Produced by small growing ovarian follicles.
Measureable from birth to near the menopause.
A granulosa cells product secreted by the early growing ovarian follicles.
It provides a more direct indicator of the ovarian oocyte reserve.
Compared with traditional ovarian function indicators such as FSH, LH, and inhibin B, anti-Mullerian hormone can reflect ovarian reserve relatively sensitively in young women.
Levels peak in the mid-20s, and then declines progressively in concert with follicle loss.
It is not produced by primordial follicles in the ovary, and it is only secreted once primordial follicle growth activation has occurred, but very low levels suggest of impending menopause.
A routine test in assisted conception.
Reflects a decline in the primordial follicle pool during the later reproductive years, and also identifying women at risk of over-response.
Its relationship with the ovarian reserve changes from an inverse one in the first quarter century to a positive one thereafter as both decline in parallel.
Levels do not vary significantly across the menstrual cycle.
Levels are not fully gonadotrophin-independent, showing delayed changes consistent with the site of production from smaller growing follicles.
Has ability to predict remaining reproductive lifespan, which clinically may be of value in the assessment of ovarian reserve following damage from chemotherapy or ovarian surgery.
AMH is markedly increased in polycystic ovarian syndrome.
Female fertility is very low for approximately a decade before menopause and is declining during the during the 30s.
The measurement of circulating sex steroids and pituitary gonadotrophins allows assessment of ovulatory function and diagnosis of the main relevant disorders of the ovary.
Ovarian and pituitary hormones do not reflect the activity of the great majority of follicles within the ovary, whose growth is necessary to support ovulation and fertility.
Smaller follicles present in the ovary are determinants of reproductive lifespan and age at menopause.
AMH expression occurs by granulosa cells and becomes detectable as soon as follicles start to grow, but later declines.
AMH is an efficient marker for predicting post chemotherapy ovarian function in pre-menopausal female patients with breast cancer older than 35 years.
The smallest growing follicles are numerically the most abundant in the ovary.
Small ovarian follicles have few granulosa cells and contribute little to serum AMH concentrations compared to larger follicles.
AMH is expressed in growing follicles throughout the pre-antral and early antral stages, and then declines with little production beyond 8 mm.
AMH production has declined when follicles are selected for dominance and when estrogen production starts to increase.
Large follicles produce little AMH and levels do not show clinically relevant changes across the menstrual cycle, making it clinically useful.
AMH measurement in clinical practice assesses a woman’s likely response to superovulation as part of an IVF cycle.
AMH is directly related to the number of oocytes that are obtained at IVF.
Can identify women likely to over respond and be at risk of ovarian hyperstimulation syndrome.
AMH is a better discriminator than FSH of ovarian reserve.
AMH reflects ovarian reserve, indicating the number of follicles that can be recruited to grow by the administration of FSH.
Ovarian reserve term reflects the pool of primordial/nongrowing follicles within the ovary.
AMH is produced by small follicles reflecting the primordial pool.
AMH concentrations decline with age.
AMH becomes undetectable approximately 5 years before the final menstrual period.
May be of value in assessing remaining ovarian function following chemotherapy or other gonadotoxic treatments.
The production of AMH by small antral follicles is to a degree FSH-regulated.
Not known which follicle sizes within the 2–10-mm range contribute most to circulating AMH concentrations.
Prolonged gonadotrophin suppression by GnRH analogues results in a progressive decline in AMH.
The administration of the combined contraceptive pills has little effect on AMH secretion.
Pregnancy significantly suppresses AMH.
AMH is detectible throughout childhood, with a transient rise in the neonatal period followed by a more sustained rise through childhood and adolescence.
The neonatal rise reflects girls as well as boys have a transient activation of the reproductive axis at that time.
A plateau or a decline in AMH occurs during puberty.
Suspected that the rise in FSH concentrations of early puberty stimulates larger numbers of follicles to reach later stages of maturation, establishing the normal follicular characteristic of the adult ovary.
Produced by granulosa cells of growing follicles, AMH is considered an established biomarker of ovarian reserve widely used in women undergoing in vitro fertilization procedures.
ZIt is more sensitive than other hormonal markers, and has the advantage of showing little variation during regular menses.
Levels continues to rise after adolescence, with peak concentration at, approximately, the age of 24.
This rise in AMH during childhood, adolescence and early adulthood occurs with declining primordial follicle pool.
IT is a promising biomarker for quantifying treatment induced gonads toxicity, aiding in the diagnosis and prediction of premature ovarian insufficiency.
Suggesting that it is inappropriate to regard AMH as a marker of ovarian reserve.
As in adults, AMH levels are a useful indicator of chemotherapy-induced gonadotoxicity in children and adolescents.
AMH associated with markedly increased levels in polycystic ovarian syndrome (PCOS), reflecting the increased numbers of small growing follicles.
High intra-ovarian AMH concentrations may contribute to a reduced responsiveness to FSH.
AMH is a granulosa cell product and is of value in the diagnosis and monitoring of granulosa cell tumors.