Correlation of ECR1 A3650G polymorphism with neonatal respiratory distress syndrome.

Abstract

This study aims to determine the correlation of erythrocyte complement receptor 1 (ECR1) A3650G (His1208Arg, rs2274567) polymorphism with the pathogenesis and development of neonatal respiratory distress syndrome (NRDS). This case-control study was conducted at the Huaihe Hospital of Henan University. Sixty-six infants who met the diagnostic criteria of NRDS were placed into the case group. There were 60 healthy infants without respiratory symptoms in the control group. Genetic analyses were conducted using peripheral blood-extracted genomic DNA. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was applied to detect SNP. No apparent differences in gender, weight, and gestational age were observed between NRDS and healthy infants (all p>0.05). However, the NRDS group had more premature infants than the control group (59.1% vs. 38.3%, p=0.019). In the NRDS group, the premature infants had shorter gestational ages than the full-term infants, while the duration of mechanical ventilation and oxygen inhalation for premature infants was longer than those of full-term infants (all p<0.05). Genotype frequencies were in Hardy-Weinberg equilibrium in both the NRDS and control groups (both p>0.05). The results showed that the A carrier (AG/GG) and the A allele of the ECR1 A3650G polymorphism were associated with risk for NRDS (both p<0.05). Furthermore, premature infants with NRDS had higher frequencies of the A carrier (AG/GG) of ECR1 A3650G polymorphism than full-term infants (p=0.002). Our findings provide evidence that the A carrier (AG/GG) and the A allele of the ECR1 A3650G polymorphism may be correlated to the pathogenesis of NRDS and, hence, might be involved in the susceptibility to NRDS.