Pelvic organ prolapse (POP) is common after menopause and can markedly impair health‑related quality of life through vaginal bulge, pelvic pressure and lower urinary tract symptoms. We hypothesized that, in postmenopausal women with POP managed in tertiary urogynecology services, metabolic status would be more strongly associated with prolapse anatomical pattern, urinary incontinence and overall quality of life than with POP‑Q stage alone, and therefore examined associations between metabolic markers and POP stage and pattern, urinary incontinence and health‑related quality of life.

This cross‑sectional study included 173 married, parous postmenopausal women aged ≥45 years with clinically confirmed POP attending tertiary urogynecology clinics. POP was staged with the Pelvic Organ Prolapse Quantification (POP‑Q) system (I–II, II–III, III–IV) and classified by detailed anatomical pattern (anterior+posterior, total, apical only, posterior only, posterior+apical, anterior+apical). Anthropometry (BMI) and fasting blood markers (fasting blood sugar, HbA1c, triglycerides, total cholesterol, LDL, HDL, vitamin D3) were obtained, diabetes was defined as fasting blood sugar ≥126 mg/dL and/or HbA1c ≥6.5%, and the triglyceride–glucose index was calculated as ln(triglycerides×fasting blood sugar/2) as an insulin‑resistance marker. Health‑related quality of life was assessed with the SF‑36, urinary incontinence was recorded as present or absent, and ANOVA, chi‑square, and multivariable linear and logistic regression (two‑sided p<0.05) were used to identify predictors of SF‑36 scores and urinary incontinence.

Mean age was 58.94±8.79 years and mean BMI 27.23±3.87 kg/m². POP stages were I–II in 5.2%, II–III in 61.85% and III–IV in 32.95%. The most frequent anatomical patterns were anterior+posterior (38.73%) and total prolapse (27.75%), and urinary incontinence was present in 34.68%. Diabetes mellitus occurred in 12.0%, obesity in 31.2% and dyslipidemia in 12.7%. Metabolic markers did not differ significantly across POP‑Q stages (all p>0.05). In contrast, POP patterns differed by BMI (p=0.019), FBS (p<0.001), HbA1c (p<0.001), TG (p=0.003), LDL (p=0.002) and TyG (p<0.001), but not by total cholesterol, HDL or vitamin D3 (all p>0.05). Apical‑involving patterns showed the most adverse profiles: in the anterior+apical pattern, mean FBS was 177.16 mg/dL, HbA1c 8.47%, TG 299.52 mg/dL and LDL 184.53 mg/dL; in the posterior+apical pattern, mean BMI was 31.5 kg/m², TG 269.94 mg/dL and LDL 177.95 mg/dL. Exploratory logistic regression suggested diabetes was associated with the posterior+apical pattern (odds ratio [OR] 7.89). Mean TyG was 9.04±0.43 and correlated inversely with SF‑36 score (r=−0.37). In multivariable linear regression, the laboratory panel explained 29.96% of SF‑36 variance (p<0.001); HbA1c (standardized β=−0.32, p<0.001) and LDL (β=−0.37, p<0.001) were independent negative predictors. In a model including obesity, diabetes and dyslipidemia, obesity (β=−0.50, p<0.001) and diabetes (β=−0.31, p<0.001) predicted lower SF‑36 scores, while dyslipidemia was not significant (p=0.129). Obesity increased the odds of urinary incontinence (OR 3.71, p<0.001), and higher TyG showed a borderline association (OR 2.08 per unit, p=0.052).

In this postmenopausal POP cohort, metabolic dysregulation was unrelated to POP‑Q stage but was clearly associated with specific prolapse patterns, particularly those involving apical support defects. Apical‑involving patterns clustered with higher BMI, poorer glycemic control and more atherogenic lipid profiles, and markers of insulin resistance and dyslipidemia (HbA1c, LDL, TyG) were strongly related to poorer SF‑36 scores, while obesity and diabetes increased the likelihood of urinary incontinence.

In summary, metabolic dysregulation in postmenopausal women with POP was linked to prolapse anatomical pattern—especially apical involvement—rather than POP‑Q stage, and was associated with poorer health‑related quality of life and more frequent urinary incontinence, supporting integration of metabolic risk assessment and optimization of weight, glycemic control and lipid profiles into comprehensive POP care pathways.