Endocrine and Anthropometric Biomarker Patterns in Iraqi Women With Idiopathic Premature Ovarian Insufficiency: A Case-Control Study
Abstract
Background: Premature ovarian insufficiency is characterized by impaired ovarian function before the age of 40 years and is associated with reproductive, skeletal, cardiovascular, and metabolic consequences. broader endocrine profiling may provide additional insight into the hormonal phenotype of idiopathic POI. This study compared reproductive and adrenal hormone profiles and anthropometric indices between Iraqi women with idiopathic premature ovarian insufficiency and healthy controls of comparable reproductive age, and explored associations among endocrine and anthropometric variables. Materials and Methods: In this case-control study, 100 women were enrolled, including 50 women with idiopathic premature ovarian insufficiency and 50 healthy controls of comparable reproductive age with regular menstrual cycles. Serum follicle-stimulating hormone, luteinizing hormone, estradiol, progesterone, testosterone, and dehydroepiandrosterone sulfate were measured, together with body mass index and waist circumference. Group differences were assessed using independent-sample tests. Correlations were evaluated using Pearson correlation analysis, and multivariable linear regression was used to identify hormonal predictors of estradiol concentrations. Receiver operating characteristic curve analysis was performed exploratorily. Results: Women with premature ovarian insufficiency had significantly higher follicle-stimulating hormone, luteinizing hormone, progesterone, and dehydroepiandrosterone sulfate concentrations and significantly lower estradiol and testosterone concentrations than controls. Follicle-stimulating hormone was strongly positively correlated with luteinizing hormone and strongly inversely correlated with estradiol. In multivariable regression, follicle-stimulating hormone remained the strongest inverse predictor of estradiol concentration. Exploratory ROC analysis showed complete separation between groups for several biomarkers; however, these findings should be interpreted cautiously because follicle-stimulating hormone was part of the diagnostic case definition. Conclusion: Idiopathic premature ovarian insufficiency in this Iraqi cohort was characterized by marked disruption of the hypothalamic–pituitary–ovarian axis, reflected by elevated gonadotropins and reduced estradiol. Increased dehydroepiandrosterone sulfate may indicate altered adrenal–ovarian endocrine interaction. Future studies should use non-circular biomarker validation designs and adjust for potential metabolic and endocrine confounders.