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

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

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

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

The ACE-inhibiting drugs enalapril and captopril may result in a chronic and sometimes severe cough for which no pathologic cause can be found. Drug-induced cough should therefore be considered in any symptomatic patient taking these medications. In such cases, prompt withdrawal of the drug and substitution of a non-ACE inhibitor is curative and conserves the time and resources of the patient and the physician by avoiding unnecessary diagnostic and therapeutic measures.
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PMID:Chronic cough due to angiotensin-converting enzyme inhibitors. 224 93

ACE inhibitors have antihypertensive efficacy similar to that of thiazides, beta-blockers and calcium antagonists. They are simple to prescribe and to take, and are relatively free from subjective side-effects apart from persistent dry cough. There are few specific concerns about safety, but experience of long-term use is still relatively limited. They are valuable additional or alternative antihypertensive drugs when standard therapy is contraindicated or fails to control blood pressure.
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PMID:The role of ACE inhibitors in the management of hypertension. 228 49

Physicians should suspect ACE inhibitors as the cause of cough in patients whose symptom begins soon after the institution of therapy with this class of drugs. This is particularly important in patients without a personal or family history of atopy, with normal physical findings, chest radiographs, and lung function tests. Rather than subjecting the patient to an extensive workup, substitution of a different antihypertensive agent is an inexpensive way to show whether the ACE inhibitor is the cause of the chronic cough.
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PMID:Chronic cough caused by angiotensin converting enzyme inhibitors. 229 44

ACE-inhibitors have long been considered to be connected with only a few side-effects. Their use in clinical practice has shown that a considerable number of patients develop a dry, non-productive cough, resistant to treatment. The cause is hitherto unknown, but ACE-inhibition has been proved to alter the cough reflex. Non-smokers seem to cough more often than smokers, and females more often than males. Registration of side-effects in 28 patients treated for arterial hypertension in general practice in the years 1985-1988 is presented.
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PMID:[Side effects in 28 patients treated with angiotensin converting enzyme (ACE) inhibitor in arterial hypertension in general practice]. 240 13

The aim of this study was to investigate whether ACE-inhibitors could influence bronchial reactivity and interfere with inflammatory skin responses. Ten hypertensive subjects, who had reacted with coughs during ACE-inhibitor therapy, were treated in a double-blind crossover fashion for two weeks with enalapril and with placebo. Enalapril reduced the PC20 value for histamine and augmented the dermal response. Circulating eosinophilic leukocyte level in venous blood dropped markedly after the histamine bronchoprovocation performed during enalapril treatment. Plasma substance P was reduced after histamine provocation performed during placebo treatment, whereas this reduction was abolished by enalapril. In this study, we have demonstrated ACE-inhibitor-induction of moderately increased bronchial reactivity in subjects with suspected ACE-inhibitor-elicited coughs. It is suggested that coughing during ACE-inhibitor therapy is due to an increased inflammatory state in the airways.
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PMID:Increased bronchial reactivity and potentiated skin responses in hypertensive subjects suffering from coughs during ACE-inhibitor therapy. 254 75

The safety and tolerability of lisinopril (1.25-160 mg daily) were assessed in 3,270 patients (2,688 hypertensives and 582 patients with congestive heart failure (CHF] and 280 healthy subjects. The duration of therapy ranged from a single dose to 43 months; 438 patients received lisinopril for at least 12 months (mean 20 months). In the hypertensive population, the most frequent adverse events reported were headache, dizziness, cough, nausea, diarrhoea and fatigue, although not all of these events were thought to be related to lisinopril; 6.1% discontinued lisinopril due to adverse clinical events, most commonly cough and nausea. Twelve hypertensive patients died (0.45%), but most of these were not receiving lisinopril at the time of death and none was considered to be drug-related. In CHF patients, the most frequently reported adverse events were dizziness, dyspnoea, diarrhoea, hypotension and fatigue. Again, not all of these reports were considered to be drug-related. Therapy was withdrawn in 9.6% of patients--hypotension, dizziness, diarrhoea and rash being the most frequent reasons. Fifty-three CHF patients died (9.1%) and in three cases death was considered to be related to lisinopril therapy. Hypotension, orthostatic effects or dizziness following the initial dose of lisinopril occurred infrequently (in 1.3% of the hypertensive group, including those receiving hydrochlorothiazide, and in 4.8% of CHF patients). Changes in laboratory parameters were generally minor and seldom resulted in discontinuation of therapy. Long-term treatment of hypertension and CHF with lisinopril for at least 3 years confirms that the drug is well tolerated. Overall, the side-effect profile is very similar to that of other ACE inhibitors with regard to class-specific effects. However, taste disturbance was rarely observed.
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PMID:Clinical experience with lisinopril. Observations on safety and tolerability. 255 Jun 41


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