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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. [ABSTRACT FROM AUTHOR]

The Coronavirus Disease 2019 (COVID-19) pandemic, a global public health emergency, has changed dermatology practice and daily routine in just under two years. Much has been written in the literature about COVID-19-associated skin manifestations. Nevertheless, much less has been written regarding skin manifestations in patients affected by severe immune-mediated skin diseases, e.g., psoriasis and hidradenitis suppurativa, undergoing biological treatment during the COVID-19 outbreak. Thus, the aim of this article is to provide the reader with an overview of the cutaneous manifestations during the COVID-19 pandemic in this subset of patients. [ABSTRACT FROM AUTHOR]

Hidradenitis suppurativa (HS) is a debilitating, chronic, (auto)inflammatory disease primarily affecting apocrine gland-rich areas of the body. Although pathogenic mechanisms responsible for HS have not yet been fully elucidated, it is a multifactorial process whose main target is the terminal follicle. The role of the inflammatory process (and consequently of cytokine milieu) and of several other factors (genetics, lifestyle, hormonal status, microbiome, innate and adaptive immune systems) involved in HS pathogenesis has been investigated (and often defined) over the years with a view to transferring research results from bench to bedside and describing a unique and universally accepted pathogenetic model. This review will update readers on recent advances in our understanding of HS pathogenesis and novel (potential) medical therapies for patients with moderate-to-severe HS. [ABSTRACT FROM AUTHOR]