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Presentation

Hormonal, Metabolic, and Microbiome-Based Management of Hidradenitis Suppurativa in PCOS and Gender-Affirming Care

Description

The speaker, an internist, presents a practical framework for managing hidradenitis suppurativa (HS) that integrates hormonal, metabolic, and microbiome factors rather than treating the skin alone. She explains that HS is often hormonally sensitive, with flares linked to menstruation, PCOS, pregnancy changes, and both endogenous and exogenous androgens. Her “three-lever” model centers on hormones, insulin resistance/metabolism, and immune-microbiome inflammation, describing a self-reinforcing cycle in which insulin resistance drives hyperinsulinemia, ovarian androgen production, fat gain, and further inflammation. She emphasizes that gut dysbiosis, low fiber intake, ultra-processed foods, and NSAID use can worsen intestinal permeability and systemic inflammation, thereby amplifying HS. In gender-affirming care, testosterone therapy may unmask or worsen HS and metabolic risk, but she stresses respecting the patient’s need for affirming treatment while monitoring A1C, lipids, blood pressure, and kidney markers and using metformin and GLP-1s early when appropriate. She also reviews contraceptive choices by androgenicity, favoring less androgenic options and warning that Depo-Provera can significantly worsen metabolic health. For broader management, she highlights metformin, vitamin D, omega-3s, and especially N-acetylcysteine as helpful adjuncts, and argues that clinicians should assess the full metabolic context, hormone exposures, and microbiome rather than relying on BMI or topical skin therapy alone.

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Conclusions

Hidradenitis suppurativa appears to be strongly influenced by hormonal sensitivity, especially androgen exposure, and is often linked with PCOS, perimenstrual flares, and pregnancy-related changes.
The speaker’s central model is that HS is driven by interacting hormone, metabolic, and immune pathways, with insulin resistance and the gut microbiome amplifying inflammatory signaling.
Insulin resistance and hyperinsulinemia may worsen HS by increasing ovarian androgen production, adipocyte expansion, and a self-reinforcing cycle of inflammation and metabolic dysfunction.
A healthy gut microbiome and adequate fiber intake are presented as important upstream regulators of inflammation, while dysbiosis, leaky gut, NSAID overuse, and ultra-processed foods may worsen disease.
Gender-affirming testosterone therapy can unmask or exacerbate HS, but the recommended approach is not to stop identity-affirming hormones reflexively; instead, clinicians should buffer metabolic and androgenic effects with individualized adjunctive therapy.
The androgenicity of contraceptives matters clinically, with more androgenic agents potentially worsening HS and less androgenic options generally preferred when contraception is needed.
Testosterone replacement in men may improve metabolic parameters, but excessive androgen exposure, especially from pellets or supraphysiologic dosing, can trigger HS or related inflammatory problems.
A systems-based treatment strategy that combines metformin or GLP-1 therapy, anti-androgens, vitamin D, omega-3s, fiber, and N-acetylcysteine is presented as more effective than treating the skin alone.
Vitamin D deficiency, low fiber intake, and other modifiable inflammatory factors are portrayed as common and important targets in HS management.
N-acetylcysteine is highlighted as a low-cost adjunct that may reduce inflammation and lesion burden, particularly in patients with metabolic features.
Overall, HS is framed as a disease of context in which hormones initiate disease signals, but metabolic health and the microbiome determine the severity of the response.
There are still major evidence gaps and no clear guidelines for HS management in several hormone-related settings, including trans populations, IVF patients, and aging populations.

Katherine Sherif, MD, FACP, Professor and Vice Chair for Academic Affairs in the Department of Medicine at Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia.