Hyperandrogenaemia and Systemic Low-Grade Inflammation in Normogonadotropic Anovulation: A Prospective Cohort Study

Abstract

Purpose

To investigate whether clinical and biochemical profiles, including inflammatory mediators, differ between hyperandrogenemia and normoandrogenemia in normogonadotropic anovulation, and to analyze the correlations of selected variables with inflammatory activity.

Methods

Clinical parameters, such as quality of life, and biochemical characteristics, including ovarian, metabolic and inflammatory parameters, were prospectively compared across hyperandrogenemia and normoandrogenemia groups of anovulatory women. Their correlations with interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), interleukin-10 (IL-10), and C-reactive protein (CRP) concentrations – potentially involved in ovulatory mechanisms – were assessed.

Results

The study groups did not differ significantly in terms of selected clinical, inflammatory, and metabolic parameters. Biochemically, the hyperandrogenemia group had significantly higher concentrations of follicle-stimulating hormone, luteinizing hormone, anti-Müllerian hormone, and free triiodothyronine. Testosterone concentration did not exhibit significant correlations with inflammatory indicators. The strongest correlations with IL-6, CRP, and TNF-α concentrations were found for metabolic parameters. Clinical parameters, such as quality of life in “Physical functioning” negatively correlated with IL-6 and CRP, while “Energy/Fatigue” correlated negatively with CRP concentration. Hyperandrogenism indicators, such as the Ferriman-Gallwey score and the free androgen index, positively correlated with IL-6 and CRP concentrations.

Conclusions

Hyperandrogenemia had no effect on clinical, metabolic, or inflammatory parameters. Since no differences in inflammatory parameters were found between hyperandrogenemia and normoandrogenemia, further investigation into the mechanisms of ovulatory defects is warranted. The observed correlations between clinical and metabolic parameters and inflammatory mediators were not driven by hyperandrogenemia. Reducing systemic inflammation and its chronicity is essential to prevent adverse metabolic health outcomes.