Comparison of Maternal Serum and Umbilical Cord Blood Leptin Level in IUGR Neonates

Document Type : Original Article


1 Assistant Professor of Pediatric Endocrinology and Metabolism,ShahidBeheshti University of Medical Sciences. Tehran, IRAN

2 Shahid Beheshti University of Medical Sciences, Tehran, Iran

3 Pediatrician, Tehran, Iran


Background: Gestational weight gain is an impressive factor in the fetal outcome. Intrauterine growth restriction (IUGR) is one of the most important problems during fetal period that may lead to many perinatal and long-term complications and growing neonatal morbidities and mortalities. The aim of the study was to ascertain the relationship between umbilical cord blood leptin concentration and fetal growth in neonates born with intrauterine growth restriction.
Methods: Maternal serum and umbilical cord blood leptin concentration were measured by immune radiometric assay at term gestation. The study was conducted on 22 women with uncomplicated singleton pregnancies as control group (group A) and 22 women with fetal growth restriction in singleton pregnancies as case group (group B). All subjects had normal pregravid body mass index (BMI).
Results: The results of the study showed that maternal serum leptin concentrations were significantly higher in group B comparing to group A (44ng/ml [28.9-58.2] vs. 24.6ng/ml [18.8-33.3]; P<0.001). However, umbilical cord blood leptin levels were significantly lower in group B comparing to group A (8.6 ng/ml [range 4.5-12.7] vs. 14.6 ng/ml [11.7-16.7]; P<0.001). Moreover, umbilical cord blood leptin levels were directly correlated with maternal BMI and neonatal birth weight in both groups.
Conclusion: In growth-restricted fetuses at term, umbilical cord blood leptin concentrations were significantly lower than normal fetuses, suggesting that fetal adipose tissue is a major source for leptin production. Maternal serum leptin concentrations were higher in the presence of a growth restricted fetuses. This increas may be due to early hypoxia or an intrinsic placental mechanism, by which small placenta produces more leptin as a compensatory mechanism. Human recombinant leptin may have some roles in the treatment of IUGR fetuses in future.


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