Hidradenitis suppurativa is a chronic inflammatory skin condition affecting primarily the axillary, perianal, and inguinal areas. Patients with hidradenitis suppurativa present with occlusion and subsequent rupture of follicular ducts, profound abscesses, fistulae, odorous discharge, fibrosis, and scar formation, causing significant morbidity. Knowledge of the pathogenesis of hidradenitis suppurativa is limited and treatment with antimicrobial drugs, immunosuppressants, and surgical procedures have shown varying results. The pathogenic role of the interleukin-17 cytokine family in chronic inflammatory skin conditions has been described. Interleukin-17A and interleukin-17F have similar properties and induce the production of cytokines, chemokines, antimicrobial peptides, and metalloproteinases, all of which take part in the inflammatory response. The efficacy of anti-interleukin-17A therapy in psoriasis has also been proven and anti-interleukin-17A drugs are already in use for this condition. There is currently no consensus on the role of interleukin-17 in the pathogenesis of hidradenitis suppurativa. Studies have demonstrated increased interleukin-17 mRNA expression in lesional hidradenitis suppurativa skin, whereas the protein concentrations of interleukin-17 were found to be normal compared to healthy control skin in one other study. A phase II clinical trial on anti-interleukin-17 therapy in hidradenitis suppurativa is ongoing.
Conclusion and future perspectives
As suggested by the studies presented herein, interleukin-17 plays a role in several chronic inflammatory skin conditions including hidradenitis suppurativa. The background knowledge on the proinflammatory properties of interleukin-17 combined with the studies revealing enhanced interleukin-17 gene expression in hidradenitis suppurativa patients provides a reason for the therapeutic value of targeting interleukin-17 and its receptors in the treatment of hidradenitis suppurativa.
Currently, a phase II anti-interleukin-17 clinical trial in hidradenitis suppurativa is ongoing (ClinicalTrials.gov – identifier: NCT02421172). As the remaining functions of interleukin-17, along with the missing links in the pathogenesis of hidradenitis suppurativa are unveiled, the future looks promising for anti-interleukin-17 therapy in hidradenitis suppurativa. Nonetheless, further research is needed to clarify the role of interleukin-17 in the pathogenesis of hidradenitis suppurativa.
Full Research: https://www.ncbi.nlm.nih.gov/m/pubmed/29469692/?i=21&from=hidradenitis%20occlusion