels of IL-6, IL-8, sTNF-RI, sTNF-RII, CRP, and ESR were significantly elevated according to Hurley staging system. Conclusions Serum proinflammatory cytokines, CRP, and ESR are increased in relation to the clinical inflammatory activity of patients with HS compared with healthy controls. Serum IL-6, CRP, and ESR are effective biomarkers for evaluating the severity of HS.

Highlights

  • Hidradenitis suppurativa (HS) is a chronic inflammatory disease originating in the follicular infundibulum [1]

  • We divided the patients with HS into the following 3 groups according to clinical inflammatory activity: a group with low inflammatory activity (LIA) (n = 22), including patients with Hidradenitis Suppurativa-Physician Global Assessment (HS-PGA) scores from 0 to 2; a group with moderate inflammatory activity (MIA) (n = 35), including patients with HS-PGA scores of 3; and a group with high inflammatory activity (HIA) (n = 17), including patients with HS-PGA scores of 4 and 5

  • We divided the patients into 3 groups according to clinical inflammatory activity based on their HS-PGA scores

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Summary

Introduction

Hidradenitis suppurativa (HS) is a chronic inflammatory disease originating in the follicular infundibulum [1]. HS is characterized by the formation of multiple inflammatory lesions such as nodules, abscesses, and fistulae, which predominantly affect the intertriginous regions. The proposed mechanism of the pathogenesis of HS begins with an alteration of the innate immune response to the commensal microbiota, which leads to epidermal hyperplasia This epidermal hyperplasia occludes the follicular infundibulum through the formation of cysts, which eventually break, free the keratin fibres, and release the commensal bacteria into the dermis. These steps amplify the inflammatory response through inflammasome activation and the interleukin- (IL-) 1β-IL-23/T-helper (Th) 17/IL-17 pathway [3, 6].

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