![]() To be diagnosed with PCOS under the ESHRE/ASRM Rotterdam criteria, which are considered to be a compromise between those of NIH and AE-PCOS, a woman must have at least two of three criteria after other related health conditions are ruled out: oligo-ovulation and/or anovulation, clinical and/or biochemical signs of hyperandrogenism, and polycystic ovaries visible by ultrasound ( 24, 25). ![]() ![]() Obstacles to timely diagnosis include the presence of multiple PCOS phenotypes and significant individual variation in clinical features, as well as competing diagnostic criteria from the National Institutes of Health (NIH), the European Society for Human Reproduction and Embryology and American Society for Reproductive Medicine (ESHRE/ASRM Rotterdam), and the Androgen Excess and PCOS Society (AE-PCOS) ( Table 1) ( 3, 15). Etiology of PCOSĭiagnosing and treating PCOS is important to preserve or restore fertility, reduce symptoms, and prevent complications that can develop in women with PCOS from adolescence to the postmenopausal period. However, research on the impact of PCOS on cardiovascular risk in the postmenopausal years is inconclusive and lacking ( 22, 23). Production of androgens tends to decrease in the years leading to menopause, so the menstrual cycles of women with PCOS often become more regular, with corresponding improvement in reproductive functioning ( 20, 21). Women who have PCOS and metabolic syndrome or type 2 diabetes are at the highest risk of CVD ( 19). PCOS and metabolic syndrome have many anthropometric and metabolic abnormalities in common, and hyperinsulinemia may be a crucial link between the two conditions ( 14). Between 35 and 60% of women with PCOS are obese ( 15), which appears to worsen both the metabolic and reproductive features of the condition, particularly in cases of visceral adiposity ( 18). Women with PCOS also have a four- to sevenfold higher risk of having a heart attack than women of the same age who do not have PCOS ( 17). In the United States, 33–47% of women with PCOS have metabolic syndrome, a rate two to three times higher than that of age-matched healthy women without PCOS ( 16). In addition to glucose and insulin abnormalities, CVD risk factors (hypertension, hyperlipidemia, impaired blood vessel function) often accompany PCOS ( 1, 2). The combination of anovulation and hyperinsulinemia can promote endometrial cell proliferation, increasing the risk of endometrial carcinomas and other abnormalities ( 16). Women with PCOS who have chronic anovulation but normal androgen levels tend to not be insulin resistant ( 15). Reduced SHBG levels lead to an increase in free testosterone levels ( 14). Insulin resistance, which occurs independently of obesity in PCOS ( 2), may affect ovulation and fertility by interfering with hepatic production of sex hormone–binding globulin (SHBG) ( 13). A 2010 systematic review and meta-analysis ( 12) of 35 studies found that PCOS is associated with a 2.5-fold increased prevalence of IGT and a fourfold increased prevalence of type 2 diabetes. Studies suggest that the annual progression rate from normal glucose tolerance to IGT and from IGT to type 2 diabetes in women is substantially enhanced among women with PCOS, with the highest risk in women who are also obese and have a family history of type 2 diabetes ( 9, 11). Conversely, the prevalence of PCOS is elevated among women who have already been diagnosed with type 1 or type 2 diabetes ( 2). An estimated 30–40% of PCOS patients have impaired glucose tolerance (IGT), and 7.5–10% have type 2 diabetes ( 7, 9). Tip: Serve this dish with a whole grain roll or bread stick.Insulin resistance with compensatory hyperinsulinemia affects ∼ 65–70% of women with PCOS ( 10).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |