Abstract / Summary
Polyendocrine metabolic ovarian syndrome (PMOS), formerly polycystic ovary syndrome (PCOS), is a heterogeneous endocrine–metabolic disorder whose biochemical profile varies across populations. The combined associations of vitamin D status, thyroid-stimulating hormone (TSH), and classical gonadotropin markers remain incompletely defined in South Asian women. We aimed to characterize demographic, clinical, hormonal, and vitamin D profiles and identify independent biochemical correlates of PMOS case status. In this case–control study, 160 women of reproductive age (80 PMOS cases diagnosed using the Rotterdam PCOS criteria and 80 age-matched controls) were enrolled at Lady Reading Hospital, Peshawar. Serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, TSH, and 25-hydroxyvitamin D were measured. Group comparisons used chi-square and Mann–Whitney U tests, and associations used Spearman correlation. Independent correlates were modelled with Firth-penalized binary logistic regression to address quasi-complete separation. Odds ratios were re-expressed for PMOS case status, and in-sample discrimination was summarized using the area under the receiver-operating-characteristic curve (AUC). Cases had markedly lower median vitamin D (12.88 vs. 30.06 ng/mL; p < .001; r = .77) and lower median TSH (1.67 vs. 2.49 µIU/mL; p < .001; r = .50), with higher LH and LH/FSH ratio (both p < .001). In penalized regression oriented to PMOS case status, each 1-ng/mL increase in vitamin D was associated with lower odds of case status (adjusted odds ratio [aOR] = 0.35; 95% CI 0.19–0.65; p = .001), as was each 1-µIU/mL increase in TSH (aOR = 0.018; 95% CI 0.001–0.251; p = .003); higher LH was associated with higher odds (aOR = 1.49; 95% CI 1.16–1.89; p = .002). Vitamin D showed excellent in-sample discrimination (AUC = 0.945), exceeding TSH (0.788) and LH (0.779). Lower vitamin D and TSH concentrations were independently associated with PMOS case status in this cohort. Although TSH differed significantly between groups, both group medians remained within the laboratory reference interval and should not be interpreted as abnormal thyroid function. These findings are associative and do not establish causality or screening utility. Not applicable.