SAT-179 - Phenotype of Polycystic Ovary Syndrome in Women with and without Obesity: Comparison of Clinical, Hormonal and Sexual Features

Background: Obesity and Polycystic Ovary Syndrome (PCOS) share key pathophysiological mechanisms, including insulin resistance, hyperandrogenism and hypothalamic-pituitary-ovarian axis dysfunction.
In literature, it is debated whether gonadal alterations in PCOS with and without obesity arise from distinct pathophysiological mechanisms. Some manifestations of PCOS are influenced by body mass index (BMI), but the specific ways in which obesity affects the gonadal axis remain unclear.

Aim: To compare clinical, hormonal, and sexual parameters between women with PCOS and severe obesity and women with PCOS without obesity, focusing on extreme BMI categories to minimize phenotypic overlap.
Materials and methods: In this retrospective cross-sectional study we collected clinical data (age, BMI, Ferriman–Gallwey [F&G] score), hormonal parameters (LH, FSH, total testosterone, sex hormone binding globulin [SHBG], Δ4-androstenedione [D4A], dehydroepiandrosterone sulfate [DHEAS], anti-Müllerian hormone [AMH]), metabolic parameters (fasting glucose, lipid profile), and sexual function data (Female Sexual Function Index [FSFI]) from ninety-six women with PCOS and BMI ≥35 kg/m² (G1) or ≤29.9 kg/m² (G2). Patients were recruited from three centers (Auxologico San Luca, Careggi Hospital and Auxologico Piancavallo Hospital).

Results: Twenty-seven patients belonged to G1 and sixty-nine to G2. We found no significant difference between the two groups in terms of age, FSFI scores, LH and FSH levels, and the LH/FSH ratio. G1 showed higher F&G scores (P = 0.0410). Total testosterone and DHEAS levels were similar between groups, whereas SHBG was significantly lower and the free androgen index was higher in G1. D4A levels were lower in G2 (P = 0.0444).
AMH levels were lower in G1 (P = 0.0106) and positively correlated with LH, D4A and the ovarian theca cell stimulation index (D4A × LH), independently of age, BMI, and HOMA index.

Discussion: We found that PCOS in patients with severe obesity is characterized by an increased clinical hyperandrogenism, exacerbated by reduced SHBG levels and increased free androgen fractions as compared with patients without obesity. In patients with severe obesity, we observed lower AMH levels correlating with reduced thecal stimulation, as suggested by the D4A×LH index. These findings support the hypothesis of blunted central stimulation in women with PCOS and severe obesity, consistent with the effects of obesity observed in male functional hypogonadotropic hypogonadism.

Conclusion: These findings seem to delineate a distinct endocrine, metabolic and reproductive clinical profile of PCOS due to severe obesity, characterized by reduced hypothalamic–pituitary stimulation, likely mediated by multiple interrelated factors.

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