Background: As described in animal models, the lectin- complement pathway is central to the propagation of ische- mia–reperfusion injuries in many tissues, including the brain. Similarly, it might affect the genesis of brain damage in pre- term infants. MBL2 gene single-nucleotide polymorphisms (SNPs), regulating mannose-binding lectin (MBL) serum levels, could predict the risk of adverse neurological outcome in these infants. Methods: To evaluate the association between SNPs of the MBL2 gene and long-term neurological outcomes in preterm infants,75infants(gestationalage(GA)≤32 wk)were observed in a prospective longitudinal study and assessed by clinical and instrumental exams at 12 and 24 mo of corrected age (CA). They were genotyped for the promoter polymorphism -221 and for the exon-1 variant alleles (at codons 52, 54, and 57) of the MBL2 gene. results: The MBL2 exon-1 OO genotype was more frequent in children with an adverse neurological outcome (5/35; 7%) than in controls (0/40; 0
MBL2 gene polymorphisms increase the risk of adverse neurological outcome in preterm infants: a preliminary prospective study / C., A., G., P., Caravale, B., M. F., C., M. P., R., F., P., C., A., V. M., D.C.. - In: PEDIATRIC RESEARCH. - ISSN 0031-3998. - STAMPA. - 76:(2014), pp. 464-469. [10.1038/pr.2014.118]
MBL2 gene polymorphisms increase the risk of adverse neurological outcome in preterm infants: a preliminary prospective study
CARAVALE, BARBARA;
2014
Abstract
Background: As described in animal models, the lectin- complement pathway is central to the propagation of ische- mia–reperfusion injuries in many tissues, including the brain. Similarly, it might affect the genesis of brain damage in pre- term infants. MBL2 gene single-nucleotide polymorphisms (SNPs), regulating mannose-binding lectin (MBL) serum levels, could predict the risk of adverse neurological outcome in these infants. Methods: To evaluate the association between SNPs of the MBL2 gene and long-term neurological outcomes in preterm infants,75infants(gestationalage(GA)≤32 wk)were observed in a prospective longitudinal study and assessed by clinical and instrumental exams at 12 and 24 mo of corrected age (CA). They were genotyped for the promoter polymorphism -221 and for the exon-1 variant alleles (at codons 52, 54, and 57) of the MBL2 gene. results: The MBL2 exon-1 OO genotype was more frequent in children with an adverse neurological outcome (5/35; 7%) than in controls (0/40; 0I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
