INTRODUCTION
Hidradenitis suppurativa (HS) is a chronic, inflammatory skin disease characterized by recurrent nodules and abscesses that may rupture, leading to the formation of sinus tracts and scarring.1 Lesions most frequently affect apocrine sweat gland-bearing areas within the intertriginous folds of the body. The initiating event is thought to be occlusion of the hair follicle secondary to follicular hyperkeratosis, leading to dilation and eventually rupture of pilosebaceous units.1 Keratin and bacteria are subsequently released into the dermis leading to sustained chronic inflammation.2 The sinus tract formation and scarring that occur as a result, are thought to be due to dysfunctional neutrophils releasing reactive oxygen species and proteases, causing tissue destruction.3 Although the rationale for the follicular occlusion has yet to be defined, altered Toll-like receptor (TLR) signaling due to a deficiency in the Notch signaling pathway on macrophages and dendritic cells may lead to increased production of pro-inflammatory cytokines. Interleukin (IL)-1beta, IL-17, and particularly, tumor necrosis factor (TNF)-alpha play a major role in HS pathogenesis as overexpression has been linked to disease severity.4
Immunomodulatory, immunosuppressive, and antibiotic medications have been used to treat HS; however, response to these treatments is variable.5 Topical clindamycin is most effective for superficial lesions and is indicated only for localized Hurley Stage I or mild Stage II disease.6 The combined use of clindamycin (300 mg bid) and rifampicin (600 mg daily) for ten weeks is beneficial for widespread Hurley Stage I or mild Stage II disease, however, disease relapse has been reported in patients receiving this combination therapy after a one-year follow-up.6-8 The combination of rifampicin (10 mg/kg daily), moxifloxacin (400 mg daily), and metronidazole (500 mg tid) for six weeks followed by rifampicin-moxifloxacin therapy is beneficial for Hurley Stage I or II disease or refractory disease.9 Infliximab and adalimumab are TNF-alpha inhibitors with benefits for moderate to severe disease (Hurley Stages II-III) and improve quality of life.10 Adalimumab was FDA-approved in 2015 for the treatment of HS. On the other hand, tetracyclines (500 mg bid) and isotretinoin are systemic treatments that have little to no effect on HS.11,12 Surgical intervention for persistent lesions may be considered alongside medical treatment.
Immunomodulatory, immunosuppressive, and antibiotic medications have been used to treat HS; however, response to these treatments is variable.5 Topical clindamycin is most effective for superficial lesions and is indicated only for localized Hurley Stage I or mild Stage II disease.6 The combined use of clindamycin (300 mg bid) and rifampicin (600 mg daily) for ten weeks is beneficial for widespread Hurley Stage I or mild Stage II disease, however, disease relapse has been reported in patients receiving this combination therapy after a one-year follow-up.6-8 The combination of rifampicin (10 mg/kg daily), moxifloxacin (400 mg daily), and metronidazole (500 mg tid) for six weeks followed by rifampicin-moxifloxacin therapy is beneficial for Hurley Stage I or II disease or refractory disease.9 Infliximab and adalimumab are TNF-alpha inhibitors with benefits for moderate to severe disease (Hurley Stages II-III) and improve quality of life.10 Adalimumab was FDA-approved in 2015 for the treatment of HS. On the other hand, tetracyclines (500 mg bid) and isotretinoin are systemic treatments that have little to no effect on HS.11,12 Surgical intervention for persistent lesions may be considered alongside medical treatment.
