Irish journal of medical science · 2026
The significance of lipocalin-2, an inflammatory and immune marker in preterm labor.
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Aliyeva Gunel, Akar Ayca Nazli, Çirkin Tekeş Gülten, Ağaoğlu Recep Taha, Öztürk Özge, Sümer Dinçer, Günday Figen, Yakut Yücel Kadriye
Аннотация
BACKGROUND: Inflammation is central to the pathogenesis of preterm labor (PTL), yet evidence on maternal serum lipocalin-2 (LCN-2) in PTL remains limited.
AIM: To investigate the significance of LCN-2, an inflammatory and immune marker, in PTL and its relationship with composite adverse perinatal outcomes (CAPOs).
METHODS: This prospective study was conducted at a tertiary perinatology clinic from June to December 2025. We enrolled 90 pregnant women at 28-37 weeks (45 with PTL, 45 controls; matched 1:1). Maternal serum LCN-2 was measured by ELISA. The PTL group was stratified into early (< 34 weeks) and late (34 + 0-36 + 6 weeks) subgroups and by CAPOs. Maternal and neonatal data were compared, and LCN-2's diagnostic performance was assessed. Multivariable logistic regression assessed its independent association with PTL and CAPO after confounder adjustment.
RESULTS: LCN-2 was higher in the PTL group than in controls (162.24 ± 53.16 vs. 131.20 ± 29.68 pg/mL; p = 0.001), with no difference between early and late subgroups (p > 0.05). It correlated weakly with neonatal intensive care unit stay (r = 0.287, p = 0.046). On ROC analysis, LCN-2 modestly discriminated PTL (AUC 0.658; 95% CI 0.550-0.754; p = 0.007; sensitivity 68.9%, specificity 60.0%; cutoff > 128.95 pg/mL). After adjustment for maternal age, gestational age at sampling, and pre-pregnancy BMI, LCN-2 remained independently associated with PTL (aOR 1.019; 95% CI 1.007-1.032; p = 0.002) but not with CAPO within the PTL group (p = 0.142).
CONCLUSIONS: Elevated maternal LCN-2 in PTL reflects involvement in inflammatory processes underlying preterm birth; however, its limited diagnostic accuracy and weak association with neonatal outcomes suggest it mainly indicates disease activity.
AIM: To investigate the significance of LCN-2, an inflammatory and immune marker, in PTL and its relationship with composite adverse perinatal outcomes (CAPOs).
METHODS: This prospective study was conducted at a tertiary perinatology clinic from June to December 2025. We enrolled 90 pregnant women at 28-37 weeks (45 with PTL, 45 controls; matched 1:1). Maternal serum LCN-2 was measured by ELISA. The PTL group was stratified into early (< 34 weeks) and late (34 + 0-36 + 6 weeks) subgroups and by CAPOs. Maternal and neonatal data were compared, and LCN-2's diagnostic performance was assessed. Multivariable logistic regression assessed its independent association with PTL and CAPO after confounder adjustment.
RESULTS: LCN-2 was higher in the PTL group than in controls (162.24 ± 53.16 vs. 131.20 ± 29.68 pg/mL; p = 0.001), with no difference between early and late subgroups (p > 0.05). It correlated weakly with neonatal intensive care unit stay (r = 0.287, p = 0.046). On ROC analysis, LCN-2 modestly discriminated PTL (AUC 0.658; 95% CI 0.550-0.754; p = 0.007; sensitivity 68.9%, specificity 60.0%; cutoff > 128.95 pg/mL). After adjustment for maternal age, gestational age at sampling, and pre-pregnancy BMI, LCN-2 remained independently associated with PTL (aOR 1.019; 95% CI 1.007-1.032; p = 0.002) but not with CAPO within the PTL group (p = 0.142).
CONCLUSIONS: Elevated maternal LCN-2 in PTL reflects involvement in inflammatory processes underlying preterm birth; however, its limited diagnostic accuracy and weak association with neonatal outcomes suggest it mainly indicates disease activity.