Polycystic ovary syndrome: antimüllerian hormone and its role in the pathophysiology of the syndrome.

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among women of reproductive age, with a prevalence estimated between 10% and 13%. It is characterized by ovulatory dysfunction, hyperandrogenism, and polycystic ovarian morphology. Antimüllerian hormone (AMH) plays a key role in regulating normal reproductive function in both males and females. Over the past few decades, significant progress has been made in understanding AMH, with numerous studies revealing its unexpected roles throughout the hypothalamic-pituitary-gonadal axis. Antimüllerian hormone and its receptor are also produced in the forebrain, where they contribute to the proper migration of gonadotropin-releasing hormone (GnRH) neurons during development. At the hypothalamic and pituitary levels, AMH has been shown to increase the frequency of GnRH pulses, which in turn leads to increased luteinizing hormone (LH) secretion. In PCOS, this regulatory mechanism appears to be disrupted. The LH/follicle-stimulating hormone ratio is often elevated because of altered GnRH pulse frequency. Elevated AMH levels contribute to this dysregulation by increasing GnRH pulsatility, which leads to enhanced LH secretion. This, in turn, stimulates theca cells to produce excessive androgens, resulting in hyperandrogenism, follicular arrest, and anovulation. Antimüllerian hormone levels are strongly correlated with these clinical features of PCOS and are predictive of outcomes in assisted reproductive treatments, including a higher risk of adverse pregnancy outcomes. Additionally, offspring born to mothers with PCOS tend to have elevated levels of AMH and androgens at birth, which may alter the hypothalamic-pituitary-gonadal axis and contribute to the development of PCOS later in life.