AMH levels and diagnosis in PCOS phenotype D

Read full text
Authors: Xiaofang Xuan, Minxia Zhang, Yaqi Fang, Liyun Su, Ke Yi Xu
Cited by: 1
References: 20

Abstract

OBJECTIVES: To evaluate the diagnostic performance of serum anti-Müllerian hormone (AMH) for polycystic ovary syndrome (PCOS) phenotype D, to define overall and age-specific AMH cut-off values, and to explore the associations between AMH and other reproductive hormones. DESIGN & METHODS: In this cross-sectional study, serum AMH levels were measured in 169 women with PCOS phenotype D and 224 age-matched healthy controls using a magnetic microparticle acridinium ester chemiluminescence immunoassay. Follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone were assessed with immunoluminescence assays. Correlations between AMH and other hormones were analyzed, and receiver operating characteristic (ROC) curves were used to evaluate diagnostic performance and derive cut-off values, including age-stratified thresholds. RESULTS: Serum AMH, testosterone, and the LH/FSH ratio were significantly higher in the PCOS phenotype D group than in controls (p < 0.0001). AMH was positively correlated with testosterone (r = 0.233, p = 0.002) but not with the LH/FSH ratio. AMH discriminated phenotype D from controls with an area under the ROC curve of 0.779 (95 % CI 0.734-0.825); the optimal overall cut-off was 43.16 pmol/L (sensitivity 71.93 %, specificity 70.67 %). Age-stratified analyses showed robust diagnostic performance across reproductive ages, with cut-off values declining progressively (e.g., 54.16 pmol/L for ≤ 25 years; 35.59 pmol/L for 31-35 years). CONCLUSIONS: Serum AMH is a valuable biomarker for diagnosing PCOS phenotype D. The use of age-specific AMH cut-off values may improve diagnostic accuracy and facilitate earlier recognition of this frequently underdiagnosed PCOS subtype.

Fields of Study & Subjects

Ovarian function and disorders Adrenal Hormones and Disorders Systemic Lupus Erythematosus Research

Publication details

Journal / source
Clinical Biochemistry
Publisher
Elsevier BV
Volume
142
Pages
111080–111080
Publication date
8 January 2026
Language
EN