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: UMLS:C0010200 (cough)
23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin converting enzyme inhibitors (ACEIs) constitute a safe and effective therapeutic class for the treatment of hypertension. However, they have been incriminated in the development of certain adverse effects, the most frequently reported being alteration in renal function, development of hypotension and cough. This justified the evaluation of renal function after short-term and long-term treatment with perindopril in hypertensive subjects. In patients with normal renal function, during short-term treatment (1 and 5 days), perindopril induced an increase in renal plasma flow without any modification of the glomerular filtration rate. During long-term administration (up to 18 months of treatment), no significant variation in plasma creatinine was observed. In elderly hypertensive patients or patients with chronic renal failure, the glomerular filtration rate was also preserved, apart from a few rare cases of decreased creatinine clearance, particularly after the addition of hydrochlorothiazide. A slight increase in plasma potassium, with no clinical significance, was observed when perindopril was used as single-agent therapy. Symptomatic hypotension was rarely reported with perindopril (0.2% of cases), even under conditions of salt and water depletion. Amongst the other adverse effects of ACEIs, cough, more recently identified, was investigated in detail. Its frequency was determined in a double-blind study comparing perindopril (1.2%) and captopril (2.4%). It was also evaluated in a long-term study in 632 hypertensive patients (391 treated for 1 year); its incidence was 2.9% and it was responsible for discontinuation of treatment in 8 cases. In this study, 36 patients stopped treatment prematurely because of an adverse effect (5.7%). No harmful drug interactions were reported. The combination of a thiazide diuretic potentiates the antihypertensive effect of perindopril and is perfectly tolerated. The favorable safety profile of perindopril should be related to the correct determination of effective doses.
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PMID:Tolerance and safety of perindopril. 269 Nov 32

In view of the pharmacological and chemical reasons for using ACE-inhibitors to treat diabetic hypertension, a group of 40 outpatients were treated with Enalapril. The sample consisted of 20 outpatients, 6 males, 14 females aged 48-76 (mean age 63.75), 18 of whom had type II and 2 type I diabetes and 11 under treatment by diet and hypoglycaemic drugs or insulin. All these patients presented slight or moderate essential arterial hypertension (diastolic pressure less than 115 mmHg). For about one year 17 of the patients were given 20 mg/die Enalapril and the remaining three 10 mg/die in a single morning dose. In 16 cases no other treatment was given. In 4 a non-potassium conserving diuretic was also given. Check-ups before six months into and at the end of treatment showed: a statistically significant reduction in systolic (p less than 0.05) and diastolic (p less than 0.01) pressure. In contrast no significant change was noted in heart beat, glycaemia before or after meals, body weight, glycosylated haemoglobin or any other blood chemical parameter considered. In one case only there was a slight increase in proteinuria that was however present at the start of treatment. As far as side effects are concerned there was one case of cardiac palmus during treatment and one case of coughing that regressed totally when treatment was suspended but nothing else of significance. It should be noted that the antidiabetic treatment remained unchanged throughout the period considered in most cases and at most was subjected to minimal qualitative and quantitative adjustments.
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PMID:[Prolonged treatment of hypertension in diabetic patients with enalapril. 1-year follow-up]. 282 79

Lisinopril is a new, nonsulfhydryl angiotensin-converting enzyme inhibitor approved for the treatment of hypertension. After oral administration, 25-29 percent of the dose is absorbed intact; biotransformation is not required for pharmacological activity. Onset of action occurs one to two hours after administration, with effects still present 24 hours later. The major route of elimination is through renal excretion and an elimination half-life of 12.6 hours has been reported in normotensive individuals. In patients with impaired renal function (creatinine clearance less than or equal to 30 ml/min) a longer half-life and accumulation have been observed. Lisinopril 20-80 mg/d has been shown to be as effective as hydrochlorothiazide, nifedipine, and beta-blocking agents in the treatment of essential hypertension. Its efficacy in renovascular hypertension has also been demonstrated. In congestive heart failure (CHF) doses of 2.5-20 mg/d appear to provide hemodynamic effects comparable to those of captopril. Dizziness and cough have been the most frequently reported side effects; rash and proteinuria have also been reported in a small number of patients. Interactions with diuretics, potassium supplements, and possibly with nonsteroidal antiinflammatory agents may occur. Lisinopril appears to be similar in efficacy to other antihypertensive agents in the treatment of essential hypertension and to captopril in the treatment of CHF. Whether lisinopril is safer or more effective than captopril or enalapril in the treatment of hypertension or CHF requires further investigation. Prolonged duration of action of lisinopril allows once daily dosing, unlike captopril for which dosing is required every 8-12 hours or enalapril which may necessitate twice daily dosing.
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PMID:Lisinopril: a new angiotensin-converting enzyme inhibitor. 283 26

Coadministration of captopril has been shown to increase serum digoxin concentration. The effects of ramipril, a new angiotensin converting enzyme inhibitor, on serum digoxin concentration after multiple dosing were studied in 12 healthy volunteers. All subjects were receiving steady-state digoxin medication (0.5 mg daily), and ramipril (5 mg daily) was coadministered for 14 days. Serum digoxin concentration was measured repeatedly before, during and up to 1 week after ramipril coadministration at 8 a.m. (trough values) and on selected trial days at 11 a.m., 3 hours after the morning medication. Simultaneously, blood levels of ramipril and its active metabolite diacid were determined. Volunteers were followed closely for side effects and for changes in blood pressure, heart rate and electrocardiogram. Safety pharmacology included serial determination of sodium, potassium, serum glutamic oxaloacetic transaminase, creatinine and a full blood count. Mean serum digoxin concentration was not significantly influenced by ramipril coadministration with trough levels of 0.90 +/- 0.24 before, 0.93 +/- 0.38 during and 0.82 +/- 0.33 ng/ml after ramipril medication. The increase in serum digoxin concentration 3 hours after the morning dose was also not significantly affected by ramipril. Serum levels of ramipril and its diacid showed a wide range of variation. Mean serum potassium increased by 0.3 mmol/liter during ramipril coadministration with development of symptomless hyperkalemia (6.0 mmol/liter) in 1 subject. The only other side effect possibly related to ramipril was a dry cough in 1 subject. Both drugs were well tolerated. Ramipril showed no significant influence on serum digoxin levels in healthy volunteers.
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PMID:Pharmacokinetic interaction study with ramipril and digoxin in healthy volunteers. 303 35

1. The potential of the potassium channel activator, cromakalim (BRL 34915), as a bronchodilator has been evaluated in guinea-pig models in comparison with nifedipine. Some effects of the compounds on guinea-pig tracheal spirals have been studied in an attempt to elucidate their different efficacies in vivo. 2. When given by the intraduodenal route to anaesthetized guinea-pigs, cromakalim (3 and 10 mg kg-1) inhibited 5-hydroxytryptamine (5-HT)-induced bronchospasm for at least 60 min. When given by the i.v. route, the dose of cromakalim producing 50% inhibition of the 5-HT response was 84 micrograms kg-1. Nifedipine failed to show any protective effect up to 100 micrograms kg-1, i.v. and was lethal at higher dose levels. 3. Cromakalim protected conscious guinea-pigs from asphyxic collapse in response to histamine aerosol. The maximal effect occurred 60 min following oral dosing, with 2.5 mg kg-1 providing complete protection for almost half of the animals. Nifedipine had only a weak protective effect even at a high dose level of 50 mg kg-1, p.o. 4. Cromakalim prolonged the time before convulsive cough in response to an antigen challenge in actively sensitized guinea-pigs. Its minimum protective dose was 1 mg kg-1, p.o. Nifedipine (50 mg kg-1, p.o.) was ineffective. 5. Cromakalim inhibited both spontaneous and prostaglandin E2-induced tone in guinea-pig isolated tracheal spirals with IC50 values, relative to the maximum inhibition achieved by isoprenaline (10(-3)M), of 1.1 x 10(-6)M and 8.9 x 10(-7)M, respectively. Its maximal effect was 89% of that produced by isoprenaline. Removal of the epithelium did not influence its activity. Studies using the two enantiomers showed that the activity of cromakalim resided almost entirely in the (-)-enantiomer. 6. Nifedipine (2 x 10-SM) achieved only 49% of the relaxant effect of 10 -3M isoprenaline in isolated tracheal spirals. Addition of cromakalim (10- 5 M) at the end of the nifedipine concentrationresponse experiment caused further relaxation to 94% of the effect of isoprenaline. 7. It is concluded that cromakalim has greater potential than nifedipine as a bronchodilator. It appears that opening of potassium channels, with consequent hyperpolarization and stabilization of the membrane potential, prevents calcium entering the cytosol through routes that are unaffected by calcium entry blockers.
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PMID:Evaluation of the potassium channel activator cromakalim (BRL 34915) as a bronchodilator in the guinea-pig: comparison with nifedipine. 320 91

This study compared the relative effectiveness of two antimicrobial preparations, amoxicillin and amoxicillin-clavulanate potassium (Augmentin), in the treatment of acute maxillary sinusitis in children 2 to 16 years of age. Of 171 children with persistent (ten to 30 days' duration) nasal discharge or daytime cough or both, 136 (80%) had abnormal maxillary sinus radiographs. These children were stratified by age and severity of symptoms and randomly assigned to receive either amoxicillin, amoxicillin-clavulanate potassium, or placebo. After the exclusion of 28 children with throat cultures positive for group A Streptococcus and 15 who did not complete their medication, the remaining 93 children were evaluated: 30 received amoxicillin, 28 received amoxicillin-clavulanate potassium, and 35 received placebo. Clinical assessment was performed at three and ten days. On each occasion, children treated with an antibiotic were more likely to be cured than children receiving placebo (P less than .01 at three days, P less than .05 at ten days). The overall cure rate was 67% for amoxicillin, 64% for amoxicillin-clavulanate potassium, and 43% for placebo.
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PMID:Comparative effectiveness of amoxicillin and amoxicillin-clavulanate potassium in acute paranasal sinus infections in children: a double-blind, placebo-controlled trial. 352 Apr 69

A 76-year-old on long-term Lasix and Pyrogastrone presented with stridor. This became worse with local irritation, e.g. on coughing or during indirect laryngoscopy. Indirect laryngoscopy showed a narrow glottis with an otherwise normal larynx. Blood investigation showed a low serum potassium with a raised bicarbonate level, and a serum calcium level just within the acceptable normal range. A diagnosis of laryngospasm secondary to drug-induced hypokalaemic alkalosis was made. This was treated with the withdrawal of the above drugs and supplementing potassium orally.
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PMID:Stridor due to drug-induced hypokalaemic alkalosis. 357 25

During eight weeks of a recent influenza epidemic 29 patients with ketoacidosis were admitted to the General Hospital, Birmingham. This was an exceptionally large number of cases. Of these, 14 had complained of a cough, nine had clinical evidence of respiratory infection, and four extensive bronchopneumonia. Hypokalaemia was present on admission in several instances and caused respiratory failure and death in three patients. Since the dangers of initial hypokalaemia are increased during the treatment of ketoacidosis, especially when sodium bicarbonate is used, serum potassium levels must be estimated initially and, if necessary, potassium chloride given intravenously at more frequent intervals than usual.
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PMID:Diabetic ketoacidosis during the influenza epidemic. 499 May 51

A 77-year-old, nonalcoholic man was admitted to the Omiya Red Cross Hospital with the complaint of fever and delirium state of two days' duration. Two months prior to admission he had had cough and sputum. Chest X-ray revealed honey comb lungs. Cultures of sputum revealed mycobacterium tuberculosis after eight weeks incubation. He had no liver disease in his past history. The patient appeared cachetic. His vital signs were as follows; temperature 38 degrees C, blood pressure 132/68 mmHg, with a pulse rate of 84/min. He was delirium and excited. Findings of the cranial, motor and sensory nerve examination were normal. Initial laboratory studies showed a serum sodium value of 133 mEq/l, potassium 4.5 mEq/l, chloride 98 mEq/l; a serum GOT value of 51 units, GPT 36 units; a total protein content of 7.8 g/dl and ESR rate of 87 mm/hr. Six days after admission, the patients' consciousness level began to stupor and nuchal rigidity was appeared. Spinal fluid examination revealed opening pressure 270 mm H2O, cell counts 720 (N 712, L 8)/cumm, sugar 57 mg/dl and protein 170 mg/dl. Spinal fluid cultures were positive in mycobacterium tuberculosis after eight weeks incubation. Laboratory studies showed a serum sodium value of 114 mEq/l, potassium 4.4 mEq/l, chloride 86 mEq/l, a serum osmorality (SeOs) 225 mOsm/l and urine osmorality (UOs) 958 mOsm/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central pontine myelinolysis--pathogenesis and review of the literature]. 663 5

This report presents data on the safety and tolerability of losartan potassium (losartan), a selective antagonist of the angiotensin II AT-1 receptor, in approximately 2,900 hypertensive patients treated in double-blind clinical trials. In these studies, headache (14.1%), upper respiratory infection (6.5%), dizziness (14.1%), asthenia/fatigue (3.8%), and cough (3.1%) were the clinical adverse experiences most often reported in patients treated with losartan. These adverse experiences were also frequently reported in patients receiving placebo: 17.2%, 5.6%, 2.4%, 3.9%, and 2.6%, respectively. Dry cough as an adverse event was reported in 8.8% of patients treated with angiotensin-converting enzyme inhibitors, and in 3.1% and 2.6% of patients treated with losartan or placebo, respectively. Only dizziness was considered "drug-related" more often in losartan-treated (2.4%) than placebo-treated (1.3%) patients. In controlled clinical trials, losartan was better tolerated than other antihypertensive agents as determined by the incidence of patients reporting any drug-related adverse experiences. Rates of discontinuation due to clinical adverse experiences in patients who received losartan monotherapy or losartan+hydrochlorothiazide were 2.3% and 2.8%, respectively, compared with placebo (3.7%). No laboratory adverse experiences were unexpected or of clinical importance. First-dose hypotension rarely occurred with losartan or with losartan plus hydrochlorothiazide, and withdrawal effects such as rebound hypertension were not observed in clinical trials. There were no clinically important differences in the clinical or laboratory safety profiles in the demographic subgroups for age, gender, or race. In controlled clinical trials, losartan demonstrated an excellent tolerability profile.
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PMID:Safety and tolerability of losartan potassium, an angiotensin II receptor antagonist, compared with hydrochlorothiazide, atenolol, felodipine ER, and angiotensin-converting enzyme inhibitors for the treatment of systemic hypertension. 771 81


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