Hidradenitis suppurativa (HS) is a debilitating, chronic, inflammatory skin disease primarily affecting apocrine gland-rich areas of the body. On the one hand, the presence of triggering factors—some identified, others only hypothesized—may initiate or perpetuate the pathogenic process of HS. In addition to cigarette smoking and diet, other trigger factors, including choice of clothing, are frequently observed in clinical practice. On the other hand, the presence of disease may influence habits of HS patients. Indeed, high incidences of sexual and sleep impairment have been reported in these patients. Consequently, alcohol and substance abuse may be a coping strategy for the emotional and psychological disease burden. Furthermore, a greater awareness of gender differences in HS may be important for dermatologists in their own clinical practice (i.e., pregnancy and breastfeeding). Consequently, in this loop interaction, comprehensive knowledge of all factors involved is crucial for the management of HS patients. Thus, the objective of this review is to (i) discuss the influence of gender on HS, (ii) summarize the most frequent triggering factors of HS and (iii) analyze the impact of HS on patient habits.

Hidradenitis suppurativa (HS) is an inflammatory skin disease whose pathogenesis remains poorly defined. Over the past decades, the bacterial role in HS patients has been a focus of research. According to the literature, the HS skin (and probably gut) bacterial composition is different to that of healthy controls. To date, a key question is whether compositional changes in the microbial populations are responsible for the development of HS (primum movens), or only secondarily reflect the ongoing inflammatory process. The great diversity of methodologies that have been used to study microbial role in HS have led to an accumulation of conflicting results. Thus, in view of these considerations, the aim of this article is to provide the reader with an overview about different hypotheses proposed to explain the bacterial role in HS pathogenesis.