Polycystic ovary syndrome (PCOS) is the com monest endocrine disturbance in women of reproduc tive years, and affects 5-10% of women of this age group1. The symptoms include: hirsutism and acne as evidence of excess androgen production, obesity, menstrual disturbances, and consequently anovula tion, and infertility. Symptoms often appear around menarche, while the biochemical abnormalities may be present around adrenarche2. PCOS is the com monest cause of anovulatory infertility and hirsutism worldwide3. However, the clinical presentation can vary widely; from an asymptomatic woman with the inci dental diagnosis of polycystic ovaries on ultrasound, to that which was first described by Stein and Leventhal4, an obese, hirsute, infertile woman with amenorrhoea and enlarged polycystic ovaries. Approxi mately 50% are obese, with significant central fat ac cumulation. A high fasting blood glucose associated with hyperinsulinaemia and insulin resistance occurs independent of the obesity in PCOS; all of which con fer an increased risk of glucose intolerance5. The range of biochemical abnormalities of PCOS include: hyper secretion of luteinizing hormone (LH), hyperandrogenaemia, acyclic oestrogen production, decreased sex hormone binding globulin (SHBG) concentrations and hyperinsulinaemia6.
Insulin resistance, accompanied by obesity, is an important risk factor for the development of longterm metabolic disease as described in the Metabolic Syndrome7. Recognized complications of PCOS are pregnancy associated diabetes mellitus and hyper tension, and” non reproductive” consequences such as, type 2 diabetes …
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