AIMS: To study the prevalence of clinical manifestations in obese and lean polycystic ovarian syndrome (PCOS) women and their health hazards. SETTINGS AND DESIGN: This prospective study was carried out in a tertiary care infertility clinic from 1.7.2005 till 31.12.2007. MATERIALS AND METHODS: These women were diagnosed to have PCOS by the European Society of Human Reproduction and Embryology and the American Society of Reproductive Medicine, Rotterdam 2003 criteria. They were further divided into two groups according to their body mass index (BMI): Group A (n = 300), overweight and obese with BMI >23 and Group B (n = 150), normal weight and lean with BMI â‰¤23. STASTICAL ANALYSIS AND RESULTS: The prevalence of menstrual irregularities [79.2% vs. 44%, P= 0.000, 95% confidence interval (CI) = 0.26Ã±0.44)] and clinical hyperandrogenism (74.2% vs. 50.6%, P= 0.000, 95% CI=0.14Ã±0.32) was signifi cantly higher in the obese group, whereas android central obesity (waist to hip ratio >0.85) was similar in both groups, irrespective of body weight (47.7% vs. 38%, P= 0.056, 95% CI=0.06 to +0.18). Comparative data of various health manifestations in lean vs. obese women with POCS [Table 4]. Of the health risk manifestations, hypertension occurred in both groups with a similar frequency (41% vs. 35.5%, P= 0.261, 95% CI=0.03 to +0.15). Group A showed an increased prevalence of IGT (25% vs. 10%, P= 0.000, 95% CI= 0.13Ã±0.29) and type two diabetes mellitus (11.7% vs. 6%, P= 0.000, 95% CI= 0.13Ã±0.29) as compared with group B. endometrial hyperplasia (EH) also showed an increase prevalence in Group A compared with Group B (5.6% vs. 2%, P= 0.055, 95% CI= 0.01Ã±0.08), although not statistically significant. CONCLUSION: PCOS emerges as a clinically heterogeneous condition with increased prevalence of health risks such as hypertension, diabetes and EH. Of these, diabetes and EH appear to be more prevalent in the obese, putting them at a greater risk of morbid problems at a much younger age than the lean ones.
Polycystic ovarian syndrome (PCOS) aff ects four to 12% women of reproductive age. In 1935, Stein and Leventhal fi rst described the association of polycystic ovaries, amenorrhea, hirsutism, and obesity. The key features necessary for the diagnosis of PCOS were detailed at a conference convened by the National Institute of Health in 1990 and they were menstrual dysfunction and hyperandrogenism, with exclusion of other causes of hyperandrogenism (congenital adrenal hyperplasia, androgen-secreting tumors, and hyperprolactinemia). Probable criteria included perimenarchal onset, insulin resistance, elevated leutenizing hormone to follicle-stimulating hormone ratio and polycystic ovaries by ultrasonography (USG). PCOS was redefi ned at a joint consensus meeting of the European Society of Human Reproduction and Embryology (ESHRE) and the American Society of Reproductive Medicine (ASRM), held in Rott erdam in May 2003. This included the presence of two of the following three criteria: (a) oligo and/or anovulation, (b) polycystic ovaries on USG and (c) hyperandrogenism (clinical and/or biochemical), with the exclusion of other etiologies. The morphology of the polycystic ovary has been redefi ned as an ovary with 12 or more follicles measuring 2Ã±9 mm in diameter and/or increased ovarian volume (more than 10 cm3 ).
Recent insights into the pathophysiology of PCOS have shown that insulin resistance is a key feature and predisposes to type two diabetes mellitus in the long run. Higher levels of plasminogen activator inhibitor (PAI) type one, decreased vascular relaxation and endothelial dysfunction.
result in increased risk of hypertension and coronary artery disease. Chronic anovulation leads to a higher risk of developing endometrial hyperplasias (EHs), with or without cytological atypia as a sequel to unopposed estrogen exposure in the absence of progesterone.
The aim of this study was to study the prevalence of clinical manifestations and health risks in obese and lean PCOS women; primarily, impaired glucose tolerance (IGT) and diabetes, menstrual irregularity, and clinical hyperandrogenism and, secondarily, EH, android obesity and hypertension.