非喫煙者におけるアンギオテンシン変換酵素 (ACE) 阻害薬による咳喇の臨床的検討  [in Japanese] ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITOR-INDUCED COUGH IN NON-SMOKING HYPERTENSIVE PATIENTS  [in Japanese]

非喫煙高血圧症患者41例(男21例, 女20例)に, ACE阻害薬を内服させ, 副作用としての咳喇発生症例について検討した. (1)非喫煙者における咳喇発生は, 41例中7例(男1例, 女6例)で, 咳喇発生率は17.1%であった. 咳喇とアレルギー歴との間, 咳喇とβ遮断薬併用との間には, 有意の関連はなかった. 咳喇症例の臨床検査について, 末梢血好酸球%, 肝機能(GOT, GPT), 腎機能(PSP 15分値, 24時間クレアチニンクリアランス), 呼吸機能(%努力肺活量, 1秒率, %V_<25>)には, 非咳喇群との間に有意差を認めなかった. (2)咳喇は, 抗コリン薬である臭化イプラトロピウムの吸入により完全に消失しないが, 抑制効果を認めた. このことから, 咳喇発生機序の一部として, 迷走神経末端からのACh放出, vagal reflex亢進などのcholinergic activationの関与が示唆された. (3)薬剤内服中止後, 平均15.6力月経過を観察したが, 慢性持続咳喇や喘息に移行した症例はなかった.

The author studied the characteristics of ACE inhibitor-induced cough in 41 non-smoking hypertensive patients. For at least 6 months, 20 patients (10 males and 10 females) were treated with enalapril, and 21 (11 males and 10 females) with aracepril. The results were as follows. 1) ACE inhibitor-induced cough was induced in 7 cases (1 male and 6 females). The incident rate of cough was 17.1%. ACE inhibitor-induced cough was not significantly related to past allergic history or to the beta-adrenergic blocker therapy. The laboratory findings of the cough sufferers-such as eosinophil percent in venous blood, serum GOT and GPT, urea nitrogen, creatinine, renal function (PSP excretion test and creatinine clearance), and pulmonary function (%FVC, FEV_<1.0>% and %V_<25>)- were not significantly different from those of the non-coughers. 2) Inhibitory effects of ipratropium bromide inhalation of ACE inhibitor-induced cough were noted in 83.3% of the patients, but their coughs did not completely disappear. From these findings, the pathogenesis of this cough may be related to be as follows. The cough seems to be related to the release of acetylcholine from vagal nerve terminals or to the stimulation of irritant receptors and vagal reflex. 3) Chronic persistant cough or bronchial asthma did not occur after stopping the treatment with ACE inhibitors. The mean follow-up period was 15.6 months.