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Published on: March 5, 2022
Anti-Müllerian Hormone Levels Across Phenotypes in Polycystic Ovary Syndrome: A Systematic Review and Meta-analysis
Patrícia Jorge Schwenck-Carvalho1, Giovana De Nardo Maffazioli1, Ricardo Santos Simões1
1Discipline of Gynecology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP 05403-000, Brazil.
Context:
Anti-Müllerian hormone (AMH) concentrations are frequently elevated in women with polycystic ovary syndrome (PCOS). However, clinical application is limited by the absence of a standardized cutoff, lack of assay harmonization, and variability across PCOS phenotypes.
Objective:
To compare AMH levels across the 4 PCOS phenotypes (A, B, C, D) defined by the Rotterdam criteria.
Data Sources:
PubMed, Embase, ScienceDirect, and Web of Science were searched for studies published between January 2009 and July 2024. Reference lists of included studies were also screened.
Study Selection:
Eligible studies included women with PCOS diagnosed by Rotterdam criteria and reported AMH levels by phenotype. Of 684 citations, 49 studies (15 535 participants) met inclusion criteria.
Data Extraction:
Two reviewers independently extracted study characteristics, AMH values, assay type, age, and body mass index (BMI). AMH levels were converted to Beckman Coulter Gen II units. Risk of bias was assessed using ROBINS-E.
Data Synthesis:
Random-effects meta-analyses showed highest AMH levels in phenotype A (11.49 ng/mL; standardized mean difference 3.06), followed by D (8.97), C (7.98), and B (6.25; standardized mean difference 1.36). Age and BMI were comparable. Heterogeneity was high (I 2 ≈ 98%). Meta-regression adjusted for phenotype, age, BMI, and region confirmed the AMH hierarchy (A > D ≈ C > B) and identified geographic region as a significant contributor to heterogeneity.
Conclusion:
AMH levels differ markedly across PCOS phenotypes, with polycystic ovarian morphology exerting the greatest influence, followed by oligoanovulation and hyperandrogenism. Findings support the use of AMH in phenotype differentiation and emphasize the need for assay standardization and population-specific interpretation.
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