The Desmoid Tumor Research Foundation

October 2026

Androgenic hidradenitis suppurativa onset linked to gamma secretase inhibitor

Author Information

Hansen Tai 1 2, Khyla T Hill 1 3, Aarthi Parvathaneni 1 4, Zahidul Islam 5, Steven R Cohen 1

1Department of Dermatology, Weill Medical School of Cornell University, New York, New York. 2SUNY Upstate Norton College of Medicine, Syracuse, New York. 3Loyola Stritch School of Medicine, Maywood, Illinois. 4McGovern (University of Texas, Houston) Medical School, Houston, Texas. 5School of Medicine, New York Medical College, Valhalla, New York.

Publication

JAAD Case Rep

Summary

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disorder of follicular origin, primarily affecting areas with apocrine gland-bearing skin. Recurrent painful nodules, abscesses, and sinus tracts characterize advanced HS. It leads to scarring, malodor, and intractable draining wounds, significantly impairing quality of life.1 Past studies have demonstrated underlying genetic etiology for HS, especially in familial HS, where genetic variation in gamma-secretase complex protein-coding genes accounts for most identified variants from genome-wide sequencing in familial and sporadic HS.2,3 Nirogacestat, a gamma-secretase inhibitor, was recently approved by the U.S. Food and Drug Administration for the treatment of desmoid tumors. It exerts its effects by blocking Notch signaling through the selective inhibition of gamma-secretase cleavage of Notch receptors.4 We present a rare and intriguing case of a patient who developed HS after 6 months of nirogacestat therapy. To our knowledge, only 1 other case report has delineated the relationship between gamma-secretase inhibitors and the development of HS.

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