title: High frequency of a deletion polymorphism of the angiotensin-converting enzyme gene in asthma.
abstract: BACKGROUND
  An insertion-deletion polymorphism of the angiotensin-converting enzyme (ACE) gene has been shown to be associated with levels of ACE. Because ACE is heavily expressed in the lungs and plays a key role in the metabolism of angiotensin II and bradykinin, which are potentially involved in the pathogenesis of asthma, we tested the hypothesis of an association between the polymorphism of the ACE gene and asthma.
  
  
  METHODS
  Seventy-nine patients with asthma, 54 healthy subjects, and 33 patients with nonasthmatic lung disease were studied. Pulmonary function tests were performed in patients with asthma, and the ACE genotypes were determined in all subjects by the polymerase chain reaction.
  
  
  RESULTS
  The ACE genotype distribution was similar in healthy subjects and in patients without asthma. By contrast, the population of patients with asthma was characterized by a higher prevalence of the DD genotype of ACE (odds ratio, 2.09; 95% confidence interval, 1.05 to 4.16; p = 0.023). No difference in pulmonary function test results was detected in asthmatic patients according to the distribution of ACE genotypes.
  
  
  CONCLUSIONS
  This study reports an association between the DD genotype of ACE and asthma, which is not related to the degree of airway obstruction. These results need to be confirmed by a larger case-control study.
authors.affiliation: Service de Biochimie A, Hôpital Bichat, Paris, France.
authors.forename: J
authors.initials: J
authors.lastname: Benessiano
authors.forename: B
authors.initials: B
authors.lastname: Crestani
authors.forename: F
authors.initials: F
authors.lastname: Mestari
authors.forename: W
authors.initials: W
authors.lastname: Klouche
authors.forename: F
authors.initials: F
authors.lastname: Neukirch
authors.forename: S
authors.initials: S
authors.lastname: Hacein-Bey
authors.forename: G
authors.initials: G
authors.lastname: Durand
authors.forename: M
authors.initials: M
authors.lastname: Aubier
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D001249:Asthma / Q000235:genetics* / Q000503:physiopathology; D005260:Female; D005541:Forced Expiratory Volume; D017353:Gene Deletion; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D014797:Vital Capacity
chemical_list: D007703:Peptidyl-Dipeptidase A