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)

A surgically treated case of left atrial myxoma is reported. A 66-year-old man with a history of cough and orthpnea had an echocardiographic and an MRI diagnosis of left atrial myxoma. He had the constitutional signs of myxoma including acceleration of E.S.R., positive CRP, hyperimmunoglobulinemia, loss of body weight, and so on, in addition to the symptoms of heart failure. Cardiac surgery was performed on him under extracorporeal circulation on June 12, 1990. A large myxoma with a diameter of 6.0 cm x 4.8 cm that was adhering to the fossa ovalis with a stalk was resected. Afterwards the symptoms of both heart failure and the constitutional signs disappeared, and the postoperative course was uneventful. Studies of the excised specimen demonstrated that this tumor produced Interleukin (IL-6). After operation the level of the serum IL-6 that was high before operation was normalized. This suggests that the symptoms and the laboratory results pointing to an autoimmune disease were due to the IL-6 produced from the cardiac myxoma. This is the first report that the localization of the IL-6 in the left atrial myxoma is demonstrated with immunohistochemical stain.
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PMID:[Left atrial myxoma with production of interleukin 6]. 159 79

Familial primary pulmonary hypertension was found in two siblings (sister and brother). The woman noted exertional dyspnea at the age of 28 yr. The younger brother noticed exertional dyspnea, cough with bloody sputum and pretibial edema at the age of 38 yr. We diagnosed them as primary pulmonary hypertension as based on hemodynamic and histopathological findings. Regardless of the treatment, both patients died of right-sided heart failure with a short time course. We examined their family members, but there were no other members with primary pulmonary hypertension.
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PMID:Familial primary pulmonary hypertension--report of two siblings. 183 76

The histologic evidence of amiodarone pulmonary toxicity is interstitial pneumonia with foamy alveolar macrophages, which ultrastructurally show lamellar inclusion bodies due to lipid storage. Bronchoalveolar lavage (BAL) fluid findings include foamy macrophages, considered characteristic, and, in certain patients, differential cell counts suggestive of active alveolitis, giving rise to an immunologic explanation for its origin. The present study was undertaken in order to investigate the findings in BAL fluid in nontoxic patients taking amiodarone and to evaluate their clinical relevance. Eleven patients taking amiodarone chlorhydrate for severe ventricular arrhythmias (345 +/- 129 mg/day during 46 +/- 31 months and an accumulated dose of 440 +/- 337 g) and without clinical or radiological evidences of pulmonary toxicity, were clinically evaluated and studied by BAL. As shown in Table 1, cough and pulmonary rales were common findings (64% and 36% respectively), chest X-Rays were normal or indicative of cardiac failure and arterial blood gases showed slight hypoxemia (PaO2 83 +/- 10). As these are usual findings in advanced cardiac diseases, the patients were considered as having no amiodarone toxicity. BAL was done and the fluid obtained was processed for cytologic study. In every patient foamy macrophages were seen with light microscopy and lamellar bodies were detected by electron microscopy. In 5/10 evaluable patients BAL fluid cell count disclosed an increase in lymphocytes, leukocytes or both, indicative of alveolitis. This group of patient had lower PaO2 and PaO2/PAO2 than "non alveolitic" patients (76 +/- 9 mmHg vs 89 +/- 5 mmHg and 0.72 +/- 0.1 vs 0.85 +/- 0.08 - p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cytologic changes in bronchoalveolar lavage in amiodarone treated patients]. 192 87

Ultrasonography revealed a renal tumour (4 x 4 cm) in a 67-year-old man with right-sided lumbar pain and macrohematuria. In addition he had marked nocturnal dyspnoea with dry cough. He had lost about 10 kg in weight. On admission he had atrial fibrillation with an irregular ventricular rate (140 beats/min) and engorgement of the neck veins. Two-dimensional echocardiography, undertaken because of signs of increasing heart failure and a fall of systolic blood pressure to below 100 mm Hg, demonstrated a space-occupying lesion in the right ventricle, 4 x 2 x 1 cm, indicating an intracardiac thrombus or solid tumour. The heart failure continued to worsen, despite treatment with cardiac glycosides, verapamil and diuretics. Hence an exploratory thoracotomy was performed. This revealed an intracardiac tumour which had markedly displaced the right ventricular inflow tract and infiltrated the entire myocardium, but not the tricuspid valve. As much of the tumour as possible was resected, but the patient died postoperatively of heart failure. The intracardiac tumour proved to be a metastasis from the papillary carcinoma of the kidney. This had infiltrated the renal capsule and pelvis and invaded the branches of the right renal vein.
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PMID:[Cardiac metastasis as cause of therapy-resistant heart failure]. 193 45

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice and are time-consuming, expensive, and stressful to the animal. Acute loss of 20-25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7-12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five per cent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10-20 ml/kg, recipient weight, is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10-15 ml of blood/kg body weight at 2-4 week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood crossmatching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 ml of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 ml) intravenously or (4 to 5 ml) intramuscularly if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of blood and blood products. 217 38

We study the hemodynamic effects of pressotherapy in 11 patients (mean age : 68 +/- 10 years) with uncomplicated acute myocardial infarction (n = 6) or with chronic ischemic heart failure (n = 5). We measure the right auricular pressure (RAP), the mean pulmonary arterial pressure (MPAP) and the pulmonary wedge pressure (PWP), before, during pressotherapy (MPAP) and the pulmonary wedge pressure (PWP), before, during pressotherapy (T 20 min) and 30 minutes after the end of pressotherapy (T 30 min). We use five-chambered leg garments with 80 mm Hg pressure during 20 minutes. The wavelike action (from the bottom to the top) is intermittent: the compression time is 10 second (sec); compression is maintained during 60 sec; deflation time is 15 sec. After 20 minutes pressotherapy (t 20) the 3 variables increase: RAP: from 3.6 +/- 5 to 7 +/- 7 mm Hg (P less than 0.001), MPAP: from 25 +/- 14 to 29 +/- 17 mm Hg (p less than 0.01) and the PWP from 10 +/- 8 to 17 +/- 11 Hg (p less than 0.01). This rise is particularly important in heart failure patients: from 18 +/- 8 to 29 +/- 8 mm Hg for the PWP, with cough in one patient. At T 30 these 3 variables decrease and return nearly to initial values: respectively 2.7 +/- 4.7 (RAP), 24 +/- 14 (MPAP), 12 +/- 8 mm Hg (PWP). In conclusion pressotherapy increases RAP and pulmonary pressures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamic impact of pressotherapy]. 221 70

Recently there has been extensive development of orally active angiotensin converting enzyme (ACE) inhibitors in addition to those already marketed, for example, captopril, enalapril, lisinopril and ramipril. It was initially thought that ACE inhibitors were likely to be most useful as antihypertensive agents in conditions in which circulating renin and angiotensin II were elevated. However, it is now clear that they can also lower arterial pressure when plasma renin is not high. In addition, they have beneficial effects in cardiac failure. Thus, captopril, enalapril, lisinopril and ramipril can be used in the treatment of mild to moderate hypertension either alone or in conjunction with diuretics or calcium antagonists. Broadly speaking, efficacy appears to be similar to that of beta-blockers or diuretics. Unfortunately, however, there are no long term studies comparing one ACE inhibitor with another or with other classes of antihypertensive agents. Furthermore, there are no prognostic studies which show that use of ACE inhibitors reduces morbidity or mortality in hypertension. Many new ACE inhibitors are undergoing clinical assessment, including alacepril, cilazapril, fosenopril, perindopril, quinapril and ramipril. The drugs vary, in that some exist in the active form whereas others are prodrugs which are converted to the active agent following absorption. In addition they each possess one of several ligands, for example, carboxyl, phosphinyl or sulfhydryl groups, and so vary in their affinity for ACE. Although many of these agents are renally excreted, a small number are metabolised via the liver (e.g. quinapril and spirapril) and this may prove advantageous in the presence of renal impairment. In common with captopril and enalapril, the new ACE inhibitors inhibit the renin-angiotensin system and initial results suggest that they are effective in lowering blood pressure in essential hypertension. Furthermore, they reduce systemic vascular resistance in the absence of a reflex tachycardia. There are a number of adverse effects which are attributable to the pharmacological mechanism of the ACE inhibitors as a group; these include hypotension, particularly in patients with high renin levels, prior diuretic use, renal impairment or in the elderly. Additional adverse effects may relate to chemical structure. The high incidence of adverse effects noted in early studies related to excess dosage and to the presence of a sulfhydryl group, which the more recently developed ACE inhibitors lack. The adverse effects most commonly reported with established and new ACE inhibitors include headache and fatigue, cough, skin rashes, hypotension and diarrhoea. As a group, ACE inhibitors have an acceptable but not negligible adverse effect burden.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin converting enzyme inhibitors and moderate hypertension. 222 19

Angiotensin converting enzyme (ACE) inhibitors are a novel class of antihypertensive and anticongestive heart failure agents with wide patient and physician acceptability. By blocking the formation of angiotensin II in blood and tissue, all ACE inhibitors significantly lower systemic vascular resistance, lower blood pressure, and improve cardiac function, while maintaining or enhancing perfusion of vital organs: kidneys, brain, and heart. Captopril is the first oral ACE inhibitor with an active sulfhydryl group. Enalapril and lisinopril are potent nonsulfhydryl inhibitors of ACE characterized by weak chelating properties. The side effects of skin rashes, pruritus, taste abnormalities, oral ulcers, pemphigus, and blood dyscrasias have been considered to be strongly characteristic of penicillaminelike drugs, including the sulfhydryl ACE inhibitors. The class effects of cough, angio-edema, hyperkalemia, nonoliguric functional renal insufficiency, and hypotension can occur with equal frequency with all ACE inhibitors. It is unclear whether the many yet investigational ACE inhibitors would have distinct advantages over captopril, enalapril, lisinopril, and enalaprilat. This paper reviews the comparative structure and clinical pharmacology of the three commercially available but chemically different oral ACE inhibitors.
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PMID:Angiotensin converting enzyme inhibitors: comparative structure, pharmacokinetics, and pharmacodynamics. 228 12

A 78-year-old woman with exertional dyspnea (Hugh-Jones Grade III) and dry cough was admitted to our hospital in April, 1983. She had marked cardiac cachexia and a loss of body weight due to long term heart failure. On physical examination a systolic ejection murmur and a diastolic rumbling murmur were heard without the opening snap sound. Chest radiography revealed pleural effusion and cardiomegaly. M-mode and two dimensional echocardiography demonstrated abnormal echoes in the left atrium, the density being 22.7 Hounsfield Unit. Radionuclide angiography and magnetic resonance imaging (MRI) provided similar findings. No other mass lesion existed in the other chambers. Based on these findings, the mass was diagnosed as a left atrial myxoma. She has been well except for periodic congestive heart failure, for about five years since her discharge. The course of her ailment is interesting because her treatment is mainly symptomatic.
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PMID:[A case of elderly (83-year-old) woman with possible left atrial myxoma]. 232 Jul 97

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.
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PMID:Converting enzyme inhibitors in the treatment of hypertension. 248 62


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