Bronchial responsiveness and angiotensin-converting enzyme gene polymorphism in sarcoidosis patients

Chest. 1998 Aug;114(2):495-9. doi: 10.1378/chest.114.2.495.

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.

Subjects: 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.

Conclusion: Patients with sarcoidosis have increased bronchial responsiveness to some extent, the degree apparently depending on the ACE genotype.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Asthma / enzymology
  • Asthma / genetics
  • Asthma / physiopathology
  • Bronchoconstriction / drug effects
  • Bronchoconstriction / genetics*
  • Bronchoconstrictor Agents
  • Cough / physiopathology
  • DNA / analysis
  • DNA / genetics*
  • DNA Primers / chemistry
  • Female
  • Genotype
  • Humans
  • Male
  • Methacholine Chloride
  • Middle Aged
  • Peptidyl-Dipeptidase A / blood
  • Peptidyl-Dipeptidase A / genetics*
  • Polymerase Chain Reaction
  • Polymorphism, Genetic*
  • Sarcoidosis, Pulmonary / enzymology*
  • Sarcoidosis, Pulmonary / genetics
  • Sarcoidosis, Pulmonary / physiopathology

Substances

  • Bronchoconstrictor Agents
  • DNA Primers
  • Methacholine Chloride
  • DNA
  • Peptidyl-Dipeptidase A