A clinical‐pathological review of hidradenitis suppurativa: using immunohistochemistry one disease becomes two

Abstract

We report the results of a re-examination of a series of 57 biopsies from 50 patients with the clinical diagnosis of hidradenitis suppurativa, submitted to the Department of Pathology at the University Hospital of Northern Norway, Tromsø, Norway. The biopsy material came from hospitals and physicians all over northern Norway in the years 2000-2007. All tissue material was resectioned and stained with the immunohistochemical reagent, cytokeratin (AE1/AE3/PKC26), and that made it possible to divide the material into two different disease categories: (1) 36 biopsies from 30 cases had tissue inflammation after rupture of keratin-rich epidermal cysts, which we call 'horny cell inflammation', followed by extensive cutaneous thrombi and infarcts, and (2) 21 biopsies from 20 cases had 'apocrinitis' defined here as an inflammatory destruction of apocrine skin glands, and partly of close eccrine glands. The two disease populations differed: the patients with a diagnosis of horny cell inflammation were younger and mainly women; those with a diagnosis of apocrinitis, as defined here, were older, men and women equally represented.

Health Care Utilization Patterns and Costs for Patients With Hidradenitis Suppurativa

“…[6][7][8] Patients develop intermittent flares with acutely painful nodules and/or abscesses, which contribute to HS being underdiagnosed or misdiagnosed as "boils" or infection by nondermatologists. 9,10 The acuity of flares and frequent diagnostic delay that patients experience may contribute to differences in health care utilization. The objective of this study was to assess how individuals with HS utilize medical care, especially emergency department (ED) care and inpatient care, both high-cost settings.…”

Purulent Hidradenitis. Part I

“…В случае поломки генов Notch-пути, кодирующих -секретазу, -никастрин (NCSTN) и пресенилины (PSEN1, PSEN2) -происходит нарушение расщепления Notch-рецептора трансмем-бранной протеазой, что в свою очередь приводит к реду-цированию HES и HEY. Утрата транскрипционных генов приводит к неконтролируемой избыточной пролиферации клеток в верхних отделах волосяного аппарата и в даль-нейшем к его закупорке богатыми кератином эпидер-мальными роговыми кистами [12,13]. Последующая иммунная дисрегуляция вызывает сильное воспаление, которое лишь дополняется бактериальными агентами и развитием мощного септического воспаления (рис.…”

Impaired Notch‐MKP‐1 signalling in hidradenitis suppurativa: an approach to pathogenesis by evidence from translational biology

“…Hidradenitis suppurativa begins with alterations of HF keratinization subsequently leading to plugging and dilatation of HFs, inflammation, epidermal cyst, abscess and sinus tract formation . Early lesions show follicular hyperkeratosis, hyperplasia of follicular epithelium, pronounced perifolliculitis and rupture of HF and epidermal cysts . Fismen et al .…”

“…Early lesions show follicular hyperkeratosis, hyperplasia of follicular epithelium, pronounced perifolliculitis and rupture of HF and epidermal cysts . Fismen et al . underlined the important role of ruptured keratin‐rich epidermal cysts as well as apocrine glands as major target structures of inflammation, which they classified as ‘horny cell inflammation’ and ‘apocrinitis’.…”

“…The activation of apocrine glands during puberty may play a pathogenic role in Notch‐dependent apocrine gland homoeostasis in HS. The observed ‘aprocrinitis’ in HS may thus represent a further compromised target structure, which activates innate immunity in HS lesions (Fig. ).…”