Antimüllerian hormone levels and cardiometabolic risk in young women with polycystic ovary syndrome

In young women with polycystic ovary syndrome, low antim€ullerian hormone levels, independently from age and race, predict a higher risk of metabolic syndrome.

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Volume 107, Issue 1, Pages 276-281


Rebecca A. Feldman, M.D., Kathleen O'Neill, M.D., Samantha F. Butts, M.D., M.S.C.E., Anuja Dokras, M.D., Ph.D.



To determine the association between antimüllerian hormone (AMH) levels and metabolic syndrome (MetSyn) in young women with polycystic ovary syndrome (PCOS).


Cross-sectional study.


Academic PCOS center.


A total of 252 women aged 18–46 years with PCOS.



Main Outcome Measure(s)

Association of AMH with markers of cardiometabolic risk and MetSyn.


The median AMH level was 5.1 ng/mL (interquartile range [IQR] 3.0–8.1), and prevalence of MetSyn was 23.8%. AMH levels positively correlated with total T, high-density lipoprotein (HDL) cholesterol, and SHBG and negatively correlated with fasting glucose, homeostasis-model assessment of insulin resistance, body mass index (BMI), and systolic and diastolic blood pressure. A single-unit decrease in AMH was associated with an 11% increase in odds of MetSyn (odds ratio [OR] 1.11, 95% confidence interval [CI] 1.03–1.20); the strength of this association was maintained in the multivariate model (OR 1.09, 95% CI 1.01–1.18) adjusting for age and race. Subjects with AMH values in the lowest tertile were twice as likely as those in the highest tertile to have MetSyn (adjusted OR 2.1, 95% CI 1.01–4.3). Total T was not associated with MetSyn or its individual components.


Our findings indicate that in young women with PCOS, low AMH levels predict a greater risk of MetSyn. The role of AMH, an established biomarker of ovarian reserve, in risk stratification of cardiometabolic risk in obese women with PCOS needs to be clarified in longitudinal studies and in the perimenopausal population.

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Fertility and Sterility

Editorial Office, American Society for Reproductive Medicine

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