title: Bronchial responsiveness and angiotensin-converting enzyme gene polymorphism in sarcoidosis patients.
abstract: BACKGROUND
  Angiotensin-converting enzyme (ACE) inactivates bradykinin and tachykinins, which are potent bronchoconstrictors and mediators of inflammatory reactions. It has recently been shown that an insertion (I)/deletion (D) polymorphism in the ACE gene accounts for variation in serum ACE level. We investigated bronchial responsiveness in patients with sarcoidosis to determine whether it might be associated with ACE gene polymorphism.
  
  
  METHODS
  Bronchial responsiveness was assessed in 21 patients with sarcoidosis, 21 patients with asthma, and 18 healthy control subjects. ACE polymorphism was also examined in the 21 patients with sarcoidosis.
  
  
  METHODS
  Bronchial responsiveness was measured by recording respiratory resistance with continuous inhalation of methacholine from 49 to 25,000 microg/mL in concentration. The ACE genotype was determined using the polymerase chain reaction.
  
  
  RESULTS
  We found a significant increase in bronchial responsiveness in sarcoidosis patients as compared with healthy control subjects (p<0.01). In the sarcoidosis group, patients with the II genotype demonstrated significantly more coughing (p<0.05) and a greater bronchial responsiveness (p<0.05) than did those with DI or DD genotypes.
  
  
  CONCLUSIONS
  Patients with sarcoidosis have increased bronchial responsiveness to some extent, the degree apparently depending on the ACE genotype.
authors.affiliation: 2nd Department of Internal Medicine, Nagoya City University Medical School, Nagoya, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Niimi
authors.forename: H
authors.initials: H
authors.lastname: Tomita
authors.forename: S
authors.initials: S
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Mori
authors.forename: H
authors.initials: H
authors.lastname: Kawaguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Sugiura
authors.forename: R
authors.initials: R
authors.lastname: Matsuda
mesh_terms: D000328:Adult; D001249:Asthma / Q000201:enzymology / Q000235:genetics / Q000503:physiopathology; D016084:Bronchoconstriction / Q000187:drug effects / Q000235:genetics*; D016085:Bronchoconstrictor Agents; D003371:Cough / Q000503:physiopathology; D004247:DNA / Q000032:analysis / Q000235:genetics*; D017931:DNA Primers / Q000737:chemistry; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D016210:Methacholine Chloride; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000097:blood / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D017565:Sarcoidosis, Pulmonary / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology
chemical_list: D016085:Bronchoconstrictor Agents; D017931:DNA Primers; D016210:Methacholine Chloride; D004247:DNA; D007703:Peptidyl-Dipeptidase A