High Fat Mass Index is Associated with Endometrial Hyperplasia in Polycystic Ovary Syndrome Patients: A Retrospective Study

Int J Womens Health. 2024 Nov 30:16:2065-2075. doi: 10.2147/IJWH.S491443. eCollection 2024.

Abstract

Aim: To assess body composition, glucolipid metabolism, and uric acid levels in PCOS (Polycystic Ovary Syndrome) patients to determine their relationship with the risk of endometrial hyperplasia (EH).

Methods: A total of 232 patients were included and divided into groups according to whether they had PCOS and endometrial pathology (Group A: non-PCOS and normal endometrium; Group B: PCOS and normal endometrium; Group C: non-PCOS and EH; Group D: PCOS and EH). Body composition differences between groups and correlations between body composition, glucolipid metabolism, and uric acid levels were analyzed.

Results: In Group D, the patient's PSM (Percent Skeletal Muscle) of Trunk, PBF (Percent Body Fat) of Arm, free mass index, FMI (Fat Mass Index), and appendicular skeletal muscle mass index were significantly higher than in Groups A, B, and C. Waist-hip rate, PBF, PBF of Trunk, PSM of Leg, skeletal muscle mass index and visceral fat level were significantly higher than in Groups A and B. FMI was an independent risk factor for EH in PCOS patients, the AUC for FMI prediction of endometrial hyperplasia in PCOS patients was 0.82. FMI had significant positive correlations with fasting glucose, fasting insulin, HOMA-IR (Homeostatic Model Assessment for Insulin Resistance), total cholesterol, triglyceride, low-density lipoprotein, triglyceride/high-density lipoprotein, and uric acid levels. FMI was correlated with HOMA-IR and uric acid at 0.602 and 0.649 respectively in PCOS patients.

Conclusion: Increased FMI and altered glucolipid metabolism as key factors associated with a higher risk of EH in patients with PCOS. Monitoring body composition and metabolic health in PCOS patients could help identify those at greater risk of EH, guiding preventive interventions.

Keywords: body composition; endometrial hyperplasia; glycolipid metabolism; metabolic syndrome; polycystic ovary syndrome.

Grants and funding

The present study was supported by the National Key Technology Research and Developmental Program of China (Program Nos. 2022YFC2704400 and 2022YFC2704402), New sharp Tianjin Young Medical (TJSQNYXXR-D2-078), National Natural Science Foundation of China (82171629), Tianjin Natural Science Foundation (23JCYBJC00720), Tianjin Key Medical Discipline (Specialty) Construction Project (TJYXZDXK-031A). The funding source played no role in the design, analysis, interpretation, or drafting of the manuscript.