Session: FP11-Pediatric Endocrinology
Room 104 (Moscone Center)
Poster Board SAT-600
Study design: We analyzed GR polymorphisms BclI, N363S and R23K with respect to recorded neonatal outcome parameters in a German Neonatal Network (GNN) multicenter cohort comprising 2.211 very low birth weight preterm (VLBW) infants.
Results: Birth parameters were not different between genotype groups. Variants BclI and R23K were associated with a significantly higher risk of culture-positive neonatal sepsis (Bcll homozygosity: OR 1.85, p=0.002; R23K-carrier: OR 2.08, p=0.016; adj. for gestational age). In addition, infants carrying BclI alleles were more likely to develop bronchopulmonary dysplasia (OR 1.41 per allele [95% CI 1.14-1.75], p < 0.01 adj. for gestational age and mechanical ventilation). A similar relative risk was seen in the subcohort of infants with antenatal betamethasone treatment (OR 1.44, p < 0.01), whereas no such effect was detectable in the small subgroup without steroid treatment (n=185, OR 1.03, n.s.). N363S-carrier tended to have lower mean arterial blood pressure at the first day of life (total cohort: beta=-0.050, p=0.010; BclI-/R23K-wildtype subcohort: beta -0.055, p=0.074) and were more likely to require catecholamine treatment (p<0.01). However, none of the analyzed GR variants significantly influenced incidence rates of intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), or retinopathy (ROP).
Conclusion: This study supports the hypothesis that endogenous differences in glucocorticoid sensitivity mediated by GR gene polymorphisms affect the neonatal outcome of VLBW preterm infants. In order to confirm the observed associations, analysis of a replication cohort is ongoing.
Nothing to Disclose: FS, CP, CH, MH, JFW, PB, EH, WG, G
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