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Objective To investigate whether vaginal microecological imbalance and group B Streptococcus (GBS) colonization are correlated with premature rupture of membranes (PROM) by activating the maternal systemic inflammatory response and to construct an individualized risk prediction model. Method This study was a prospective single-center cohort study. A total of 162 singleton pregnant women at 28–37 weeks of gestation who were admitted to Jilin Provincial Maternal and Child Health Hospital from January 2023 to June 2024 were included. Among them, 81 cases were in the PROM group, and 81 cases were in the matched control group. Vaginal secretions were collected for microbiological testing (Nugent score, H 2 O 2 , and leukocyte esterase), and GBS colonization was detected by the constant temperature amplification method; serum levels of CRP, PCT, IL-6, and IL-10 were determined by electrochemiluminescence and chemiluminescence methods. LASSO-penalized multivariable logistic regression analysis was used to identify independent risk factors, and a nomogram model was constructed with internal validation by bootstrap resampling (1,000 iterations). Result The GBS colonization rate in the PROM group was significantly higher (16.0% vs. 3.7%, aOR = 4.87, 95% CI 1.89–12.56). The incidence rates of abnormal vaginal microscopic evaluation (grades III–IV), H 2 O 2 depletion, and leukocyte esterase positivity were all significantly higher than those in the control group ( P < 0.01). The ratio of IL-6/IL-10 in the PROM group was significantly increased ( P < 0.001). The multivariate model showed that GBS colonization, IL-6 >12 pg/mL, and H 2 O 2 depletion were independent risk factors. The nomogram model constructed based on these indicators had an apparent AUC of 0.89 (95% CI 0.83–0.95) and a bootstrap-corrected AUC of 0.86 (95% CI 0.80–0.92) and excellent calibration (Brier score 0.158, Hosmer–Lemeshow P = 0.423). Conclusion GBS colonization is associated with a higher incidence of PROM by inducing vaginal microecological imbalance and systemic inflammatory responses. The “microecology–inflammation” nomogram model we have developed shows potential for individualized prediction of the risk of PROM pending external validation, providing a basis for early intervention.
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Xu et al. (2026) studied this question.
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