POLYCYSTIC OVARIAN SYNDROME AND ITS METABOLIC CONSEQUENCES: A MINI REVIEW

Polycystic ovarian syndrome (PCOS) is a reproductive metabolic disorder affecting nearly 20% females, globally. Though Rotterdam consensus is widely used for assessment, it lacks definite diagnostic guidelines. Absence of PCOS guidelines for adolescent and post-menopausal women might be influencing the prevalence data. The prevalence varied with ethnicities and found high in urban than rural. Among women in reproductive age, the obese rural population also found vulnerable to PCOS, indicates the role of lifestyle factors in this syndrome. Erratic lifestyle predisposes to insulin resistance, or obesity leads to subsequent hyperinsulinemia and hyperandrogenemia. Also, genetic predisposition to hypothalamic pituitary gonadal (HPG) axis dysfunction and impaired ovarian steroidogenesis further influence the disorder. It dysregulates the oocyte maturation leading to polycystic ovaries, thereby, affects the normal ovarian functions. The environmental toxins which are endocrine disruptors further worsens the consequence of the disorder. Multiple factors make it difficult to decipher the independent pathway of pathogenesis. Apart from ovulatory and reproductive dysfunctions, PCOS have chronic metabolic consequences: cardiovascular disease (CVD), obesity, dyslipidemia, obstructive sleep apnoea, and non-fatty liver. These factors are interdependent and progressive. Since the studies have contradicting results; it’s difficult to determine the impact of these consequences. Both non-obese and obese PCOS women found vulnerable to the same metabolic consequences. Hence, further long term, controlled studies are required to understand the exact pathogenesis and metabolic consequences both in obese and non-obese PCOS women. Moreover, both regional and multicentre cohort studies are required to understand the progression of disease in different ethnicities.