Immunosuppressive therapy in hidradenitis suppurativa

Abstract

Hidradenitis suppurativa (HS) is an inflammatory skin disease. The clinical presentation and historical concept of the disease have traditionally been interpreted to indicate that bacteria have a pathogenic role, but specific microbiological investigations have suggested that the role of bacteria is generally not that of a simple infection. Routine cultures are more often than not found to be sterile, and recognized pathogens such as Staphylococcus aureus can be found mainly in rapidly evolving lesions [1, 2]. Heavy bacterial overgrowth of known pathogens is therefore not a main feature of the disease, and the pathogenic role of bacteria may be an immunological one. Bacteria may only be the antigen that starts an immunological disease. Similar mechanisms have been described in guttate psoriasis and atopic dermatitis. In acne, bacterial antigens have also been shown to elicit an immunological response, suggesting a similar mechanism. Similarly scarring is a prominent feature of more advanced disease [3]. Whereas scarring is currently not amenable to medical therapy, preventive medical therapy may be of clinical interest. Since the primary pathogenic event in HS is not known, treatment directed at minimizing scar formation is of independent interest to all involved. Immunosuppressive therapy has a potential in reducing the inflammatory phase of the disease, which may result in subsequent scar formation. Accepting the possibility of such a mechanism, a different range of therapeutic options becomes available to the dermatologist.