Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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, FEV1.0% and %V25)--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 persistent cough or bronchial asthma did not occur after stopping the treatment with ACE inhibitors. The mean follow-up period was 15.6 months.
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PMID:[Angiotensin converting enzyme (ACE) inhibitor-induced cough in non-smoking hypertensive patients]. 183 7

Since dry cough has recently been recognized as a side effect of angiotensin converting enzyme (ACE) inhibitors employed in the treatment of hypertension or congestive heart failure, the incidence of dry cough in elderly patients receiving ACE inhibitors was investigated. There were 237 out-patients on either captopril, enalapril, or delapril, in August and November 1989. Questionnaires concerning dry cough and smoking were completed by 184 patients. Patients either less than 50 years of age, or with chronic pulmonary disease were excluded. The remaining 168 patients, 63 males, 105 females, with a mean age of 73 years were analyzed for the incidence of a dry cough in relation to age, sex, smoking, and type of drugs. The overall incidence of a dry cough was 21/168 (12.5%), 7/63 (11.1%) for males and 14/105 (13.3%) for females, and was less frequent with advancing age; in the 51-60 age group 4/11 (36.4%), in the 61-70 age group 5/39 (12.8%), in the 71-80 age group 9/75 (12.0%), in the 81-90 age group 3/40 (7.5%), in the 91- age group 0/3 (0%). Enalapril showed significantly higher incidence of dry cough than captopril (16/93, 17.2% vs 7/88, 8.0%, p less than 0.05). Delapril showed an incidence 4/11, 36.4%, however, 9 out of the 11 patients who were given delapril had had a history of a dry cough with captopril or enalapril, and in 4 out of these 9 patients the dry cough disappeared by replacement of captopril or enalapril by delapril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dry cough in the elderly patients treated with angiotensin converting enzyme inhibitor]. 189 31

To determine the frequency of ACE inhibitor cough in an outpatient medical clinic population, a cross-sectional epidemiologic survey using mailed questionnaires was done. Patients were randomly selected from a computerized hospital pharmacy data base. The overall prevalence of cough was 19 percent in the ACE inhibitor groups compared with 9 percent in the hydrochlorothiazide-treated group. The observed odds ratio for cough among ACE inhibitor users was 2.3 (95 percent CI, 1.02 to 5.00). This study is the first systematic investigation of frequency and characteristics of ACE inhibitor cough that includes a control group. Our results suggest that cough may more frequently accompany treatment with ACE inhibitors than has been previously reported. We recommend that physicians specifically inquire about cough in patients taking an ACE inhibitor. Recognition of this side effect may prevent unnecessary testing and treatment of patients receiving ACE inhibitors.
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PMID:Angiotensin-converting enzyme inhibitors and cough. Prevalence in an outpatient medical clinic population. 198 82

Delapril, a nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor, which has an indanylglycine moiety differing from the proline moiety of captopril or enalapril, is an esterified prodrug that is converted in vivo to its active metabolites. Delapril effectively inhibits rabbit lung ACE activity and lowers blood pressure in spontaneously hypertensive rats. Delapril has several characteristics that differ from captopril and enalapril, including high lipophilicity and weak bradykinin potentiating action. Delapril is a more potent inhibitor of vascular wall ACE activity than enalapril or captopril. It also shows a weaker potentiating action on the citric acid-induced cough in the guinea pig model compared with captopril and enalapril. In 12 out of 150 patients with essential hypertension who complained of cough during treatment with enalapril, changing to delapril resulted in resolution of the cough in 6 out of 12 of these patients: the percentage of patients in the total population with cough decreased from 8% to 4%.
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PMID:Characteristics of a new angiotensin converting enzyme inhibitor: delapril. 200 44

To compare the effects of three different angiotensin converting enzyme (ACE) inhibitors on the cough reflex, capsaicin and citric acid challenge tests were done in normal subjects and hypertensive patients before and after administration of delapril, captopril, or enalapril. Two groups of 7 normal subjects (single dose study: 15 mg delapril v 18.75 mg captopril or 2.5 mg enalapril) and a group of 6 mildly hypertensive patients (1 week study: cross-over administration of 30 mg/day delapril, 37.5 mg/day captopril, or 5 mg/day enalapril) were studied. Another group of 6 patients with essential hypertension was treated with three ACE inhibitors for 4 weeks in a randomized order, with a 2 week washout period between active therapies. Aerosols of 1 mumol/L and 3 mumol/L capsaicin and 0.68% citric acid in 0.9% NaCl were generated by an ultrasonic nebulizer, and the frequency of cough was counted during inhalation. Delapril treatment resulted in substantially fewer patients with a significant increase (greater than or equal to 4 coughs during treatment than during the control period) in the frequency of cough than did captopril treatment. In the 1 and 4 week studies, enalapril and captopril had substantially more occurrences of significantly increased capsaicin-induced cough than did delapril. These results indicate that delapril has the least cough stimulatory effect among these ACE inhibitors, which may be clinically beneficial.
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PMID:Comparative study of the effects of three angiotensin converting enzyme inhibitors on the cough reflex. 200 48

In recent years, studies of the regulation of the airways have focused to an increasing degree on the roles of neuropeptides. Several peptides have been shown to be present in airways and mediate such diverse responses as ion transport, mucus secretion, bronchospasm or relaxation, edema, cough, changes in vascular permeability, and neutrophil chemotaxis. More recently, studies have described the roles of peptidases, most notably neutral endopeptidase (NEP, also known as enkephalinase, or E.C. 3.4.24.11) and kininase II (also known as angiotensin-converting enzyme, or E.C. 3.4.15.1) in modulating peptide-induced responses. The enzymes cleave a wide variety of peptides, generating metabolites that are inactive in the systems studied to date. Thus inhibitors of NEP potentiate responses to peptides that are cleaved by it. Therefore, NEP plays roles in modulating peptide-induced effects analogous to the role of acetylcholinesterase in modulating cholinergic neurotransmission. In several experimental respiratory diseases, the activity of neutral endopeptidase is decreased, resulting in increased responses to peptides. The therapeutic application of recombinant NEP protects the airways from the adverse actions of stimuli that release inflammatory peptides, and induction of the NEP gene expression by glucocorticoids suggest a possible mechanism for the action of these steroids in treating airway diseases such as asthma, chronic bronchitis, or cystic fibrosis.
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PMID:Roles of neutral endopeptidase in airways. 201 45

Cough is one of the possible untoward adverse drug effects of angiotensin converting enzyme inhibitors. We describe the available information on 50 cough episodes attributable to captopril and 18 episodes attributable to enalapril reported to the Spanish Drug Surveillance System. Cough represented 37% and 39% of the reports of side effects of captopril and enalapril, respectively. There was a remarkable female predominance among the patients with cough. Cough developed at very low doses (15 mg of captopril and 5 mg of enalapril daily), although the patients on captopril who developed cough were receiving higher doses than those who presented other side effects. A high proportion of patients (29%) continued with the drug for more than six months after cough had developed, suggesting the need for a wider knowledge of this side effect.
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PMID:[Cough caused by angiotensin-converting enzyme inhibitors. A series of cases collected by spontaneous notification of adverse reactions]. 202 85

The incidence and prevalence of cough related to enalapril was assessed by spontaneous reporting and a visual analogue scale during a 6 month random double-blind parallel-group study comparing enalapril with nifedipine. Cough was reported spontaneously by 6.2% of enalapril-treated patients, and by none on nifedipine (NS). No patient had to discontinue enalapril because of cough. After 24 weeks treatment increases in visual analogue scale scores for cough frequency greater than or equal to 8 mm were more common for enalapril than nifedipine (difference 21.5%, 95% CI 7.3-35.7%). Increased cough frequency by visual analogue scale was present throughout the study in women, but less consistently in men. High scores for cough were not related to the dose of enalapril. Cough with enalapril was not an important problem during the 6 months of treatment. However increased cough frequency could be detected by visual analogue scale, with a frequency consistent with that observed in open clinic-based studies of longer duration. These findings suggest that ACE inhibitor-induced cough may increase in severity over time, and that even a period of 6 months treatment is too short to evaluate this side-effect adequately.
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PMID:Cough and enalapril: assessment by spontaneous reporting and visual analogue scale under double-blind conditions. 205 77

During the past few years, dry cough has been described as a possible adverse effect of treatment with angiotensin converting enzyme (ACE) inhibitors. There have been several studies of the effect of long-term administration of ACE inhibitors on pulmonary function. We examined spirometrically the effect of a single oral dose of captopril (25 mg) on bronchial tonus in those who had not received the drug previously, in 4 patients who had previously had dry cough during ACE inhibitor therapy, in 20 patients with obstructive pulmonary disease and in 20 control subjects without pulmonary disease. 1 hour after ingestion of captopril there were no significant changes in the spirometric tests of any group. These findings supplement the results of similar tests done during longterm administration of ACE inhibitors, indicating that the pathogenesis of cough elicited by ACE inhibitor therapy does not seem to have an asthmatic basis.
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PMID:[Effect of captopril on pulmonary function]. 206 20

The occurrence of a dry, nonproductive cough during ACE inhibitors therapy has been described in several reports. However, the mechanism of this effect is still unknown. In order to clarify whether ACE inhibitor-induced cough is a symptom of an asthmatic disturbance, six patients (age 54-68) with cough related to captopril or enalapril were rechallenged with ACE inhibitors after an adequate washout period. Baseline airway function and bronchial reactivity to metacholine were measured at the end of the washout period and on the fourth day of rechallenge which was accompanied by the reappearance of cough without wheezing. Rechallenge did not cause changes in dynamic lung function; a low and not significant (p less than 0.1) increase in metacholine dose causing a 15% and a 20% reduction in baseline FEV 1 was observed. It is concluded that cough and bronchoconstriction are likely to be mediated through different nervous pathways and that ACE inhibitor-induced cough is not a variant of asthmatic cough.
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PMID:[Bronchial reactivity and cough due to ACE inhibitors]. 207 84


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