Novel Therapeutic Approaches and Targets for the Treatment of Hidradenitis Suppurativa

Background: Hidradenitis Suppurativa (HS) is a chronic, recurrent and disabling inflammatory skin condition, clinically characterized by nodules, bullae, abscesses, fistulae, and draining sinus tracts mainly located in axillae, inguinal folds, inframammary region and buttocks, often leading to pain, scarring, disfigurement and decreased quality of life. Due to its complex nature, with still no completely elucidated etiology and pathogenesis, the management of IIS can be challenging. In fact, many patients do not respond to the traditionally available systemic treatments, including anti-inflammatories, antibiotics and surgery. Research has provided new insights into the mechanisms of HS, mainly investigating the inflammatory cytokine pathways underlying the disease. Methods: We review the current knowledge on newer therapeutic approaches and targets for the treatment of HS, through a PubMed-based literature search. Results: In this setting, studies on tumor necrosis factor-alpha, IL-1 beta, IL-10, and the IL-23/T-helper (Th) 17 and IL12/Th1 axes in immune dysregulation in HS have helped in developing new regimens. Inhibitor of phosphodiesterase 4 and laser treatments have shown clinically meaningful efficacy with good short-term safety and tolerability. Conclusion: Target therapy has revolutionized the treatment of moderate to severe HS, based on the inhibition of specific molecular or cellular targets, directly involved in the pathogenesis of the condition.

Automated summary

Research on newer therapeutic approaches targeting specific molecular or cellular targets, such as tumor necrosis factor-alpha, IL-1 beta, IL-10, and the IL-23/T-helper (Th) 17 and IL12/Th1 axes, has shown promising results in the management of HS. Inhibitors of phosphodiesterase 4 and laser treatments have demonstrated good short-term safety and effectiveness. Target therapy has revolutionized the treatment of moderate to severe HS by directly inhibiting the pathogenesis of the condition.