1. Polycystic ovarian syndrome (PCOS). The diagnosis is based on ultrasound or endocrine features plus the usual clinical presentation (oligomenorrhoea, infertility, obesity, hirsutism).
   
2. 1. Semen analysis on her husband.
   2. Test of tubal patency. Although the obvious cause appears to be PCOS, dual pathology may be present. A test of tubal patency may be ordered immediately or may be delayed and performed if a pregnancy fails to ensue after successful ovulation induction.
   
3. Apart from attention to weight reduction, the traditional first-line therapy is clomiphene citrate. Cumulative ovulation rates of approximately 80% and cumulative pregnancy rates of 40-50% can be expected.¹
4. Resistance to treatment with clomiphene citrate is in part related to the degree of obesity. The propensity for women with PCOS to hyperstimulate with usual doses of gonadotrophins has led to the use of low-dose incremental regimens for women with this condition. Gonadotrophin releasing hormone (GnRHa) pretreatment may be needed if there is a high baseline luteinising hormone (LH) concentration. Ovarian diathermy is as effective as gonadotropin therapy² with ovulation rates of > 80% and cumulative pregnancy rates of approximately 50%.
5. 1. Endometrial hyperplasia and endometrial carcinoma. Women with PCOS are at increased risk of developing endometrial hyperplasia and carcinoma.³ This is due partly to the action of unopposed oestrogen on the endometrium, but hyperandrogenism and hyperinsulinaemia may also contribute.
   2. Type II diabetes mellitus or impaired glucose tolerance. Most women with PCOS are insulin resistant. Hyperinsulinaemia stimulates ovarian testosterone production and decreases levels of sex hormone binding globulin; this in turn suppresses ovulation. Diabetes mellitus or impaired glucose tolerance develops in 25-35% of obese women with PCOS by age the age of 30 years.⁴ Thus, part of the general healthcare of women with PCOS should include routine screening for diabetes. Women with PCOS should also be screened for hypertension and hyperlipidaemia, as the combination of obesity, hyperinsulinaemia, hypertension and hyperlipidaemia increases the risk of cardiovascular disease.

1. Kelly AC, Jewelewicz R. Alternate regimens for ovulation induction in polycystic ovarian syndrome. Fertil Steril 1990;54:195-202.
2. Abdel Gadir A, Mowafi RS, Alnaser HMI, et al. Ovarian electrocautery versus human menopausal gonadotrophins and pure follicle-stimulating hormone therapy in the treatment of patients with polycystic ovarian syndrome. Clin Endocrinol 1990;33:585-592.
3. Gibson M. Reproductive health and polycystic ovary syndrome. Am J Med 1995;98:67-75S.
4. Ehrmann DA. Obesity and glucose intolerance in androgen excess. In: Azziz R, Nestler JE, Dewailly D, eds. Androgen excess disorders in women. Philadelphia: Lipincott Williams &Wilkins, 1997, pp 705-712.
   
   

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