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Background <p>Inflammation is central to the pathogenesis of preterm labor (PTL), yet evidence on maternal serum lipocalin-2 (LCN-2) in PTL remains limited.</p> Aim <p>To investigate the significance of LCN-2, an inflammatory and immune marker, in PTL and its relationship with composite adverse perinatal outcomes (CAPOs).</p> Methods <p>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 (&lt; 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.</p> Results <p>LCN-2 was higher in the PTL group than in controls (162.24 ± 53.16 vs. 131.20 ± 29.68 pg/mL; <i>p</i> = 0.001), with no difference between early and late subgroups (<i>p</i> &gt; 0.05). It correlated weakly with neonatal intensive care unit stay (<i>r</i> = 0.287, <i>p</i> = 0.046). On ROC analysis, LCN-2 modestly discriminated PTL (AUC 0.658; 95% CI 0.550–0.754; <i>p</i> = 0.007; sensitivity 68.9%, specificity 60.0%; cutoff &gt; 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; <i>p</i> = 0.002) but not with CAPO within the PTL group (<i>p</i> = 0.142).</p> Conclusions <p>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.</p>

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The significance of lipocalin-2, an inflammatory and immune marker in preterm labor

  • 期刊论文

  • 发表日期：

    2026年7月20日

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  • Gunel Aliyeva,
  • Ayca Nazli Akar,
  • Gülten Çirkin Tekeş,
  • Recep Taha Ağaoğlu,
  • Özge Öztürk,
  • Dinçer Sümer,
  • Figen Günday,
  • Kadriye Yakut Yücel

摘要

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.