Tuberc Respir Dis > Volume 58(1); 2005 > Article
Tuberculosis and Respiratory Diseases 2005;58(1):25-30.
DOI: https://doi.org/10.4046/trd.2005.58.1.25    Published online January 1, 2005.
Polymorphisms of Angiotensin-converting Enzyme Gene Associated in Patients with COPD with or without Bronchial Hyperresponsiveness.
Seung Soo Kim, Eu Gene Choi, Seoung Ju Park, Heung Bum Lee, Yong Chul Lee, Yang Keun Rhee
1Department of Internal Medicine, College of Medicine, The Catholic University of Korea.
2Department of Internal Medicine, College of Medicine, Konyang University, Korea.
3Department of Internal Medicine, Medical School, Chonbuk National University, Korea. lhbmd@chonbuk.ac.kr
4Research Institute of Clinical Medicine, Chonbuk National University, Korea.
Abstract
BACKGROUND
An insertion-deletion polymorphism of angiotensin converting enzyme (ACE) gene has been shown to be associated with enzyme activity levels of ACE. Reported results that have been mutually contradictory about asthmatic hypersensitiveness and occurrence according to ACE gene insertion (I)/deletion (D) polymorphism. Also, the involvement of the ACE genes as the genetic basis of bronchial asthma is currently controversy. We investigated whether there was any association between polymorphisms of the ACE genes and airway hyper-responsiveness in chronic obstructive pulmonary disease (COPD). METHODS: A total of 100 patients with COPD were enrolled in this study. The ACE genotypes were determined in all subjects by polymerase chain reaction. Pulmonary function test including bronchodilator response (BDR), methacholine bronchial provocation test (MBPT) were done in those patients. Airway hyper-responsiveness include any findings of positive BDR or MBPT. RESULTS: In COPD patients, the ACE genotype distribution did not differ significantly among groups of patients with severities of COPD, and with or without airway hyper-responsiveness. CONCLUSIONS: These results suggest that polymorphisms of the ACE gene may not be associated with airway hyper-responsiveness, development and severity of COPD.
Key Words: Angiotensins, Enzymes, Polymorphism, COPD


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