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Polycystic ovary syndrome (PCOS) is the most common female endocrine disorder, present in 5 – 7% of women of reproductive age. The diagnosis of PCOS was made according to Rotterdam criteria in presence of at least two of the following: 1) oligomenorrhea and/or anovulation; 2) hyperandrogenism (clinical and/or biochemical); 3) polycystic ovaries with the exclusion of other etiologies (1). The disorder is characterized by irregular menstrual cycle, chronic anovulation and hyperandrogenism. Women with PCOS demonstrate marked clinical heterogeneity: the commonly associated features of hirsutism, acne, polycystic-appearing ovaries, obesity and acanthosis nigricans are neither uniform nor universal (2-3). In time the disorder may lead to onset of hyperinsulinemia, insulin resistance, gestational diabetes, early onset of type 2 diabetes mellitus (DM), dyslipidemia and cardiovascular disease (CVD) (4-5). PCOS is characterized by a complex physiology implicating an interaction with environmental and genetic factors, resulting in a broad spectrum of reproductive and metabolic disorders. (6-7) Adult females with PCOS may be at increased risk for atherosclerotic cardiovascular disease (CVD) due to increased prevalence of obesity and central adiposity as well as to hypertension, hyperinsulinemia, type 2 DM, and dyslipidemia in these patients (8).The prevalence of obesity and consequently the presence of metabolic abnormalities reported in Italian and American published studies differs considerably, underlining the presence of important ethnic differences. (9, 10, 11, 12). A percentage ranging from 30-75% of women with PCOS are obese, European women generally weighing less than their American counterparts (20,21). Hyperinsulemia and/or insulin resistance (IR) are frequently manifested in obese, and to a lesser extent (50%) in lean, PCOS patients (3, 13, 14). Hyperandrogenaemia, hyperinsulemia and obesity are considered as risk factors for the development of hypertension and dyslipidemia, diabetes mellitus and coronary disease in PCOS (15-16). The causes of metabolic disorders in PCOS remain to be clarified, but include obesity-related IR, an intrinsic abnormality of postreceptor insulin signaling (e.g. excess serine phosphorylation), and abnormal insulin secretion. On the other hand, increased resistance to insulin is a hallmark of the onset of normal pubertal development with natural to pre-pubertal values at the end of puberty in non-obese subjects. Consequently, in early adolescence a physiological resistance to insulin should be taken into account (12). |
