title: The Angiotensin Converting Enzyme Insertion/Deletion polymorphism is not associated with an increased risk of death or bronchopulmonary dysplasia in ventilated very low birth weight infants.
abstract: BACKGROUND
  The ACE gene contains a polymorphism consisting of either the presence (insertion, I) or absence (deletion, D) of a 287 bp alu repeat in intron 16. The D allele is associated with increased ACE activity in both tissue and plasma. The DD genotype is associated with risk of developing ARDS and mortality. The frequency of the D allele is higher in patients with pulmonary fibrosis, sarcoidosis and berylliosis. The role of this polymorphism has not been studied in the development of BPD in the premature newborn.
  
  
  METHODS
  ACE I/D genotype was determined in 245 (194 African-American, 47 Caucasian and 4 Hispanic) mechanically ventilated infants weighing less than 1250 grams at birth and compared to outcome (death and/or development of BPD).
  
  
  RESULTS
  The incidence of the D allele in the study population was 0.58. Eighty-eight (35.9%) infants were homozygous DD, 107 (43.7%) were heterozygous ID and 50 (20.4%) were homozygous II. There were no significant differences between genotype groups with respect to ethnic origin, birth weight, gestation, or gender. There was no effect of the ACE I/D polymorphism on mortality or development of BPD (O2 on 28 days or 36 weeks PCA). Secondary outcomes (intraventricular hemorrhage and periventricular leukomalacia) similarly were not influenced by the ACE ID polymorphism.
  
  
  CONCLUSIONS
  The ACE I/D polymorphism does not significantly influence the development of BPD in ventilated infants less than 1250 grams.
authors.affiliation: Department of Pediatrics Louisiana State University Health Sciences Center 1501 Kings Highway Shreveport, Louisiana 71130-3932, USA. KYanam@lsuhsc.edu
authors.forename: Krishna
authors.initials: K
authors.lastname: Yanamandra
authors.forename: John
authors.initials: J
authors.lastname: Loggins
authors.forename: R John
authors.initials: RJ
authors.lastname: Baier
mesh_terms: D001741:Black or African American / Q000235:genetics; D001997:Bronchopulmonary Dysplasia / Q000235:genetics*; D002543:Cerebral Hemorrhage / Q000235:genetics; D005260:Female; D005838:Genotype; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D019102:Infant, Very Low Birth Weight; D007969:Leukomalacia, Periventricular / Q000235:genetics; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D012121:Respiration, Artificial; D044465:White People / Q000235:genetics
chemical_list: D007703:Peptidyl-Dipeptidase A