Anti-Müllerian hormone and polycystic ovary syndrome: a mountain too high?

Abstract

Anti-Mü llerian hormone (AMH) was initially thought to be produced solely by the foetal male during sexual differentiation to promote regression of the Mü llerian ducts. Over the last decade, however, a new and interesting role has emerged for AMH in the ovary. In human ovaries, AMH is produced by granulosa cells from 36 weeks of gestation until menopause, with the highest expression being in small antral follicles. AMH production gradually declines as follicles grow; once follicles reach a size at which they are dominant, it has largely disappeared. Its removal from these larger follicles appears to be an important requirement for dominant follicle selection and progression to ovulation as AMH has an inhibitory role in the ovary, reducing both primordial follicle initiation and follicle sensitivity to FSH by inhibition of aromatase. It is for this reason that AMH is a focus of interest in polycystic ovary syndrome (PCOS). Serum levels are doubled, and granulosa cell production is greatly increased. Interestingly, there appear to be two groups of women with PCOS who can be distinguished by their AMH level: one group consists of those who have high levels which do not reduce with treatment and who respond less well to induction of ovulation, and a second group consists of those in whom the level is less elevated and reduces on treatment and who seem to respond rather better. Understanding the reason for the raised AMH in PCOS may give clues as to the mechanism of anovulation. To conclude, AMH appears to have a major inhibitory role during folliculogenesis, which may contribute to anovulation in PCOS.

Differences of the association of anti-Müllerian hormone with clinical or biochemical characteristics between women with and without polycystic ovary syndrome

“…Considering that AMH and total testosterone were the main determinants of ovarian volume [26], correlation of testosterone with AMH might be true for all women, irrespective of the PCOS status. AMH is considered to be a marker of severity of PCOS [22]. These findings support the belief that intraovarian hyperandrogenism may cause follicular arrest and follicle excess followed by increased intraovarian AMH level.…”

“…These different relationships between AMH and biochemical/ clinical factors in the PCOS and control groups suggest that loss of control over AMH production by factors other than testosterone might contribute to the pathogenesis of PCOS. In normal follicle growth and development, a decrease in AMH has an inhibitory effect, allowing larger follicles to become responsive to FSH and stimulating aromatase and E2 production [22]. The lack of correlation between AMH and E2 in the PCOS group suggests that AMH no longer has an effect on aromatase and E2 production, resulting in dysregulation of folliculogenesis.…”

Different diagnostic power of anti-Mullerian hormone in evaluating women with polycystic ovaries with and without hyperandrogenism

“…Androgen contributes to enhance the secretion of AMH by inducing the recruitment of small follicles. The excessive secretion of AMH leads to polycystic ovaries by inhibiting follicular growth [23]. Considering the important role of androgen in PCOS, the patient can be categorized into two main clinical subtypes patients with hyperandrogenism [HA+] and patients without hyperandogenism [HA−].…”

Anti-Müllerian hormone in women with polycystic ovary syndrome

“…또한 다낭성 난소증후군 여성 중에 무월경의 여성에서 희발월경의 여성보다 높은 수치의 항뮐러관 호르몬이 측정되었으며 고안드로겐혈증 (hyperandrogenemia)이 있는 경우에 정상 안드로겐 수치를 보이는 여성 보다 항뮐러관 호르몬이 높다고 보고되었다 [15]. 즉, 항뮐러관 호르몬 농 도는 고안드로겐혈증, 희발월경 또는 무배란, 다낭성 난소 형태 등 다낭 성 난소증후군의 특징적 진단 소견과 비례하는 것으로 나타났다 [16,17] …”