The News in pathogenesis of Hidradenitis suppurativa

Abstract

Introduction and objectives Hidradenitis suppurativa (HS) – chronic, inflammatory, progressive skin, subcutaneous and hair follicle disease. A mean illness incidence of 6.0 per 100,000 person-years and an average prevalence of 1% has been reported in Europe [1]. The pathophysiology of HS was still poorly understand until recent years. It is known that genetics, immune response, smoking and obesity play a vital role in this disease onset. This summary aim is to summarize the most recent aspects of HS pathogenesis. Methods and materials During the period July 7st to April 20th 2020, PubMed database was searched for studies publicized in the last ten years employing the keywords “hidradenitis suppurativa”, “acne inversa” and “pathogenesis”. The following inclusion criteria were claimed to the search: review, articles in English. In total, nine articles match inclusion criteria and were reviewed for further data research. Results One of the most important gene dysfunction is related to γ secretase gene mutation. γ secretase comprises four subunits: presenilin (PSEN), presenilin enhancer 2 (PSENEN), nicastrin protein (NCSTN) and anterior pharynx defective 2. Mutations to any of the component genes can result in disease onset but mutations in the NCSTN gene are commonly observed in hidradenitis suppurativa and are related to familial HS [2]. Moreover, follicular occlusion stimulate bacterial proliferation and production of biofilms on skin to increase overexpression of Tolllike receptors type 2 which are vital components of the innate immunity[3]. Nicotine, by stimulating the skin's cholinergic receptors, promotes skin hyperkeratosis and hair follicle occlusion. Obesity is another pathway to HS. Classically activated macrophages are rich in obese adipose tissue and produce pro-inflammatory cytokines IL-1β, IL-6 ir TNF-α to start or maintain immunological reactions of HS [4]. [...].