Hidradenitis suppurativa and immune dysregulation

This is the authors' abstract. We don't add key points for this paper.

Conflicts of interest None declared. Hidradenitis suppurativa (HS) is a disease in dire need of more efficient treatment options. The development of new treatments has hitherto been empirical as the aetiology of HS remains a topic for speculation.1 Nevertheless, significant progress has recently been achieved leading not only to more therapeutic options for patients, but also increasing our understanding of the pathogenesis of this disease. In contrast to the common view of HS as primarily an infectious disease, the concept of HS as an immunological disease has gradually been accepted. The use of immunosuppressive agents in the treatment of HS has been recognized for a long time, but has been poorly evidenced.2 In 2001, a serendipitous observation of the therapeutic success of infliximab in a patient with concomitant Crohn disease suggested that tumour necrosis factor (TNF)‐α blockers could have an effect on HS.3 In consequence, several further cases were reported, and the initial enthusiasm was supported by small randomized controlled trials of infliximab and adalimumab.4–6 More recently, a larger controlled trial has indicated that adalimumab, at a dosage commonly used for Crohn disease, has a significant effect.7 In a back‐handed way, the rising level of evidence in favour of treating HS with anti‐TNF‐α antibodies is now providing a stronger footing for studies concerning the aetiology of the disease.