Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Persistent dry cough is a common unwanted effect of angiotensin converting enzyme (ACE) inhibitors and the most frequent reason for the drug being stopped. This article reviews the incidence and aetiology of ACE inhibitor cough and considers its management.
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PMID:Cough caused by ACE inhibitors. 763 22

As a symptom of an underlying condition, cough is one of the most common reasons patients see physicians. To the majority, a cough means that 'something is wrong' and it causes exhaustion and/or self-consciousness. Patients find these reasons as well as effects on lifestyle, fear of cancer and/or AIDS or tuberculosis to be the most troublesome concerns for which they seek medical attention. The treatment of cough can be divided into two main categories: (a) therapy that controls, prevents or eliminates cough (i.e. antitussive); and (b) therapy that makes cough more effective (i.e. protussive). Antitussive therapy can be either specific or nonspecific. Definitive or specific antitussive therapy depends on determining the aetiology or operant pathophysiological mechanism, and then initiating specific treatment. Since the cause of chronic cough can almost always be determined, it is possible to prescribe specific therapy that can be almost uniformly successful. Non-specific antitussive therapy is directed at the symptom; it is indicated when definitive therapy cannot be given. Practically speaking, the efficacy of nonspecific therapy must be evaluated in double-blind, placebo-controlled, randomised studies of pathological cough in humans. Such studies have demonstrated the efficacy of dextromethorphan, codeine and ipratropium bromide aerosol in patients with chronic bronchitis. While the preferred treatment for patients with cough due to angiotensin converting enzyme (ACE) inhibitor therapy is withdrawal of the offending drugs, it may be possible to ameliorate the cough by adding nifedipine, sulindac or indomethacin to the treatment regimen. The efficacy of protussive therapy has not been well documented. Although hypertonic saline aerosol and erdosteine in patients with bronchitis, and amiloride aerosol in patients with cystic fibrosis have been shown to improve mucus clearance, their clinical utility has not been adequately studied.
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PMID:Appropriate use of antitussives and protussives. A practical review. 769 10

1. The reproducibility of angiotensin converting enzyme inhibitor induced cough was examined in a double-blind cross over study in patients previously shown to have exhibited this side effect. 2. Ninety-seven patients who had experienced angiotensin converting enzyme inhibitor cough within the last 2 years were challenged with enalapril 20 mg daily for 4 weeks to establish eligibility. Eighty-eight of 97 (91%) patients experienced a repeat of their cough symptoms. Sixty-four patients entered the double-blind part of the study where they were treated with enalapril 20 mg and a renin inhibitor for up to 4 weeks in random order. These periods were separated by a minimum 4 week placebo wash out. 3. Of 59 evaluable patients who received enalapril a second time, 37 (62.7%) experienced cough again. Of 62 patients on the renin inhibitor 16 (25.8%) experienced cough, however as it was not equi-efficacious to enalapril no valid comparison could be made. 4. Angiotensin converting enzyme inhibitor cough is not reproducible within patients, as other factors are involved in the aetiology. Objective testing with blinded assessment together with symptom reporting, would give a more accurate measure of the incidence, and mechanism of this side effect.
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PMID:Reproducibility of angiotensin converting enzyme inhibitor induced cough: a double-blind randomised study. 774 49

The objectives of this study were to determine the risk for coughing as an adverse reaction to angiotensin converting enzyme (ACE) inhibitors under everyday circumstances in a large population and to study whether this adverse effect is more common in women. A population-based case-control study was used. The study was set in the practices of 161 Dutch general practitioners (GPs), in which all consultations, morbidity, mortality, medical interventions and prescriptions were registered during 4 consecutive 3-month periods in 4 consecutive groups of 40-41 GPs. The subjects were 2436 patients with incident coughing and up to 3 controls per case were obtained (total group: 7348 controls), matched for GP and a contemporary consultation in the same 3 months. All cases and controls were 20 years or older and had no notification of respiratory infections, influenza, tuberculosis, asthma, chronic bronchitis, emphysema, congestive heart failure, sinusitis, laryngitis, haemoptysis or respiratory neoplasms during the 3-month period. The results showed that cases were 3.6 times as likely as controls to have been exposed to ACE inhibitors (95% CI: 2.4-5.5) but after adjustment for potential confounders the odds ratio was 2.5 (95% CI: 1.6-3.9). The crude odds ratio for males was 2.7 (95% CI: 1.4-5.1) and for females 4.2 (95% CI: 2.4-7.5). The adjusted odds ratio for males was 1.8 (95% CI: 0.9-3.5) and for females 2.7 (95% CI: 1.5-4.8).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin converting enzyme inhibitor associated cough: a population-based case-control study. 776 16

Forty-seven patients with pulmonary sarcoidosis stage II-III, fulfilling clinical indications for starting treatment with corticosteroids, received oral methylprednisolone for 8 weeks in gradually decreasing doses (starting dose 48 mg per day). From week 5 onwards, they also received inhaled budesonide, 1.6 mg daily. Treatment was continued for 18 months and all patients have been followed for at least 3 years. At 18 months treatment could be discontinued in 38 patients, who had used individually adjusted doses of budesonide depending on the clinical response (reduced doses in 14, initial dose in 16, and increased doses in 8 patients). Budesonide treatment alone was satisfactory in 31 of these 38 cases. An additional seven patients could stop treatment after receiving supplementary courses of oral steroids for 3-12 months. Treatment is ongoing in 9 patients in which 6 have extrapulmonary manifestations requiring oral steroids. The chest radiograph became normal in 22 patients and improved in 14. Significant improvements were noted in FVC and DLco in relation to predicted normal values. Serum ACE, lysozyme and beta 2-microglobulin values decreased significantly. Transient cough was seen in 5 and hoarseness in 3 patients. No systemic side-effects were noted; one patient taking 2.4 mg budesonide daily had a plasma cortisol value below the normal range. Inhaled budesonide seems to offer an effective and safe alternative to oral steroids for long-term maintenance treatment of patients with pulmonary sarcoidosis.
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PMID:Inhaled budesonide for maintenance treatment of pulmonary sarcoidosis. 780 97

The objectives of this study were to evaluate the specific effect of the ACE-inhibitor lisinopril on myocardial mass and diastolic function in uremic patients using a protocol designed to leave blood pressure unchanged. Nineteen hemodialysis patients (7 males; mean age: 55 +/- 13 years; mean time on dialysis: 44 +/- 35 months) received lisinopril for 6 months in addition to their preexistent antihypertensive treatment regimens (mean: 1.4 +/- 0.8 drugs). Doses of antihypertensive drugs were adjusted to keep both systolic and diastolic blood pressure stable. Nine patients were withdrawn from lisinopril treatment after 43 +/- 33 days because of hypotension (n = 4), withdrawn consent (n = 3), stroke (n = 1) and cough (n = 1). Seven of them were further studied as controls. Ten patients received 6.4 +/- 4 mg lisinopril as a mean for 6 months. Mean myocardial mass, calculated by M-mode echocardiography, was 324 +/- 103 g before, and 313 +/- 79 g after 6 months of lisinopril treatment. In the control patients, myocardial mass was 318 +/- 110 g initially, and after 6 months, it was 334 +/- 159 g. Early and late transmitral diastolic flow velocities were not significantly influenced by lisinopril. Throughout the study, both the systolic and diastolic 24-h mean blood pressure levels remained stable (systolic: before: 145 +/- 19 mmHg, at 6 months: 147 +/- 17 mmHg; diastolic: before: 87 +/- 12 mmHg, at 6 months 87 +/- 10 mmHg). Thus, no specific effect of lisinopril on regression of myocardial hypertrophy or improvement of diastolic function could be observed within a 6-month period in this small group of hemodialysis patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of ACE-inhibition on myocardial mass and diastolic function in chronic hemodialysis patients with adequate control of blood pressure. 785 Oct 32

Angiotensin-converting enzyme inhibitors (ACE-I) have become the mainstem of antihypertensive therapy and first-choice agents for vasodilatation in congestive heart failure (CHF). A typical dry cough is the main cause for discontinuation of ACE-I therapy. Data about the incidence, course, and clinical significance of this side effect are conflicting. This study determined the incidence of cough in ACE-I treated patients with hypertension and with CHF and to appreciate its clinical significance; 268 ACE-I treated patients, 164 with hypertension and 104 with CHF were prospectively followed for at least 1 year and specifically questioned about cough and other side effects. In those in whom cough developed, a second and then a third ACE-I were tried. Cough developed in 50 (18.6%) of the 268 patients; 23 patients with hypertension (14%) had coughs 24.7 +/- 17.1 (SD) weeks after initiation of therapy; 27 patients with CHF (26%) had coughs 12.3 +/- 12 (SD) weeks after the start of ACE-I therapy (P = 0.005). All but three patients had coughs also on the second and third ACE-I. The time from the beginning of therapy to the onset of cough was significantly shorter with the second than the first drug. ACE-I agents had to be discontinued in 50% of the patients in whom coughs developed, most of them in the CHF group. In the others, cough was well tolerated or disappeared during subsequent months. The incidence of cough, which necessitated discontinuation of ACE-I treatment, was 4% among patients with hypertension and 18% among patients with CHF (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors and cough: a prospective evaluation in hypertension and in congestive heart failure. 787 4

Chronic cough is a common symptom presenting to all clinicians. Every effort should be made to determine the cause(s) of cough because specific therapy has a higher likelihood of success than empiric therapy. Evaluation begins with a complete history, physical examination, routine health screen laboratory testing, chest film, and pulmonary function testing. Further investigation should be guided by the response to treatment of the most likely diagnostic possibilities: postnasal drip, cough-variant asthma, gastroesophageal reflux, chronic bronchitis, bronchiectasis, and ACE inhibitor induced. The majority of each patient's workup can be performed and ordered by the primary care physician.
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PMID:Chronic cough. 787 96

We examined the effect of trandolapril ((-)-(2S, 3aR, 7aS)-1-[(S)-N-[(S)-1-ethoxycarbonyl-3- phenylpropyl]alanyl]hexahydro-2-indolinecarboxylic acid), a potent angiotensin converting enzyme (ACE) inhibitor, on the number of capsaicin-induced coughs in guinea pigs and compared it with that of enalapril. Chronic treatment with enalapril, at a dose of 3 mg/kg, p.o., significantly enhanced the number of capsaicin-induced coughs. Chronic treatment with trandolapril, at doses of 1 and 3 mg/kg, p.o., slightly enhanced the number of capsaicin-induced coughs. However, there were no significant differences in the number of capsaicin-induced coughs between trandolapril-treated and vehicle-treated animals. These results suggest that cough induced activity, one of the most serious side effects associated with chronic treatment with ACE inhibitors, of trandolapril is relatively lower than that of enalapril.
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PMID:Cough-induced activity of (-)-(2S, 3aR, 7aS)-1-[(S)-N-[(S)-1-ethoxycarbonyl-3- phenylpropyl]alanyl]hexahydro-2-indolinecarboxylic acid (trandolapril) in guinea pigs. 795 88

The effects of inhibition of angiotensin converting enzyme (ACE) and glycopyrrolate on cough caused by inhaled capsaicin were investigated in a double-blind, randomised cross-over study in twelve normal volunteers. The capsaicin challenge was performed before and 2 h after dosing with 75 mg captopril or matched placebo given orally, and 20, 40 and 60 min after giving 1 mg glycopyrrolate i.v. to each subject. Captopril and placebo did not alter the cough response when compared to baseline. Glycopyrrolate, however, caused a significant increase in the threshold sensitivity (D2) from baseline, and a significant decrease in the total cough response at 40 and 60 min both after captopril and placebo. The D2-baseline and D2-40 min after glycopyrrolate (mean SD), respectively, were 3.2 (1.0); 17.9 (4.2) after placebo and 2.5 (8.5); 23.6 (6.9) after captopril. Elimination of vagal influences implies attenuation of the effects of tachykinins but not those prostaglandins. We postulate that tachykinins, such as substance P, play a more important role than prostaglandins in capsaicin-induced cough. We conclude that the vagus is important in the capsaicin-induced cough reflex, but, as suppression of this reflex by glycopyrrolate was delayed, the relevant receptors are either poorly accessible peripheral receptors or they are located in the central nervous system.
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PMID:Effects of glycopyrrolate on capsaicin-induced cough in normal volunteers treated with captopril. 795 39


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