Antibiotic therapy

Abstract

Antibiotic therapy is widely recommended and mentioned in all textbooks of dermatology as a prominent form of treatment of hidradenitis suppurativa (HS). Curiously, the literature reveals only a handful of primary studies on the use of antibiotics in this chronic, destructive disease. The original descriptions of chronic, recurrent abscesses in the axillary, mammary, and perineal skin and then the possible linkage to apocrine glands by Verneuil in 1854 formed a logical basis for thinking of this disease as an "infection of apocrine glands" [1]. In 1956, Pillsbury, Shelley and Kligman proposed the concept of the follicular occlusion triad and brought together acne conglobata, HS, and dissecting cellulitis of the scalp. The central event in these conditions was viewed to be follicular hyperkeratinization leading to retention of corneocytes and secondary bacterial infection [2]. This concept was strengthened by the work of Shelley and Cahn in 1955 [3]. They occluded the axillae of volunteers with impermeable plastic film and reported the subsequent formation of dermal abscesses. Their analysis was that poral occlusion of follicles led to hyperkeratosis of the distal apocrine duct, and dilatation of apocrine ducts with subsequent ductal rupture and inflammation. They described the presence of bacteria in the inflammatory infiltrate and hypothesized that bacteria trapped beneath the hyperkeratotic plug proliferated in apocrine sweat milieu with neutrophils pouring into the apocrine duct. Rupture of the duct leads to "spread of infection" and abscess formation. In this work epithelial sinus tracks were not described. In our view Shelley and Cahn more likely induced bacterial furunculosis than a chronic inflammatory process associated with epithelial sinus tract formation. In more recent years, the concept of infection of apocrine glands has been questioned. For example, the absence or paucity of apocrine glands in lesions on the buttocks, inframammary folds, inguinal, and thigh areas argues against apocrine glands being the primary site of pathology. Furthermore, histopathologic studies indicate that the dominant feature are epithelial-lined cysts and sinuses of follicular origin [4, 5]. The latter authors [5] proposed the term acne inversa and believe that lesions begin in terminal follicles with hyperkeratosis of the infundibulum giving rise comedo-like horny impactions with subsequent rupture of the follicular canal, and dermal inflammation with strands of epithelia extending into the dermis in an attempt to encapsulate the inflammatory reaction. Bacterial infection, when present, is a secondary, aggravating factor.