Identification of Metabolic Phenotypes in Polycystic Ovary Syndrome Using Unsupervised Clustering: A Case-Control Study
Metabolic Phenotypes in Polycystic Ovary Syndrome Using Unsupervised Clustering
DOI:
https://doi.org/10.54393/pbmj.v9i7.1385Keywords:
Polycystic Ovary Syndrome, Insulin Resistance, Sex Hormone-Binding Globulin, Cluster Analysis, Hirsutism, Body Mass Index, ROC Curve, Phenotype, HyperandrogenismAbstract
PCOS is an endocrine disorder of women. It remains unclear whether adding biomarkers to clinical assessment improves diagnosis, or if androgens explain clinical hirsutism severity. Objectives: To identify metabolic phenotypes via clustering; test if a biomarker panel predicts PCOS better than clinical assessment; and explore the serum androgen-hirsutism correlation. Methods: This retrospective case-control study analyzed Kaggle data (208 PCOS cases and controls). Clinical, biochemical (total/free testosterone, DHEAS, LH/FSH, HOMA-IR, SHBG), and ultrasound (ovarian volume, follicle count) variables were recorded. Logistic regression (clinical vs. full panel) was compared using AUC, DeLong's test, LRT, bootstrap correction, and Hosmer-Lemeshow. K-means clustering (k=2) applied to standardized BMI, HOMA-IR, and SHBG. Pearson correlation assessed FG score. Results: The full model (test AUC 0.596) did not outperform the clinical model (AUC 0.592; DeLong p=0.886; LRT p=0.835). Optimism correction reduced the full AUC to 0.507 versus 0.526 for clinical, with poor calibration (p=0.005). No biomarker independently predicted PCOS. No serum hormone correlated with FG score (|r|≤0.111). Clustering revealed obese/low-SHBG (n=98) and lean/insulin-resistant (n=110) phenotypes, differing in BMI, SHBG, and HOMA-IR (p<0.050), but not testosterone or LH/FSH. Conclusions: Adding biomarkers does not improve diagnosis and is overfitted. Serum androgens do not explain hirsutism. Clustering identifies distinct metabolic subtypes, supporting phenotype-based management.
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