Dr Surveen Ghumman Sindhu MD (Obst & Gyne), FICOG
MAX IVF & Reproductive Medicine, Department of Gynecology
MAX Superspeciality Hospitals, Panchsheel, Saket, Vaishali & Patparganjlhi
Polycystic ovarian syndrome (PCOS) is a heterogeneous collection of signs and symptoms which form a spectrum of mild to severe disturbance of reproductive, endocrine and metabolic functions. Normal menstrual cycles occur in 20% of women. According to definition, introduced in Rotterdam in 2003, presence of two out of the following three are essential for diagnosis – Oligo and/or anovulation, hyperandrogenism (clinical and/or biochemical), and polycystic ovaries on ultrasound with exclusion of other etiologies.
Earlier, two phenotypes were described, the severe PCOS with all three criterion present (phenotype 1) and the anovulatory hyperandrogenic PCOS without evidence on ultrasound (phenotype 2). These are still the most common 48.2% and 30.7 % respectively. Based on the new Rotterdam criteria, two additional phenotypes of PCOS arise – the mild PCOS with anovulation and ultrasound picture of PCOS but no hyperandrogenemia (phenotype 4 – 11.4%), and the least common, ovulatory PCOS with hyperandrogenia and ultrasound picture of PCOS (phenotype 3- 9.7%)
There are differences in the hormonal and metabolic profile of the ovulatory and anovulatory PCOS. Circulating androgens were higher in women with phenotypes 1–3 than in controls. Women with phenotypes 1 and 2 were more insulin resistant. Phenotype 3 did not differ from controls in any marker of insulin resistance. AMH, which have been shown to inhibit the initial follicle recruitment, and also to cause follicular arrest, are increased in this syndrome. AMH was higher in PCOS groups 1 and 2 compared with groups 3 and 4 and the control group and may reflect the severity of the syndrome. However, AMH levels do not predict the phenotype of PCOS or the metabolic disturbances. Patients with classic PCOS had higher LH to FSH ratios and serum testosterone in comparison with ovulatory PCOS.
Problems with PCOS who ovulate are a raised basal LH, high androgens and a premature LH surge. Raised LH can be brought down with oral contraceptive pills in previous cycle or GnRH agonists. High androgens can be reduced by dexamethasone, oral contraceptive pills if conception is not being planned, metformin if insulin resistance is also present or laparoscopic ovarian drilling. Premature luteinisation has been defined as the rise of progesterone on the day hCG. In stimulated cycles, it was seen that intense ovarian response with more number of follicles led to an early rise in estradiol which initiated a LH surge before follicles reach an optimum size. Premature LH surge can be prevented by using a GnRH agonist or antagonist. Ovulatory PCOS response to metformin is the best among all phenotypes in terms of pregnancy rate.
The ovulatory PCOS do not conceive because of subtle defects in endocrine factors. It remains to be established whether these differences in endocrine features and insulin resistance between phenotypes will also translate into different cardiovascular and long term outcomes.