Artículo de publicación IS

SummaryBackground There is a dearth of information on the precise pathogenesis of hidradenitis suppurativa (HS), but immune dysregulation is implicated. Objectives To determine the nature of the immune response in HS. Methods Skin biopsies -lesional, perilesional (2 cm away) and uninvolved (10 cm away) -were obtained from patients with HS and healthy controls. The expression of various cytokines was determined by enzyme-linked immunosorbent assay, flow cytometry and real-time polymerase chain reaction. Results The expression of the inflammatory cytokines interleukin (IL)-17, IL-1b and tumour necrosis factor-a was enhanced in lesional skin of patients with HS. In addition, IL17A and IL1B mRNA were enhanced in clinically normal perilesional skin. CD4 + T cells produced IL-17 in HS, while CD11c + CD1a À CD14

many dimensions of sleep are adversely associated with CLBP. Management strategies for CLBP need to address these to maximize quality of life in this patient cohort.

Hidradenitis suppurativa (HS) is a chronic relapsing inflammatory disease of follicular occlusion characterized by boils, sinus tracts, fistulae, and scarring. It has a significant underestimated morbidity. Antimicrobial, immunosuppressive, anti-androgenic, and surgical approaches have been used with varying results. Knowledge of the pathogenesis of HS is fragmented, and treatment choices have hitherto been empiric without an exact understanding of the scientific basis for their use. Tumor necrosis factor-α inhibitors have shown promise in the treatment of HS in recent years, and the concept of HS as an immunological condition has come to the fore. The focus of this review is to discuss the immunological abnormalities underpinning HS as elucidated to date.