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)

One hundred malignant pleural mesotheliomas have been treated in our hospital since 1955. Clinical and autopsy findings are analyzed and compared to X-ray changes. The most common symptoms were dyspnea (49%), pain (40%) and cough (36%). The main initial X-ray signs were pleural effusion (62%), pleural thickening (29%) and solitary nodules (6%). Prior to death a combination of effusion and pleural thickening was the usual finding. Histologically there were 49 biphasic, 32 mesenchymal and 18 epithelial malignant pleural mesotheliomas. At autopsy 82% of the cases had distant metastases, most of which had not been expected clinically. The median survival time was 7.3 months following the first clinical symptoms, and only 4 months after the first radiological signs.
Thorac Cardiovasc Surg 1985 Oct
PMID:Follow-up study of 100 malignant pleural mesotheliomas. 241 79

In a multicenter, parallel, double-blind study, lisinopril was compared with atenolol in the treatment of mild to moderate essential hypertension. Four hundred ninety patients were randomized to a once-a-day treatment with lisinopril 20 mg or atenolol 50 mg for 4 weeks, and the doses of lisinopril or atenolol were increased up to 80 mg or 200 mg, respectively, at 4-week intervals if sitting diastolic blood pressure (SDBP) was not well controlled. Hydrochlorothiazide (HCTZ) 12.5 or 25 mg was added after 12 weeks, if necessary, and titrated upward after 4 weeks to a maximum dose of 25 or 50 mg/day. Lisinopril and atenolol reduced SDBP to a similar extent. All reductions from baseline in sitting diastolic and systolic blood pressure were significant (less than 0.01). Lisinopril produced a significant (less than 0.01) greater reduction in sitting systolic blood pressure (SSBP) than atenolol. Addition of HCTZ caused further blood pressure reductions (p less than 0.01). Five patients (1.7%) on lisinopril and four (2.0%) on atenolol developed skin rashes during weeks 1-12. Two patients (0.7%) on lisinopril 80 mg developed proteinuria (greater than 1 g/day). Cough occurred more often with lisinopril (4.5%), and elevated triglycerides occurred more often with atenolol (2.0%).
J Cardiovasc Pharmacol 1987
PMID:The antihypertensive effect of lisinopril compared to atenolol in patients with mild to moderate hypertension. 244 51

Eleven patients (five women and six men), aged 24-60 years, were treated with the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, with a once-daily dose as the only antihypertensive treatment. Renal artery stenosis was unilateral in eight patients and bilateral in the remaining three. Fibromuscular dysplasia was present in seven patients, and renal arteriosclerotic narrowing was present in the remaining four. All completed a 6-month treatment and went on to a long-term treatment program for a final 24 months, now completed by five patients. Mean pretreatment blood pressure, 187 +/- 19/112 +/- 5 mm Hg (systolic/diastolic; mean +/- SD), was reduced to 148/87 following the drug titration period (1 week), and the same antihypertensive control was maintained throughout the study. Plasma concentration of angiotensin II, aldosterone, and serum ACE activity were effectively reduced for at least 24 h following drug administration. Serum concentrations of lisinopril varied individually and rose in two patients with moderate renal failure. Renal function was well maintained, and control renography revealed no worsening of renal artery stenosis or renal function. The drug was well tolerated without side effects other than cough in one patient. We conclude that lisinopril monotherapy is highly effective in renovascular hypertension. Drug safety was demonstrated by the lack of serious side effects.
J Cardiovasc Pharmacol 1987
PMID:Long-term monotherapy with lisinopril in renovascular hypertension. 244 55

The safety and tolerability of lisinopril were assessed in 1,476 patients [1,165 hypertensives and 311 patients with congestive heart failure (CHF)] and 211 normal volunteers. The duration of lisinopril therapy ranged from 1 day to 16 months, with a mean duration of 105 days. In the hypertensive population, the most frequent clinical adverse experiences on lisinopril alone were headache, dizziness, cough, and diarrhea. Not all of these adverse experiences were thought to be drug related. Five percent of patients were discontinued because of adverse clinical experiences; cough and dizziness were the most common reasons for discontinuation. Two of 1,165 (0.17%) hypertensive patients treated with lisinopril died, compared to 0.41% of hypertensive patients on other therapies. Neither case was considered to be drug related. In patients with CHF, the most frequent clinical adverse experiences were dizziness, diarrhea, hypotension, fatigue, headache, and rash. Not all of these adverse experiences were thought to be drug related. The percent of CHF patients discontinuing because of an adverse clinical experience was 7.4%; the most frequent causes for discontinuation were hypotension, dizziness, or renal impairment. Twelve deaths occurred in 311 CHF patients treated with lisinopril (3.9%) compared to 4/104 (3.8%) of CHF patients treated with placebo and 2/65 (3.1%) treated with captopril. Hypotension, orthostatic effects, or dizziness following the initial lisinopril dose occurred infrequently in patients treated with lisinopril. In hypertensive patients with normal renal function, including those treated previously or concomitantly with diuretic therapy, a first-dose hypotensive episode was reported in six of 955, or 0.6%. The incidence was higher (6.7%) in hypertensive patients with impaired renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1987
PMID:The safety and tolerability of lisinopril in clinical trials. 244 61

The therapeutic inhibition of angiotensin converting enzyme (ACE) is associated with the production of a dry cough, which occurs more commonly in women than men and appears to be unrelated to concurrent illness. At present the exact incidence of ACE inhibitor cough and the substrate of ACE responsible for this effect is unknown. Cough challenge by inhalation of aerosols of tussive agents such as citric acid and capsaicin may be used to study the effect of drug administration on the cough reflex. In normal subjects, an oral dose of captopril (25 mg) causes a significant shift in the dose-response curve to capsaicin inhalation, but not that to distilled water or citric acid. The exacerbation of artificially induced cough by ACE inhibition may be the result of a local increase in perineuronal substance P or bradykinin concentrations within the lung.
J Cardiovasc Pharmacol 1989
PMID:Cough associated with angiotensin converting enzyme inhibition. 247 6

Angiotensin converting enzyme (ACE) inhibitors produce a dry, nonproductive cough in some patients. Retrospective surveys have suggested an incidence of cough of between 0.7 and 14%. Those patients who develop cough show a marked increase in the sensitivity of the cough reflex to inhalation of the extract of red pepper, capsaicin. They have a normal response before treatment, and the sensitivity of the cough reflex returns to normal when therapy is discontinued. The mechanism of this important side effect is not known. Further studies are required to clarify the mechanism of cough, both as a side effect of therapy and as a common symptom of respiratory disease.
J Cardiovasc Pharmacol 1989
PMID:Angiotensin converting enzyme inhibitors and cough. 247 8

The treatment of hypertension in patients with airway dysfunction is a delicate problem. This article focuses on the airway effects of some antihypertensive drugs. Early on, the beta-adrenoceptor antagonists were shown to be hazardous in patients with asthma. Nonselective beta-blockers could induce severe asthma attacks and the bronchodilating effect of beta-agonists was totally blocked. Also, the beta-blockers with partial agonist activity totally blocked the effect of bronchodilating beta-agonists. The selective beta 1-adrenoceptor antagonists were shown to have less pronounced effects on the airways, and it was possible to overcome the beta-blockade in the airways with high doses of beta-agonists. beta-Blockers are contraindicated in asthma patients, even if it is possible to give selective beta 1-adrenoceptor antagonists in some patients together with high doses of beta 2-agonists. Angiotensin converting enzyme (ACE)-inhibitors were recently shown to induce cough and bronchial hyperresponsiveness in some patients. This is probably due to an increased inflammation in the bronchial mucosa as substances (e.g., bradykinin) are not metabolized. Therefore, ACE inhibitors could be hazardous in asthmatic patients, as they can increase the underlying bronchial hyperresponsiveness. Calcium channel blockers were earlier considered to be beneficial in asthma, as it was shown that they had a small relaxant effect on bronchial tone, and could amplify the effect of bronchodilators. In studies of provoked bronchoconstriction, calcium channel blockers were shown to have some protective effect against allergens, histamine, methacholine, or exercise-induced bronchoconstriction. Calcium channel blockers do not have a major place in asthma treatment, but as they have no severe side effects on the airways, they could preferably be given to hypertensive patients with airways disease instead of other antihypertensive agents.
J Cardiovasc Pharmacol 1989
PMID:Antihypertensive drugs and airway function, with special reference to calcium channel blockade. 248 71

The renin-angiotensin system has a wide range of physiological actions, and thus interference with the system has attractive therapeutic potential. The orally active angiotensin converting enzyme (ACE) inhibitors have so far been the most successful drugs in this area. They lower arterial pressure both in renovascular and essential hypertension, and their effects are enhanced by concomitant diuretic therapy or dietary salt restriction. Since, in renovascular hypertension, the affected kidney depends on enhanced local generation of angiotensin II to help preserve its function, the circulation and excretory capacity of this kidney may be compromised with ACE inhibition. ACE inhibitors can improve exercise tolerance and diminish cardiac ventricular arrhythmias in patients with heart failure. Because these drugs lower plasma aldosterone, they tend to correct potassium deficiency and hypokalemia, which may have been induced by diuretic treatment. Hypotension can occur with the first dose of ACE inhibitor, especially in sodium-depleted subjects; in patients on prior antihypertensive therapy, particularly if this includes a diuretic; and in the elderly. Not all of the actions of ACE inhibitors are necessarily due to lowering of plasma angiotensin II: accumulation of kinins may be responsible for some of the effects and side effects. Common to all ACE inhibitors are occasional rashes, cough, and, more rarely, angioedema. Apparently peculiar to captopril, and less often seen with the lower doses now employed, are taste disturbance, proteinuria, and marrow depression. ACE inhibitors, should not be used in pregnant women.
J Cardiovasc Pharmacol 1987
PMID:Converting enzyme inhibitors in the treatment of hypertension. 248 62

Orthotopic en bloc transplantation of the heart and one lung has been done in two patients with end-stage cardiopulmonary disease and a prior thoracic operation. The first patient had undergone right pulmonary thromboembolectomy with caval ligation 5 years earlier, and the second had had left lower lobectomy for bronchiectasis 15 years before the heart and contralateral lung transplantation. Surgical procedures followed the techniques that had been developed in animals. Transplantation of the unoperated contralateral lung made it possible to avoid dissection in the obliterated pleural space and to minimize bleeding, which simplified the procedure considerably. Dramatic reduction in pulmonary artery pressure and improved respiratory function allowed both patients to be weaned from cardiopulmonary bypass without problems. Although the first patient died of liver and renal failure soon after the operation, an intact cough reflex facilitated recovery in the second patient, who has been discharged with essentially normal respiratory function. This report describes heart and unilateral lung transplantation as a procedure of choice for patients with extensive pleural adhesions that made total cardiopulmonary replacement unfeasible.
J Thorac Cardiovasc Surg 1989 Sep
PMID:Heart and unilateral lung transplantation in patients with end-stage cardiopulmonary disease and previous thoracic operations. 252 34

Cough-CPR, a deep rhythmic forceful cough repeated 30-60 times per minute, can be an effective resuscitative technique during emergencies occurring in the cardiac catheterization laboratory. We provide documented evidence on the potential of cough-CPR to maintain adequate systemic arterial blood pressure and consciousness during malignant ventricular arrhythmias, including the longest cough-CPR episode (75-90 sec), with continuous hemodynamics recorded. Results in three patients disclose that 1) mean arterial pressure during cough-CPR was 47-66% of nonarrhythmic baseline at a cough rate of 38-46% of normal sinus rhythm heart rate; 2) mean arterial pressure during hypotensive ventricular tachycardia was 17-60 mm Hg higher with than without cough-CPR; 3) at comparable diastolic pressures (33 vs. 31 mm Hg), systolic arterial pressure during cough-CPR was 40 mm Hg higher than basic CPR; and 4) consciousness can be maintained with cough-CPR during prolonged malignant ventricular arrhythmias. Thus cough-CPR can be a valuable adjunct in maintaining patient stability while definitive therapy for the malignant ventricular arrhythmia is administered.
Cathet Cardiovasc Diagn 1989 Nov
PMID:Cough-cardiopulmonary resuscitation in the cardiac catheterization laboratory: hemodynamics during an episode of prolonged hypotensive ventricular tachycardia. 259 Sep 33


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