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)

Asthma is a chronic inflammatory disease of the airways that may affect individuals at any age, and can be especially challenging to diagnose and treat in the elderly. The hallmarks of asthma--bronchial hyperreactivity and reversible airflow obstruction--lead to symptoms of intermittent wheezing, dyspnoea and cough. Occasionally, atypical symptoms such as chest pain or tightness occur and may mimic other diseases more common in the elderly, such as ischaemic heart disease. It is therefore important to use objective measures such as spirometry or bronchoprovocation testing to make a diagnosis. In recent years, trends in the treatment of asthma have changed from reliance on shorter-acting bronchodilating drugs to long term preventative therapy with inhaled corticosteroids. In some elderly asthmatic patients, symptoms may be mild and intermittent, and treatment with an inhaled beta 2-adrenergic agent may be all that is required. Most, however, experience persistent symptoms, and pharmacological therapy should begin with daily inhaled corticosteroids and be increased in a stepwise fashion according to the patient's needs. In such patients, short-acting beta 2-agonists should be continued as needed for acute symptomatic relief. Longer-acting beta 2-agonists, oral theophylline and inhaled anticholinergic therapy may be useful. When symptoms are more severe and potentially life-threatening, oral corticosteroids should be given. Since elderly patients are more likely to develop complications of asthma therapy and more likely to manifest adverse interactions with other therapeutic agents, more intense monitoring of asthma treatment is required in dealing with this population.
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PMID:Drug treatment of asthma in the elderly. 888 79

Underlying causes and precipitating causes of congestive heart failure (CHF) should be treated when possible. Older persons with CHF and normal left ventricular (LV) ejection fraction should have maintenance of sinus rhythm, treatment of hypertension and myocardial ischemia, slowing of the ventricular rate below 90 beats/minute, and reduction of salt overload. First-line drug treatment in the management of these persons is the use of loop diuretics combined with beta blockers as tolerated. Angiotensin-converting enzyme (ACE) inhibitors should be administered if CHF persists despite diuretics and beta blockers. If persons are unable to tolerate ACE inhibitors because of cough, rash, or altered taste sensation, angiotensin II type 1 receptor antagonists should be given. If CHF persists despite diuretics, beta blockers, and ACE inhibitors or the person is unable to tolerate beta blockers, ACE inhibitors, and angiotensin II type 1 receptor antagonists, isosorbide dinitrate plus hydralazine should be administered. Calcium channel blockers should be used if CHF persists despite administration of diuretics and the person is unable to tolerate beta blockers, ACE inhibitors, angiotensin II type 1 receptor antagonists, and isosorbide dinitrate plus hydralazine. Digoxin, beta blockers, verapamil, and diltiazem may be used to slow a rapid ventricular rate in persons with supraventricular tachyarrhythmias. Digoxin should not be used in persons with CHF in sinus rhythm with normal LV ejection fraction.
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PMID:Left ventricular diastolic heart failure with normal left ventricular systolic function in older persons. 1157 22

Epidemiological studies have demonstrated an association between different levels of air pollution and various health outcomes including mortality, exacerbation of asthma, chronic bronchitis, respiratory tract infections, ischaemic heart disease and stroke. Of the motor vehicle generated air pollutants, diesel exhaust particles account for a highly significant percentage of the particles emitted in many towns and cities. This review is therefore focused on the health effects of diesel exhaust, and especially the particular matter components. Acute effects of diesel exhaust exposure include irritation of the nose and eyes, lung function changes, respiratory changes, headache, fatigue and nausea. Chronic exposures are associated with cough, sputum production and lung function decrements. In addition to symptoms, exposure studies in healthy humans have documented a number of profound inflammatory changes in the airways, notably, before changes in pulmonary function can be detected. It is likely that such effects may be even more detrimental in asthmatics and other subjects with compromised pulmonary function. There are also observations supporting the hypothesis that diesel exhaust is one important factor contributing to the allergy pandemic. For example, in many experimental systems, diesel exhaust particles can be shown to act as adjuvants to allergen and hence increase the sensitization response. Much of the research on adverse effects of diesel exhaust, both in vivo and in vitro, has however been conducted in animals. Questions remain concerning the relevance of exposure levels and whether findings in such models can be extrapolated into humans. It is therefore imperative to further assess acute and chronic effects of diesel exhaust in mechanistic studies with careful consideration of exposure levels. Whenever possible and ethically justified, studies should be carried out in humans.
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PMID:Health effects of diesel exhaust emissions. 1140 Oct 72

Vasopeptidase inhibitors are a new class of cardiovascular drug that simultaneously inhibit both neutral endopeptidase and angiotensin-converting enzyme (ACE). They increase the availability of peptides that have vasodilatory and other vascular effects; they also inhibit production of angiotensin II. In animal models vasopeptidase inhibitors decrease blood pressure in low, medium, and high renin forms of hypertension, and they also appear to confer benefits in models of heart failure and ischaemic heart disease. Studies in human hypertension show that these agents are effective in decreasing blood pressure regardless of race or age. Experience with omapatrilat, the most clinically advanced of these drugs, has shown it to be more effective than currently available ACE inhibitors or other widely used antihypertensive agents. Studies with omapatrilat in congestive heart failure have shown beneficial effects on haemodynamics and symptoms. The vasopeptidase inhibitors appear to have safety profiles similar to ACE inhibitors, though the frequency of side-effects such as angio-oedema and cough remains to be established. Large trials with clinical endpoints, some already in progress, are needed to establish the place of this class of drug beside that of established therapies in conditions such as hypertension, heart failure, ischaemic heart disease, and nephropathy.
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PMID:Vasopeptidase inhibitors. 1194 97

Previous studies showed that increased QT dispersion (QTd) has been observed during episodes of myocardial ischemia or infarction and identify the patients at risk of arrhythmia or sudden death. The objective of this study is to investigate the relationship between coronary artery disease and QTd during the Valsalva maneuver. The study population included 85 subjects (21 with normal coronary arteries, 35 with stable angina pectoris, and 29 with unstable angina pectoris). Twelve-lead surface ECGs were recorded at 50-mm/sec paper speeds and were obtained before the Valsalva maneuver and during the strain phase. The results indicate a significant difference in mean time increase between the control group and the group with stable angina pectoris (mean difference = 16.10 milliseconds, p<0.000), and between the control group and the group with unstable angina pectoris (mean difference = 35.26 milliseconds, p<0.000). The mean difference in time between these groups was also compared (mean difference = 19.17 milliseconds), and was statistically significant (p<0.000). There are some conditions like constipation, severe coughing spells, nausea, vomiting, and carrying or lifting heavy objects that increase intrathoracic pressure and may increase QT dispersion. Therefore, all these conditions should be treated appropriately and carrying or lifting heavy objects is forbidden, especially in patients with coronary artery disease.
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PMID:Effects of Valsalva maneuver on QT dispersion in patients with ischemic heart diseases. 1171 25

The aim of the study was assessment of bronchial capacity in the treatment with ACE inhibitors. 92 patients with essential hypertension stage I-II (mean age 52 years), ischemic heart disease and bronchial asthma (a mild, moderate and severe course) in a relative remission were treated for arterial hypertension with ACE inhibitors enalapril and diroton. Enalapril improved cough indices by 38.3%, diroton--by 13.3%. This was accompanied by a rise in the level of natural antibodies to bradikinin.
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PMID:[Bronchoconstriction in administration of ACE inhibitors]. 1247 41

The results of the analysis of diagnostic significance of examination of natural antibodies (Nab) to agiotensin-converting enzyme (ACE) and its substrates in the serum of hypertensive patients indicate that concentration of Nab to ACE differ from this mean concentration in donors. An elevated level of Nab to ACE may be considered as a compensatory reaction to increased content of the enzyme in vascular endothelium and blood flow. The same patients were examined for antibodies to peptide angiotensin II (AT-II). Enzyme immunoassay has shown that a significantly elevated level of antibodies to AT-II was only in 5 examinees. The same patients had also high Nab to ACE. The study of a group of ischemic heart disease patients with adverse effects attributed to bronchial affection treated with enalapril and diroton (ACE inhibitors) demonstrates that deterioration of cough and external respiration function is not related to exacerbation of existing chronic pulmonary inflammation. None of the patients had elevated body temperature or inflammatory changes in the blood, other signs of inflammation. Enzyme immunoassay also proved that the initial level of Nab equaled mean value for donors or was insignificantly lower. Blood serum patients with side effects contained a significantly (p < 0.02) elevated quantities of Nab to bradikinin vs initial values. Thus, the proposed method of solid phase enzyme immunoassay quantifies Nab to ACE and its substrates in the patients.
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PMID:[Diagnostic implications of detecting antibodies to angiotensin-converting enzyme and its substrates]. 1459 88

Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ss-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: maximal tolerated dosages of ACE inhibitors;ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema;adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; relatively low dosages of digoxin (serum concentrations of < or = 1.0 ng/dl) if not contraindicated; and diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy.
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PMID:Congestive heart failure: what should be the initial therapy and why? 1472 93

Heart failure is a common and costly medical condition. Ischemic heart disease and hypertension account for most cases of heart failure in developed countries. Estimates of the one-year mortality rates for patients with New York Heart Association (NYHA) Class II, III, and IV are 10%, 20%, and 40%, respectively. Angiotensin-converting enzyme (ACE) inhibitors reduce mortality of heart failure patients by approximately 25% (odds ratio 0.77, 95% CI 0.67 0.88). Larger doses of ACE inhibitors are more effective in preventing hospitalization than are lower doses. Angiotensin II receptor blockers (ARBs) are an alternative for patients who cannot tolerate ACE inhibitors because of their side effects (e.g., cough). Evidence for benefits of using combination of ACE inhibitors and ARBs is encouraging, but requires further study. For patients who cannot tolerate either ACE inhibitors or ARBs, vasodilator therapy with hydralazine and nitrates will probably provide benefit. (Diuretic therapy, while a mainstay of heart failure treatment, is primarily used for symptom relief.) There is also evidence that spironolactone reduces mortality (relative risk reduction 30%, 95% CI 18 40%) for patients with NYHA class III and IV heart failure. When administering spironolactone to heart failure patients, monitoring for hyperkalemia is essential. After two centuries of use, randomized controlled trials have finally demonstrated that digoxin is effective in preventing hospitalizations (relative risk reduction 28%, 95% CI 21 34%). There is now overwhelming evidence that beta-blockers are safe for heart failure patients but that they reduce the risk of death for these patients by approximately 30%. In addition to these medical interventions, heart failure patients may also benefit from a number of non-pharmacological interventions.
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PMID:A review of heart failure treatment. 1477 Feb 50

We report three patients aged 75-80 years observed in the Emergency Room with severe anaemia (requiring transfusion) due to a large abdominal wall haematoma while receiving standard prophylaxis against venous thromboembolism (40 mg/day enoxaparin for 6 days on average). All of them concomitantly received 100 mg/day aspirin because of previous ischaemic heart disease and presented similar clinical features: sudden onset of abdominal pain during a severe cough episode due to bronchial infection. A giant haematoma in the rectus abdominis muscle was recognized (by computed tomography) in every case. The cough has been related with this complication in some reports but its association with antiplatelet drugs and low molecular weight heparin could increase the risks in older patients. Sudden abdominal pain must alert the clinician to the rectus muscle sheath haematoma in order to avoid the risks of an exploratory laparotomy.
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PMID:Prophylaxis with enoxaparin can produce a giant abdominal wall haematoma when associated with low doses of aspirin among elderly patients suffering cough attacks. 1579 43


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