title: Mannose-binding lectin gene polymorphism and early neonatal outcome in preterm infants.
abstract: BACKGROUND
  Mannose-binding lectin (MBL) as a component of innate immunity plays an important role in preterm infants in whom adaptive immunity is not sufficiently developed. Polymorphisms in immunoregulatory genes influence the response to infection and subsequent inflammation. Infection and inflammation have been implicated in the mechanisms responsible for many of the diseases in the preterm newborns.
  
  
  OBJECTIVE
  The aim of the study was to investigate the relationship between MBL gene polymorphism and early neonatal outcome in preterm infants.
  
  
  METHODS
  Codon 54 and 57 polymorphisms in MBL2 gene were genotyped in 99 preterm infants admitted to the Neonatal Intensive Care Unit at Ege University Children's Hospital.
  
  
  RESULTS
  Overall frequencies of sepsis and early-onset sepsis were higher in the group of infants with MBL polymorphism when compared to infants with wild-type MBL genotype (p = 0.008, 0.009, respectively). Maximum Tollner sepsis score in the first 3 days of life was higher for the infants with variant MBL genotype (p = 0.0278). More infants in the variant MBL group had significant patent ductus arteriosus when compared to infants with wild-type MBL (27.8 vs. 9.5% respectively, p = 0.037).
  
  
  CONCLUSIONS
  MBL gene polymorphism was associated with increased frequency of clinical sepsis particularly with early neonatal sepsis and also with higher Tollner sepsis scores and increased frequency of patent ductus arteriosus in infants. Overall mortality and incidence of culture proven sepsis, respiratory distress syndrome, bronchopulmonary dysplasia, intraventricular hemorrhage, periventricular leukomalacia and necrotizing enterocolitis were not found to be related to MBL genotype.
authors.affiliation: Division of Neonatology, Department of Pediatrics, Ege University Faculty of Medicine, Bornova/Izmir, Turkey. ozgekoroglu @ mail.ege.edu.tr
authors.forename: Ozge Altun
authors.initials: OA
authors.lastname: Koroglu
authors.forename: Huseyin
authors.initials: H
authors.lastname: Onay
authors.forename: Gulin
authors.initials: G
authors.lastname: Erdemir
authors.forename: Mehmet
authors.initials: M
authors.lastname: Yalaz
authors.forename: Bilin
authors.initials: B
authors.lastname: Cakmak
authors.forename: Mete
authors.initials: M
authors.lastname: Akisu
authors.forename: Ferda
authors.initials: F
authors.lastname: Ozkinay
authors.forename: Nilgun
authors.initials: N
authors.lastname: Kultursay
mesh_terms: D005260:Female; D005317:Fetal Growth Retardation / Q000453:epidemiology / Q000235:genetics / Q000473:pathology; D020022:Genetic Predisposition to Disease; D005838:Genotype; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007235:Infant, Premature, Diseases / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology; D008297:Male; D037601:Mannose-Binding Lectin / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D018805:Sepsis / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology; D012720:Severity of Illness Index; D014421:Turkey
chemical_list: C445619:MBL2 protein, human; D037601:Mannose-Binding Lectin