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Resistin levels in preterms: are they influenced by fetal inflammatory course?
T Gursoy1, D Aliefendioglu, O Caglayan
1Department of Pediatrics, Zeynep Kamil Maternity and Children's Education and Training Hospital, NICU, Istanbul, Turkey. tugbagursoy@gmail.com
Insights
Resistin levels are elevated in preterm neonates with preterm prelabour rupture of membranes (PPROM) and reduced in those whose mothers received antenatal steroids, suggesting a role in fetal inflammation.
Area of Science:
- Neonatal research
- Inflammatory markers
- Maternal-fetal medicine
Background:
- Preterm delivery pathogenesis involves maternal/perinatal infections and inflammation.
- Resistin is implicated in inflammatory cytokine cycles and neonatal growth.
- Limited research exists on resistin's role in neonatal inflammation.
Purpose of the Study:
- To evaluate resistin levels in premature neonates.
- To assess the impact of preterm prelabour rupture of membranes (PPROM) on resistin levels.
- To investigate the effect of antenatal steroid use on neonatal resistin levels.
Main Methods:
- Included 118 preterm neonates and their mothers' medical data.
- Measured serum resistin, IL-6, CRP, and procalcitonin in neonates within 2 hours of birth.
- Analyzed data based on PPROM status and antenatal steroid exposure.
Main Results:
- Babies with PPROM showed significantly higher resistin levels (70.7 ng/mL) compared to those without (25.9 ng/mL).
- Neonates whose mothers received antenatal steroids had significantly lower resistin levels (20.8 ng/mL) than those who did not (34.6 ng/mL).
- Resistin correlated with IL-6, procalcitonin, and CRP in neonates without antenatal steroid exposure, but not in those with exposure.
Conclusions:
- Preterm delivery and PPROM involve complex inflammatory cascades.
- Elevated resistin in PPROM neonates and suppressed levels with antenatal steroids suggest a role in fetal inflammation.
- Resistin may serve as a marker for inflammatory responses in premature neonates.
Objective:
Many different factors are involved in the pathogenesis of preterm deliveries and among them maternal or perinatal infections and inflammatory response have the major role. Researches were carried out about resistin, which is thought to have a role in inflammatory cytokine cycle and it was shown to be associated with growth in neonates. However, no research has been carried out showing its relationship with inflammation in neonates. In this study, we aimed to evaluate the resistin levels in premature neonates and the effect of events such as preterm prelabour rupture of the membranes (PPROMs) and the use of antenatal steroids on these levels.
Study Design:
The study included 118 preterm neonates. Their medical data together with their mothers' were recorded. Serum resistin levels together with interleukin (IL)-6, C-reactive protein (CRP) and procalcitonin were evaluated in the first 2 h of life.
Result:
Mean gestational age and birth weight of babies included in the study were 29.6 ± 2.7 weeks and 1306.4 ± 393.4 g, respectively. Babies with PPROMs had significantly higher levels of resistin ((n=30); 70.7 (7.8 to 568.4) ng ml(-1)) than babies without PPROM ((n=88); 25.9 (5.5 to 528.9) ng ml(-1)) (P=0.005), and the babies of mothers who received antenatal steroids had significantly lower resistin levels ((n=44); 20.8 (5.5 to 159.9) ng ml(-1)) than the babies of mothers who did not ((n=66); 34.6 (7.2 to 568.4) ng ml(-1)) (P=0.015). There were significant correlations between resistin and IL-6 levels and between IL-6 and procalcitonin and CRP levels in babies whose mothers did not receive antenatal steroids. However, no correlation was found between these parameters in babies whose mothers received antenatal steroids.
Conclusion:
Preterm delivery and PPROM involve complex cascade of events including inflammation, and steroids are potent anti-inflammatory agents. Elevated resistin levels in babies with PPROM and suppressed levels in babies whose mothers received antenatal steroids reported in this study might have been observed as a result of the effects of fetal inflammation on resistin levels.
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