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 authors report the case of a 28-year-old woman referred to their department by a respiratory medicine department with an inferior mediastinal tumour arising from the right atrium, presenting in the form of dysponea, dry cough and chest pain associated with a general syndrome composed of fever, weight loss and physical asthenia. Physical examination revealed a superior vena cava syndrome, the electrocardiogram showed diffuse repolarization disorders and the chest x-ray showed an opacity of the anterior and inferior mediastinum. The diagnosis of tumour of the right atrium was based on echocardiography and thoracic CT scan. Subtotal surgical resection under cardiopulmonary bypass allowed examination of the histological type of the tumour. After routine chemotherapy, despite negative secondary staging and a favourable immediate course, the patient died 11 months after the operation in a context of local recurrence and hepatic and bone metastases.
Ann Cardiol Angeiol (Paris) 1997 Dec
PMID:[Angiosarcoma of the right atrium. Presentation of a surgically treated case and comparison with data of the literature]. 958 34

We studied the oral actions of antihistamines from six chemical classes, namely: the ethanolamines (ENA, diphenhydramine and clemastine); ethylenediamines (EDA, pyrilamine and tripelennamine); piperidines (PPD, terfenadine and astemizole); piperazines (PPZ, hydroxyzine and cetirizine); phenothiazines (PTZ, promethazine), and the alkylamines (ALA, chlorpheniramine and bromopheniramine) on cough reflexes, pentobarbital-induced sedation and minute ventilation in the conscious guinea pig. Antihistamines of the ENA class had minimal effects on capsaicin-induced cough although both diphenhydramine (30 and 100 mg/kg p.o.) and clemastine (30 and 100 mg/kg p.o.) increased sedation time (ST). The PPZ class demonstrated both antitussive and sedating activity. The minimum effective oral antitussive dose (MED) of cetirizine and hydroxyzine was 30 and 10 mg/kg, respectively. The EDA did not exhibit antitussive activity. Tripelennamine (10, 30 and 100 mg/kg p.o.) but not pyrilamine enhanced ST. The MED for the PTZ, promethazine, was 10 mg/kg, and at 100 mg/kg promethazine increased ST. The ALA group displayed antitussive activity but only chlorpheniramine (10 mg/kg p. o.) had any effects on ST. The MED for chlorpheniramine and bromopheniramine was 3 and 10 mg/kg p.o., respectively. The PPD antihistamines, namely terfenadine and astemizole, inhibited cough (MED 30 and 10 mg/kg p.o.) without sedative effects. Of the antihistamines tested only promethazine (100 mg/kg p.o.) depressed ventilation responses; however, this dose of promethazine was associated with adverse behavioral effects. The present findings indicate that the antitussive actions of antihistamines are not directly related to histamine H1-receptor blockade because several antihistamines did not antagonize capsaicin-induced cough. In addition, the antitussive actions of antihistamines are independent of their sedative or ventilation effects.
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PMID:Antitussive action of antihistamines is independent of sedative and ventilation activity in the guinea pig. 969 Dec 25

Most antihypertensives have advantages and disadvantages. The ideal antihypertensive drug should be effective in lowering blood pressure, well tolerated, safe in the long term, and easy to use. Ideally, it should be relatively inexpensive. Most importantly it should reduce the risk of the adverse effects of high blood pressure, such as myocardial infarction, sudden death, stroke, heart failure, renal damage, and retinal changes. Most antihypertensive drugs effectively reduce blood pressure, are available as once daily preparations, and are safe long-term. Unfortunately, most antihypertensive drugs cause adverse effects in some patients and for few drugs is there good evidence that they protect the heart, the brain, the kidney, and the eye? Reducing the effects of Angiotensin II (using an ACE inhibitor) has been shown to reduce the incidence of coronary events, sudden death, heart failure, renal damage, and fundal changes. AT1 blocking drugs offer the same pharmacological advantages but also very good tolerability, in particular no cough. Therefore, they have the potential to meet all the criteria for an ideal antihypertensive drug.
Basic Res Cardiol 1998
PMID:Therapeutic advantages of AT1 blockers in hypertension. 983 62

Tolerability and not efficacy is the limiting factor for long-term successful antihypertensive treatment. Since the discontinuation rate of first line antihypertensives may be as high as 50-60% over six months, it is important to develop new agents with an improved efficacy/tolerability ratio. Candesartan cilexetil is particularly promising in this respect. Candesartan is a potent and selective angiotensin II type 1 (AT1) receptor blocker that binds selectively and tightly (insumontable binding) to the receptor. Candesartan is not associated with any increased risk of cough or angiodema. It is an orally effective vasodilator that does not cause reflex tachycardia or first dose hypotension or orthostatic hypotension. In the dose range from 4-16 mg, once daily candesartan cilexetil is not associated with any dose-dependent adverse events and it is equally well tolerated in men and women and by older (> 65 years) and younger (< 65 years) patients. Furthermore, the drug has no adverse effect on glucose homeostasis or plasma lipid profile. In a double-blind comparison with losartan 50 mg od, candesartan cilexetil 16 mg once daily was significantly more effective in lowering the diastolic blood pressure at the end of the 24 h dose interval but was equally well tolerated. In meta-analyses of clinical trials, candesartan cilexetil showed a tolerability profile comparable to that of placebo therapy.
Basic Res Cardiol 1998
PMID:Tolerability of a modern antihypertensive agent: candesartan cilexetil. 983 64

This study examines whether there are differences between Mexican Americans and non-Hispanic whites in reported symptoms of acute myocardial infarction (AMI). The symptoms experienced by patients identified in a community-based surveillance program were examined to determine whether between-group differences existed by ethnicity, gender, and diabetic status. Data were available regarding the symptoms of 589 patients, between the ages of 25 and 74 years, who were hospitalized and diagnosed as either having definite or possible AMI in special care units at 1 of 7 hospitals in Corpus Christi, Texas. The most frequently reported symptoms were chest pain (83.2%), chest pressure or discomfort (67.6%), sweating (64.2%), fatigue (62.6%), dyspnea (60.3%), and arm or jaw pain (58.2%). After adjusting for age, diabetes mellitus, and gender, and relative to non-Hispanic whites, Mexican Americans were more likely to report chest pain, upper back pain, and palpitations, and less likely to report arm or jaw pain. Likewise, relative to men, women were more likely to report fatigue, dyspnea, dizziness, upper back pain, palpitations, and cough, and were less likely to report chest pain. Significant differences were also observed when older patients' symptoms were compared with younger patients' symptoms.
Am J Cardiol 1998 Dec 01
PMID:Comparison of reported symptoms of acute myocardial infarction in Mexican Americans versus non-Hispanic whites (the Corpus Christi Heart Project). 985 14

A 69-year-old male presented with a diagnosis of idiopathic pericarditis, first treated with prednisone for a few weeks with resolution of the symptoms. A few days after stopping the medication, he presented with malaise, cough and signs of pericardial constriction confirmed by echocardiography. He was diagnosed with pulmonary tuberculosis with pericardial involvement and treated accordingly. Pericardiectomy was performed after a few days of treatment because the symptoms related to constriction progressed. The procedure was successful, and the patient was completely asymptomatic after 10 months. The removed pericardium stained positive for acid-fast bacilli.
Can J Cardiol 1998 Dec
PMID:Rapidly evolving constrictive tuberculous pericarditis: case presentation and review of the literature. 991 6

One possible intervention to interrupt the deleterious effects of the renin-angiotensin system is suppression of angiotensin II (Ang II) formation by inhibition of angiotensin-converting enzyme (ACE). However, ACE inhibition incompletely suppresses Ang II formation and also leads to accumulation of bradykinin. Angiotensin II type 1 (AT1) receptors are believed to promote the known deleterious effects of Ang II. Therefore, AT1 receptor antagonists have been recently introduced into therapy for hypertension and congestive heart failure (CHF). Although there are significant differences between the effects of AT1 receptor antagonists and ACE inhibitors including the unopposed stimulation of angiotensin II type 2 (AT2) receptors by AT1 receptor antagonists, the discussion of whether ACE inhibitors, AT1 receptor antagonists or the combination of both are superior in the pharmacotherapy of CHF is still largely theoretical. Accordingly, AT1 receptor antagonists are still investigational. Angiotensin-converting enzyme inhibitors remain first line therapy in patients with CHF due to systolic dysfunction. However, in patients not able to tolerate ACE inhibitor induced side effects, in particular cough, AT1 receptor antagonism is a good alternative. In clinical practice, emphasis should be placed on increasing the utilization of ACE inhibitors, as more than 50% of patients with CHF do not receive ACE inhibitors. In addition, the majority of those on ACE inhibitors receive doses lower than the dosage used in the large clinical trials. Although not yet completely proved, it is likely that high doses of ACE inhibition are superior to low doses with respect to prognosis and symptoms.
J Am Coll Cardiol 1999 Apr
PMID:Recent insight into therapy of congestive heart failure: focus on ACE inhibition and angiotensin-II antagonism. 1019 12

There is a sexual dimorphism in blood pressure: men tend to have higher blood pressures than women with functional ovaries, whereas ovariectomy or menopause tends to abolish the sexual dimorphism and cause women to develop a "male" pattern of blood pressure. Synthetic estrogens and progestins, found in oral contraceptives, tend to elevate blood pressure, whereas naturally occurring estrogens, used in postmenopausal hormone replacement therapy, lower it or have no effect. Women are more likely than men to be aware of their hypertension, to be treated with antihypertensive drugs, and to have their blood pressure controlled. Antihypertensive therapy induces similar blood pressure reductions in men and women. However, men experience larger reductions in total cardiovascular risk with successful treatment of high blood pressure, because their absolute risk of coronary events at baseline is so much higher. Special considerations that can dictate antihypertensive treatment choices for women include increased vulnerability to the adverse effects of some drugs, including angiotensin-converting enzyme inhibitor-induced cough, calcium channel blocker-induced edema, and minoxidil-induced hirsutism. Beta-adrenergic blockers tend to be less effective in women than in men, and diuretics are particularly useful in women because they protect against hip fracture. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers are contraindicated during pregnancy or if pregnancy is planned because of the risk of fetal developmental abnormalities.
Cardiol Rev 1998 Nov
PMID:The Sexual Dimorphism of High Blood Pressure. 1034 60

The history of antiarrhythmic therapy reveals these agents to be associated with a high incidence of toxicity. Although several agents have ocular effects, amiodarone is the most widely recognized for producing adverse effects in the eyes. Corneal microdeposits are almost ubiquitous in patients being treated with amiodarone. However, they are, for the most part, benign and produce no changes in visual acuity. Lack of microdeposits should prompt the physician to investigate whether there is a problem with drug absorption or adherence to therapy. Other effects on the eye have been reported including optic neuropathy, but no causal link has been proved with amiodarone. The population of patients treated with amiodarone often have ischemic disease and/or diabetes, which affect retinal and optic nerve health. Many antiarrhythmic agents also affect lung function. The frequent association of procainamide with a lupus-like syndrome, where half the cases develop pleural-pericardial involvement, may require discontinuation of that drug. Although beta blockers and to a lesser degree, calcium antagonists, may cause bronchospasm in some patients, this is not usually a major clinical problem. Again, it is amiodarone that has the most widespread reputation for causing pulmonary toxicity. Although infrequent (< 1% incidence), it generates the most fear as it is sometimes fatal. Because of the lack of a diagnostic "gold standard," it is often overdiagnosed, placing patients at risk from overlooked congestive heart failure and infections and from recurrent arrhythmias after drug withdrawal. Patients with pre-existing pulmonary disease appear to be more at risk. Common features include indolent onset of cough, malaise and fever associated with patchy peripheral infiltrates, and severely decreased diffusion capacity. Several cases of pulmonary toxicity have had inordinately high serum desethylamiodarone to amiodarone ratios. Most cases recover with cessation of amiodarone therapy. Steroids are commonly used, but are of unproved efficacy. In terms of its toxicity, amiodarone remains the most feared of the antiarrhythmic agents. In the future, a better understanding of its pharmacokinetics, mechanisms of toxicity, and optimal dosing regimens should provide a possibility of better strategies for avoidance, early diagnosis, and more directed therapy of toxicities associated with amiodarone.
Am J Cardiol 1999 Nov 04
PMID:Clinical organ toxicity of antiarrhythmic compounds: ocular and pulmonary manifestations. 1056 58

Angiotensin converting enzyme inhibitors (ACEI) and angiotensin II receptor antagonists (AIIA) are both pharmacological groups that inhibit the actions of angiotensin II. ACEI prevent the formation of angiotensin II from angiotensin I, whereas A II A inhibit the final crucial step of angiotensin II binding with the AT1 receptor site. A similar antihypertensive efficacy has been described for both groups but A II A drugs have a better safety profile above all due to the absence of dry cough. Despite the fact that evidence with ACEI is more conclusive, A II A seems to achieve the same protective effects on the target organ damage in hypertensive patients. At present, ACEI are the drugs of choice in the treatment of patients with cardiac dysfunction and failure. The information of ongoing trials with A II A will be of great value in deciding the optimal treatment for hypertensive patients with different cardiovascular diseases.
Rev Esp Cardiol 2000 Jan
PMID:[Do angiotensin II receptor antagonists substitute angiotensin converting enzyme inhibitors in the treatment of high blood pressure?]. 1070 16


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