Resistin levels in preterms: are they influenced by fetal inflammatory course?

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.