Alterations in leucocyte subsets and histomorphology in normal-appearing perilesional skin and early and chronic hidradenitis suppurativa lesions

Abstract

Psoriasiform hyperplasia, follicular plugging and low-grade leucocytic infiltration are already present in normal-appearing perilesional skin. Keratin fibres in the dermis are associated with clinical disease. Early lesions are characterized by neutrophilic abscess formation and influx of mainly histiocytes, and chronic lesions mainly by expansion of B cells and plasma cells in 'pseudo' follicles. Proliferating strands of follicular epithelium may initiate fistula formation. Mast cells are increased in all stages of HS including perilesional skin.

Hidradenitis suppurativa: why isn’t it a form of acne?

“…A laphámrák kialakulására nagy valószínűséggel a HS-ben fennálló krónikus bőrgyulladás hajlamosít. Ezzel szemben a B-sejtes lymphomák emelkedett előfordulása rávilágít a limfociták és a termelt immunglobulinok szerepére (20), melyek előrehaladott esetekben válnak jellegzetessé és mutatnak malignus transzformációt.…”

Can Animal Skin Diseases or Current Transgenic Mice Serve as a Model for Hidradenitis Suppurativa?

“…Recently we demonstrated the presence of free keratin remnants in the dermis and in multinucleated giant cells and proposed that this is a key histological hallmark of HS [6]. We hypothesized that that these keratin remnants are derived from ruptured infundibular cysts and that HS is the result of an aberrant clearing/inflammation reaction of these remnants [6].…”

“…We hypothesized that that these keratin remnants are derived from ruptured infundibular cysts and that HS is the result of an aberrant clearing/inflammation reaction of these remnants [6]. Moreover, it has been demonstrated that experimentally punctured dilated human hair follicles do form fistulas [43], which are a hallmark of severe HS.…”

“…Yet, it is now generally accepted that the infundibulum of the hair follicle is the primary origin of the disease rather than the apocrine glands [1]. The typical histology of HS yields infundibular occlusion, epidermal psoriasiform hyperplasia, involution of the sebaceous glands, cyst formation, free keratin remnants in the dermis phagocytosed by multinucleated giant cells, and a mixed inflammatory cell infiltrate with abscess formation [6,7,8]. …”

Failure of Anti-Interleukin-1 Therapy in Severe Hidradenitis Suppurativa: A Case Report

“…It is a chronic disease with natural flare-ups and remissions, but in severe disease inflammation, pain and discharge are continuously present, resulting in a significantly compromised quality of life [2]. HS is probably the result of environmental factors in a genetically predisposed individual in which infundibular occlusion results in cyst formation, subsequent rupture and inflammation [3]. Putative risk factors include smoking, obesity and mechanical friction [1].…”