TY - JOUR
T1 - Correlation between angiotensin-converting enzyme (ACE) inhibitor induced dry cough and ACE gene insertion/deletion (I/D) polymorphism
AU - Je Hyeong Kim, Hyeong Kim
AU - Hye Cheol Jeong, Cheol Jeong
AU - Kyung Kyu Kim, Kyu Kim
AU - Sung Yong Lee, Yong Lee
AU - Young Hwan Kwon, Hwan Kwon
AU - So Ra Lee, Ra Lee
AU - Sang Youb Lee, Youb Lee
AU - Sin Hyung Lee, Hyung Lee
AU - Dae Ryong Cha, Ryong Cha
AU - Jae Youn Cho, Youn Cho
AU - Jae Jeong Shim, Jeong Shim
AU - Won Yong Cho, Yong Cho
AU - Kyung Ho Kang, Ho Kang
AU - Hyoung Kyu Kim, Kyu Kim
AU - Se Hwa Yoo, Hwa Yoo
AU - Kwang Ho In, Ho In
PY - 1999
Y1 - 1999
N2 - Background: Persistent nonproductive cough is a major adverse effect encountered with ACE inhibitor treatment and the most frequent reason for withdrawal of the drug. The mechanism of cough was postulated to be associated with accumulation of bronchial irritants which are substrates of ACE. It has been speculated that occurrence of this adverse effect is genetically predetermined; in particular, variants of the genes encoding ACE. To investigate this relationship, we determined ACE gene Insertion/Deletion polymorphism in subjects with and without a history of ACE inhibitor-induced cough. Methods: Among the 339 patients with ACE inhibitor treatment, subjects who developed cough that resolved when not taking medication were designated to cough group and other subjects who did not complain cough were designated to non-cough group. Clinical characteristics of the patients were collected by review of medical records. ACE genotypes were determined by PCR amplification of DNA from peripheral blood and agarose gel electrophoresis. Results: 37 patients complained of dry cough(cough group) and 302 patients did not complained of cough (non-cough group). The incidence of ACE inhibitor induced dry cough was 10.9%. There was a preponderance of females in the cough group (M : F=24.3% : 75.7%) compared to the non-cough group (M : F=49.7% : 50.3%, p=0.004). There was no significant difference in mean age, underlying diseases, and kinds and frequencies of ACE inhibitors and their mean dosage between the both groups. ACE genotypic frequencies were I/I : I/D : D/D=16.2% : 18.9% : 64.9% in the cough group and 18.9% : 18.2% : 62.9% in the non-cough group which showed no significant difference between the both groups (p=0.926). Allelic frequencies were I : D = 25.7% : 74.3% and 28.0% : 72.0% in the cough and non-cough group respectively and the difference was not significant (p = 0.676). Conclusion: The incidence of ACE inhibitor- induced cough are 10.9%, and women are more susceptible to ACE inhibitor- induced cough. ACE inhibitor-induced dry cough is not associated with ACE gene Insertion/Deletion polymorphism.
AB - Background: Persistent nonproductive cough is a major adverse effect encountered with ACE inhibitor treatment and the most frequent reason for withdrawal of the drug. The mechanism of cough was postulated to be associated with accumulation of bronchial irritants which are substrates of ACE. It has been speculated that occurrence of this adverse effect is genetically predetermined; in particular, variants of the genes encoding ACE. To investigate this relationship, we determined ACE gene Insertion/Deletion polymorphism in subjects with and without a history of ACE inhibitor-induced cough. Methods: Among the 339 patients with ACE inhibitor treatment, subjects who developed cough that resolved when not taking medication were designated to cough group and other subjects who did not complain cough were designated to non-cough group. Clinical characteristics of the patients were collected by review of medical records. ACE genotypes were determined by PCR amplification of DNA from peripheral blood and agarose gel electrophoresis. Results: 37 patients complained of dry cough(cough group) and 302 patients did not complained of cough (non-cough group). The incidence of ACE inhibitor induced dry cough was 10.9%. There was a preponderance of females in the cough group (M : F=24.3% : 75.7%) compared to the non-cough group (M : F=49.7% : 50.3%, p=0.004). There was no significant difference in mean age, underlying diseases, and kinds and frequencies of ACE inhibitors and their mean dosage between the both groups. ACE genotypic frequencies were I/I : I/D : D/D=16.2% : 18.9% : 64.9% in the cough group and 18.9% : 18.2% : 62.9% in the non-cough group which showed no significant difference between the both groups (p=0.926). Allelic frequencies were I : D = 25.7% : 74.3% and 28.0% : 72.0% in the cough and non-cough group respectively and the difference was not significant (p = 0.676). Conclusion: The incidence of ACE inhibitor- induced cough are 10.9%, and women are more susceptible to ACE inhibitor- induced cough. ACE inhibitor-induced dry cough is not associated with ACE gene Insertion/Deletion polymorphism.
KW - ACE gene polymorphism
KW - ACE inhibitor
KW - Cough
UR - http://www.scopus.com/inward/record.url?scp=0032984169&partnerID=8YFLogxK
U2 - 10.4046/trd.1999.46.2.241
DO - 10.4046/trd.1999.46.2.241
M3 - Article
AN - SCOPUS:0032984169
SN - 1738-3536
VL - 46
SP - 241
EP - 250
JO - Tuberculosis and Respiratory Diseases
JF - Tuberculosis and Respiratory Diseases
IS - 2
ER -
