The significance of lipocalin-2, an inflammatory and immune marker in preterm labor
Irish Journal of Medical Science, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s11845-026-04534-5
- Dergi Adı: Irish Journal of Medical Science
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, MEDLINE, Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest)
- Anahtar Kelimeler: Lipocalin-2, Preterm labor, Preterm birth, Inflammation, Neonatal outcomes, Composite adverse perinatal outcomes
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
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.