Abstract
CONTEXT: Increased circulating insulin levels contribute to hyperandrogenism in polycystic ovarian syndrome (PCOS) which causes a derangement in folliculogenesis, thus contributing to polycystic morphogenesis of the ovaries and a higher than normal anti-Mullerian hormone (AMH). A high AMH is an indicator of either stubborn anovulation or a predictor of ovarian hyperstimulation syndrome. Hence, it is postulated that the use of insulin sensitizers will reduce insulin resistance, hyperandrogenism, and subsequently serum AMH levels and will convert anovulatory cycles to ovulatory. AIM: To study the effect of insulin sensitizers on raised serum AMH levels in infertile women with PCOS. SETTINGS AND DESIGN: This was a prospective interventional randomized single tertiary center study. METHODOLOGY: The study was conducted from August 2015 to April 2016. Infertile patients with PCOS as defined by the Rotterdam criteria with raised AMH (>5 ng/ml) levels were enrolled in the study under strict inclusion and exclusion criteria. The sample size was 105 patients. Cycle regularity, day 2-antral follicle count (AFC), luteinizing hormone, AMH levels, modified Ferriman-Gallwey score (mFGS), and acne score were recorded before starting the intervention. Patients were randomized into three equal groups of 35 each. Group A received metformin alone, Group B metformin plus myoinositol, and Group C only myoinositol. After completion of 3 months of pretreatment, the same parameters were rechecked. STATISTICAL ANALYSIS USED: Univariate analysis and Chi-square test were used for statistical analysis. RESULTS: Of 105 patients, 95 completed treatment and the rest 10 dropped out. There was a reduction in AMH in all groups of insulin sensitizers with significant fall in the metformin only group. Cycle regularity, reduction in AFC, mFGS, and grade of acne were also obtained. CONCLUSIONS: Therapy with insulin sensitizers in PCOS women with raised AMH reduces the AMH levels, converts irregular menstrual cycles to regular, and reduces clinical hyperandrogenism.