Eradicating hyperandrogenism? Hormonal changes following Helicobacter pylori eradication in women with polycystic ovary syndrome: an observational case series

11.06.2026

Joanna Wutke-Ostręga, Mateusz Szul, Dagmara Pluta

Abstract

Introduction: Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder in which hyperandrogenism represents a central pathophysiological feature. Increasing attention has been directed toward chronic inflammatory factors that may modulate androgen excess. Helicobacter pylori (H. pylori) infection is a prevalent chronic bacterial infection associated with systemic low-grade inflammation. However, its potential relationship with androgen-related hormonal parameters in PCOS remains poorly explored.

Material and methods: This observational mini case series included seven women with PCOS diagnosed according to the Rotterdam criteria and confirmed active H. pylori infection. Hormonal parameters including total testosterone, androstenedione, dehydroepiandrosterone sulfate (DHEAS), sex hormone-binding globulin (SHBG), anti-Müllerian hormone (AMH), and free androgen index (FAI) were assessed during active infection and after confirmed eradication. No hormonal contraception, antiandrogens, metformin, incretin-based therapies, or inositol supplements were used during the study period.

Results: Following successful H. pylori eradication, consistent changes in androgen-related parameters were observed. Median DHEAS, androstenedione, and total testosterone concentrations decreased, while SHBG levels increased. Consequently, the free androgen index decreased in all patients. AMH levels showed a downward trend after eradication. Due to the descriptive nature of the study, no inferential statistical analyses were performed.

Conclusions: In this observational case series, H. pylori eradication was associated with coherent changes in androgen-related hormonal parameters and reduced androgen bioavailability in women with PCOS. Although causality cannot be established, these findings suggest that chronic infection-related inflammation may influence the androgenic milieu in PCOS.