Regulation of Inflammatory Genes in Hidradenitis Suppurativa

Hidradenitis Suppurativa

The purpose of this protocol is to examine the cytokine profi le of pati ents with hidradeniti s suppurati va (HS) and idemechanisms responsible for post-transcripti onal regulati on of these genes. The primary objecti ve is to determinfollowing cytokines linked to hidradeniti s suppurati va are diff erenti ally expressed in hidradeniti s pati ents versus controlalso doing a sub-study to determine the eff ect of childhood trauma on HS. The parti cipati on in the sub-study is opti onal

Hidradeniti s suppurati va (HS) is a chronic infl ammatory cutaneous disease which involves the pilosebaceous-apocrwhich typically presents aft er puberty with painful nodules and abscesses which can form sinus tracts and scars in theapocrine gland-bearing sites of the body. 1 Esti mates of disease prevalence range from 0.0003% to 4%, with youngparti cularly women as the most eff ected group. Racial predilecti on has also been demonstrated, with a higher likeldisease in African American and biracial individuals when compared to whites.1 HS is an under-recognized enti ty, ontaking 7.2 years from symptom onset to formal diagnosis.2 A notable aspect of HS is the profound impact it can have oof life in pati ent's suff ering with the disease, with an increase in depression, pain, and social and work impairment.pathogenesis conti nues to be elucidated but is primarily thought to be due to follicular hyperkeratosis, leading formati on, dilati on, and rupture. This in turn causes infl ammati on, abscess and sinus tract formati on. 1, 4 Whiunderstanding of a role of tumor necrosis factor (TNF) alpha, interleukin (IL)-1, IL-17A, IL-23, C-reacti ve protein (Cinterferon (IFN) gamma have been previously shown, much is sti ll unknown of the molecular involvement of infl ammarkers in HS.1, 2, 4. Currently, management varies from topical treatment, to surgical excision, to prescribing manbiologic medicati ons used for hidradeniti s suppurati va and infl ammatory bowel disease. However, there can be vasvariability in response to these medicati ons, and a proper understanding of the infl ammatory markers involved inpathogenesis will allow for more specifi c treatment, while hopefully avoiding the adverse eff ects related to these isuppressive medicati ons. Thus, in this study we will assess the cytokines, TNF-alpha, IFN-gamma, IFN-alpha, IFN-beta, IIL-12, IL-23, IL-17A, and study their regulati on in HS lesions of pati ents, with the ulti mate goal of identi fying potenti al tafuture therapies and interventi ons.

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