Aetiology and Pathogenesis of Hidradenitis Suppurativa

K. Wolk; O. Join-Lambert; R. Sabat


The British Journal of Dermatology. 2020;183(6):999-1010. 

In This Article


HS is a complex, immunologically mediated disease that involves different components simultaneously: an inflammasome-driven innate component with dominance of neutrophilic granulocytes, a significant anti-inflammatory component, and strong activation of the Th1 and the Th17 pathways, but not the Th22 pathway. Anaerobic bacteria and cell-damage-associated molecules play an inflammation-triggering role. Activated pathways induce inflammatory vicious circles resulting in pain, purulence, tissue destruction and scarring. Several clinical studies are currently being carried out that aim to prevent the action of cytokines such as IL-17, IL-23p19 and IL-1,[1] the roles of which are described above. Prevention of cytokine action is possible by neutralization of the cytokines themselves, blocking their specific receptors or interfering with their signal transduction (Figure 4). Not only the pathogenetic complexity but also the destructive nature of HS represents a challenge for the development of therapeutic approaches for this disease. In fact, once the skin architecture is damaged, it cannot be repaired with medications. Therefore, great efforts are needed to reduce the current intolerable delay in the diagnosis of HS[162] as a prerequisite for an early start of anti-inflammatory treatment. An early treatment start may also prevent or counteract the systemic comorbidities and reduced life expectancy of patients with HS.