
Neither group regards polycystic ovaries without other clinical features as sufficient for diagnosing PCOS. The syndrome should be diagnosed once conditions such as Cushing’s syndrome, thyroid disorders, idiopathic hirsutism and hyperprolactinaemia have been ruled out.

There is unanimous agreement that PCOS is a diagnosis of exclusion. Three different groups, the Rotterdam European Society for Human Reproduction and Embryology/American Society for Reproductive Medicine (ESHRE/ASRM), the National Institutes of Health/National Institute of Child Health and Human Disease (NIH/NICHD) and the Androgen Excess and PCOS Society, have proposed diagnostic criteria for PCOS (Table (Table1) 1). Women with PCOS often have elevated serum insulin and IR, regardless of androgen concentrations and their levels of ‘adiposity’.
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Another effect of insulin is to decrease sex hormone binding globulin (SHBG) synthesis in the liver, resulting in elevated levels of free androgens. However, the steroidogenic ovaries and adrenal glands remain sensitive to the actions of insulin. In PCOS, IR affects the liver, adipose tissue and skeletal muscles. During puberty, only glucose metabolism is affected by IR while protein metabolism is spared. Subsequent elevations in insulin-like growth factor-1 (IGF-1) and growth hormone levels mean that more amino acids are available for growth. During puberty, there may be a temporary increase in insulin levels and IR. Puberty is also thought to have a major effect on hyperinsulinaemia and IR. Although the exact mechanisms are yet to be elucidated, genetic, intra- and extra uterine factors and adaptations to consumption of high energy food items are considered to be factors causing IR in PCOS. IR results from inadequate tissue utilisation of insulin for glucose metabolism. Insulin resistance (IR) is another important component of PCOS. High LH combined with low FSH levels and decreased oestradiol synthesis through the conversion of androgens results in anovulation due to the absence of a dominant follicle. High luteinising hormone (LH) levels are required for androgen synthesis by ovarian theca cells. The characteristic polycystic appearance of ovaries in PCOS is due to large numbers of primordial follicles growing and undergoing subsequent growth arrest. AMH is produced by ovarian granulosa cells and is important in preventing primordial follicles from transitioning into primary follicles. In PCOS, an imbalance between androgens, anti-Müllerian hormone (AMH) and follicle stimulating hormone (FSH), cause a halt of follicular growth. The rate at which primordial follicles are selected for growth is strictly controlled, in order to maintain ovarian reserve and ensure fertility is intact. In a normal fertile female, a single follicle matures and undergoes ovulation from a pool of primordial follicles present in the ovaries since birth. Ovarian pathology is a major element of PCOS. The pathophysiology is complex and is thought to be a result of interactions between genetics, epigenetics, ovarian dysfunction, endocrine, neuroendocrine and metabolic alterations, amongst other changes. PCOS remains an enigmatic condition, despite years of research. With the aid of up to date scientific literature, we discuss the evidence based diagnostic approach and therapeutic algorithm for patients with lean PCOS in this review. Other endocrine and genetic disorders with similar clinical picture need to be excluded in such cases before the clinicians can make appropriate management plans. Īlthough a majority of cases with PCOS are obese/overweight, a small but significant proportion of patients present with normal body mass index (BMI ≤25 kg/M 2) that makes diagnostic work up and therapeutic approach more difficult. Acne is also a marker of hyperandrogenism, albeit rare and less specific. Up to 70% of women with hyperandrogenism present with hirsutism, or excess body hair.


Characteristic features include polycystic ovaries, menstrual disturbance and hyperandrogenism. It is the commonest cause of anovulatory infertility, and around 90–95% of women with anovulatory infertility presenting to infertility clinics are affected by the syndrome. Polycystic ovary syndrome (PCOS) is a heterogeneous endocrinopathy affecting 4–8% of women of reproductive age.
