Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 P483

1Medical and Surgical Sciences Department-Clinica Medica 3, University-Hospital of Padua, Padua, Italy; 2Laboratory Medicine Department, University-Hospital of Padua, Padua, Jamaica.


Background: Hyperandrogenism and disrupted folliculogenesis are prominent features of polycystic ovary syndrome (PCOS) and are causatively linked to ovarian dysfunction. In PCOS, increased anti-Müllerian hormone (AMH) serum levels have been observed and related to the severity of the phenotype. However, the regulation of AMH in PCOS remains poorly understood. Therefore, we compared AMH secretory pattern after acute exposure to a GnRH-analogue in women affected by PCOS or by other causes of anovulation and hyperandrogenism, such as functional hypothalamic amenorrhea (FHA) and extra-ovarian hyperandrogenaemia (non-PCOSH).

Patients and methods: Of 26 PCOS (23.9±4.8 years), 9 FHA (26.6±2.6 years) and 8 non-PCOSH (21.2±4.5 years) women were studied. Testing was performed at 4–7 day/cycle, after Liddle test. AMH, LH, FSH, DHEA-S, 17-OHP, A, T, DHT, E2, Inh-B were evaluated at 0-h, and over a 20 and 24-h period after a s.c. injection of Triptorelin (0.1 mg).

Results: Our results are summarized in Table:

PCOSFHANon-PCOSH
BaselinePeakBaselinePeakBaselinePeak
E2 (pM)160±671546±67576±27*1453±350123±361056±537
InhB (ng/l)114±40400±121154±43566±10081±24.6205±97
AMH (pM)43±1844±14§70±26*78±44†,§21±10*,†24±12‡,§
*P<0.05 versus PCOS baseline; P<0.05 versus FHA baseline; P<0.05 versus PCOS peak; §NS versus baseline values.

Conclusions: AMH serum levels were increased in PCOS and FHA patients when compared with non-PCOSH subjects, suggesting that extra-ovarian androgens may not be directly involved in the complex AMH regulation network. In contrast with conventional markers of early follicular growth, such as inhibin-B and E2, AMH secretion appears to be independent of gonadotropin acute stimulation in vivo both in PCOS and non-PCOS patients.

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