Endocrine Abstracts (2008) 16 P639

Weight loss determines a complete remission of the polycystic ovary syndrome in most of obese women

Ilaria Grassi, Lara Giovannini, Giulia Forlani, Laura Patton, Alessandra Gambineri & Renato Pasquali


Endocrinology Unit, Bologna, Italy.


Obesity is strictly connected with Polycystic Ovary Syndrome (PCOS). However, we still do not know whether a form of PCOS secondary to obesity exists or whether obesity exacerbates manifestations of the syndrome. To answer this question we contacted seventy obese patients with PCOS that attended our Endocrinology Unit in the last 3 years and that lose weight after at least 6 months of dietary treatment. Sixty-five out of 70 patients agreed to take part to the study and gave their informed consent. The diagnosis of PCOS was performed at baseline according to the NIH criteria (oligo/amenorrhea and hyperandrogenism or hyperandrogenemia) and was re-evaluated after weight loss using the same criteria. At baseline 59/65 women executed also a pelvic ultrasonography that confirmed the diagnosis of PCO, whereas only 23/65 repeated it after weight loss. After weight loss PCOS disappeared in 45/65 women (Responders – R), whereas PCOS did not disappeared in 20/65 patients (Non-Responders – NR). This result was not related to the reduction of body weight that did not differ between the two groups (mean reduction of body weight: R −14.3±7.3 kg; NR −14.7±8.8 kg, P NS). At baseline NR had higher waist, waist-to-hip ratio (WHR) and androstenedione levels respect to R (waist: R 97.3±10.4 cm; NR 106.5±15.9 cm, P<0.01; WHR: R 0.851±0.077; NR 0.915±0.097, P<0.01; androstenedione: R 354±147 ng/dl; NR 482±151 ng/dl, P<0.01). All the other anthropometric, hormonal, and metabolic parameters did not differ between the two groups. Only R group significantly reduced DHEAS (−0.31±0.89 μU/ml, P<0.01), LH (−4.51±8.45 mIU/ml, P<0.05), and FSH (−0.99±2.28 mIU/ml, P<0.05) levels after weight loss. Insulin resistance and hyperinsulinemia similarly improved in both groups. These data show that a secondary form of PCOS related to obesity does exist and that insulin-resistance and hyperinsulinemia are not the main pathogenetic mechanisms of this variant.

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