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

---

Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pharmacotherapy of hypertension in the aged does not differ qualitatively but only quantitatively from that in use for younger patients. Adjusted, usually lower doses of diuretics, beta-blocking agents, ACE-inhibitors and calcium-channel blockers are the basic drugs. Individual aging processes and concomitant diseases determine the choice of drugs in the elderly (individualized therapy). All substances are initially prescribed at very low dose. The increasing infirmity of the aged often associated with tiredness, dyspnea and dizziness even without treatment requires careful instruction of the patient about effects and side effects of the prescribed medication. The old WHO-guidelines (systolic BP greater than or equal to 160, diastolic BP greater than or equal to 95 mm mercury) should be maintained for diagnosis and treatment of hypertension. However antihypertensive therapy in patients over 80 years of age and in those with marginally elevated diastolic or solely elevated systolic pressure is controversial today.
...
PMID:[Hypertension and old age]. 268 25

Several studies have shown symptomatic and haemodynamic improvement after the introduction of angiotensin converting enzyme inhibitors in patients with heart failure treated with diuretics. The concomitant long term effects of the new orally effective long acting angiotensin converting enzyme inhibitor, enalapril, on symptoms, exercise performance, cardiac function, arrhythmias, hormones, electrolytes, body composition, and renal function have been further assessed in a placebo controlled double blind cross over trial with treatment periods of eight weeks. Twenty patients with New York Heart Association functional class II to IV heart failure who were clinically stable on digoxin and diuretic therapy were studied. Apart from the introduction of enalapril, regular treatment was not changed over the study period; no order or period effects were noted. Enalapril treatment significantly improved functional class, symptom score for breathlessness, and exercise tolerance. Systolic blood pressure was significantly lower on enalapril treatment. Echocardiographic assessment indicated a reduction in left ventricular dimensions and an improvement in systolic time intervals. In response to enalapril, the plasma concentration of angiotensin II was reduced and that of active renin rose; plasma concentrations of aldosterone, vasopressin, and noradrenaline fell. There were significant increases in serum potassium and serum magnesium on enalapril. Glomerular filtration rate measured both by isotopic techniques and by creatinine clearance declined on enalapril while serum urea and creatinine rose and effective renal plasma flow increased. Body weight and total body sodium were unchanged indicating that there was no overall diuresis. There was a statistically insignificant rise in total body potassium, though the increase was related directly to pretreatment plasma renin (r = 0.5). On enalapril the improvement in symptoms, exercise performance, fall in plasma noradrenaline, and rise in serum potassium coincided with a decline in the frequency of ventricular extrasystoles recorded during ambulatory monitoring. Adverse effects were few. In patients with heart failure, enalapril had a beneficial effect on symptoms and functional capacity. The decline in glomerular filtration rate on enalapril may not be beneficial in early heart failure.
...
PMID:Effects of enalapril in heart failure: a double blind study of effects on exercise performance, renal function, hormones, and metabolic state. 299 98

A major problem in pulmonary sarcoidosis is the assessment of disease activity. We established a clinical score system composed of degree of dyspnea, chest radiographic stage, forced vital capacity, and clinical assessment of disease activity (normal = 0, maximum = 16). We evaluated this score in 50 patients with sarcoidosis along with other proposed measures of disease activity: bronchoalveolar lavage percent lymphocytes (% lymphs), Gallium-67 lung uptake measured as total lung to background ratio (TL/B ratio), and serum angiotensin converting enzyme (SACE) levels. The patients we studied had an average clinical score of 5.6 +/- 2.7 (+/- SD). Though bronchoalveolar lavage % lymphs (32 +/- 20%), TL/B ratio (192 +/- 73), and SACE (137 +/- 66) were all significantly elevated in these patients, Gallium-67 uptake was most frequently abnormal (80% of patients). However, the TL/B ratio was higher in smokers (231 +/- 91) than nonsmokers (178 +/- 64, p less than 0.05). There was no correlation between our clinical score, or any part of the clinical score, and other laboratory measures of alveolitis. Bronchoalveolar lavage % lymphs and TL/B ratio correlated weakly (n = 50, r = 0.36, p less than 0.02), while % lymphs and SACE correlated less well (n = 29, r = 0.36, p = 0.051). There was no correlation between TB/L ratio and SACE.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Comparison of clinical parameters, bronchoalveolar lavage, gallium-67 lung uptake, and serum angiotensin converting enzyme in assessing the activity of sarcoidosis. 303 84

Chronic obstructive pulmonary disease (COPD) is equated with chronic bronchitis and emphysema as one disease entity. In COPD airflow limitation is relatively persistent--unlike asthma. Tests for "small-airways disease" form no part of routine practice, for their accuracy in detecting pathological change is debatable. The proteolytic theory of the pathogenesis of emphysema highlights the role of neutrophil elastase, antielastases, oxidants, antioxidants, and thus of potential new treatments. Clinical features of COPD include breathlessness, cough, and sputum, with airflow obstruction and lung hyperinflation. The differential diagnosis includes bronchiectasis, cystic fibrosis, and pulmonary hypertension, but pulmonary fibrosis, etc., is distinguished by radiological infiltrates. Plain chest radiography cannot reliably diagnose emphysema in life, but a new method measuring lung density from the computed tomographic (CT) scan allows location, quantitation, and diagnosis of emphysema (defined by enlargement of distal air spaces) in humans in life. "Pink puffers" with breathlessness, hyperinflation, mild hypoxemia, and a low PCO2 are contrasted with "blue bloaters" with hypoxemia, secondary polycythemia, CO2 retention, and pulmonary hypertension and cor pulmonale. Antismoking measures are a major aim in management. A bronchodilator regimen combining a slow-release oral theophylline with an inhaled beta 2-agonist, ipratropium, and high-dose inhaled steroids is proposed because even modest improvement in obstruction can help these patients. In acute exacerbations with purulent sputum, antimicrobials against Streptococcus pneumoniae and Hemophilus influenzae are used with controlled oxygen therapy aiming to keep the arterial PO2 over 50 mm Hg without the pH falling below 7.25. Influenza prophylaxis is recommended, but pneumococcal vaccination remains debatable. Chronic under-nutrition in "emphysema" implies controlled trials of feeding regimens--but these remain to be assessed. Long-term oxygen therapy is the only treatment known to prolong life in blue bloaters, and oxygen concentrators and transtracheal oxygen delivery are discussed. Pulmonary vasodilators (e.g., beta 2-agonists, hydralazine, nifedipine, angiotensin-converting enzyme [ACE] inhibitors, etc.) have not yet been proved to provide long-term reduction in pulmonary arterial pressure. Blue bloaters have severe nocturnal hypoxemia in rapid eye movement (REM) sleep that is corrected by oxygen or the investigational drug almitrine.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Chronic obstructive pulmonary disease. 304 40

Ten patients with congestive heart failure (CHF) (NYHA II-IV) on adjusted doses of digitalis and diuretics underwent a careful clinical assessment including an evaluation of exertion dyspnoea and the usual echocardiographic indices of cardiac performance. A cardiopulmonary exercise test with an increment of 20W every 3 minutes was prolonged until exhaustion. Systemic arterial pressure, ECG, VO2, VCO2 and VE were monitored throughout. Gas tensions, plasma catecholamines and lactate were measured in blood samples taken at the first and third minute of each exercise stage. The above measurements were carried out before and after 3 months of treatment with Captopril, 50 mg b.i.d. or t.i.d. A highly significant correlation between arterial lactate and plasma norepinephrine (NE) was observed in each patient during both exercise tests (r = 0.77 to 0.99; p less than 0.05 at least). Left ventricular end-diastolic dimensions were reduced by Captopril (from 69.9 +/- 1.7 to 65.2 +/- 1.4 mm, p less than 0.01) along with a concomitant increase in percent fractional shortening. Most of the patients were reclassified at a lower NYHA class and a significant decrease in dyspnoea score was observed. The exercise time was significantly increased (from 11.2 +/- 1.8 to 12.9 +/- 1.9 min; p less than 0.05), but the peak values of NE, arterial lactate and VO2 were not affected by the treatment. The predicted value of VE at a VCO2 of 1 L/min, regarded as an index of dyspnoea, was significantly decreased by Captopril (from 41.4 +/- 2.9 to 38.9 +/- 2.7 L/min; p less than 0.05). The positive effects of long-term treatment with Captopril on cardiac performance in CHF are confirmed. Sympathetic activity is linked to anaerobic muscular metabolism during exercise and seems to be independent of pharmacological ACE inhibition. The discrepancy between the exercise tolerance and the peak VO2 might be explained by a better utilization of the available energy.
...
PMID:Sympathetic activation on effort in patients with chronic heart failure. Long term effects of captopril. 314 3

Steroids are used in progressive lung sarcoid despite arguments that spontaneous remission occur and therapy may not alter outcome. We studied a unique group of 6 patients with dyspnea and advancing pulmonary sarcoid, who had documented untreated progressive disease for 6.8 +/- 2.4 years. Raised SACE, Ga 67 lung uptake, and lymphocyte counts in lung lavage fluid indicated continued active alveolitis. After 3-6 months on steroid, MRC dyspnea grade fell from 2.5 to 0.3 and FVC, FEV, and DLCO increased by 36%, 27% and 16% respectively. This was associated with a fall in small opacity profusion scores on x-ray lung uptake of Ga 67 and serum ACE. These improvements were sustained for the duration of follow up (mean 22 months). These data show that steroids can alter the natural history of progressive sarcoid and reversible alveolitis may coexist with established fibrosis.
...
PMID:Evidence that steroids alter the natural history of previously untreated progressive pulmonary sarcoidosis. 357 16

The acute toxicity of captopril, a potential inhibitor of angiotensin converting enzyme, was studied in Sprague-Dawley rats and ICR mice. In the oral administration, a decrease of spontaneous motor activity, lacrimation, salivation and decline of body temperature was noted in the rats and mice. In the mice, tarry stool was also noted. The LD50 was estimated as: 4249 mg/kg in male mice, 5050 mg/kg in female mice, 4336 mg/kg in male rats and 4245 mg/kg in female rats, In the dead animals, a hemorrhagic erosion or ulcer was recognized in the glandular stomach. An intravenous captopril in mice, caused immediate death by dyspnea in some animals within 3 minutes, but delayed death was also occurred within 24 hours showing a decrease of spontaneous motor activity and decline of body temperature. The LD50 was estimated as 3154 mg/kg in male mice and 3225 mg/kg in female mice. A single intravenous administration of captopril in dose of 1600 mg/kg did not cause any death in the rats of both sexes. The mice of both sexes well tolerated a single subcutaneous administration of captopril in a dose of 2400 mg/kg. No death occurred in rats of both sexes received subcutaneously captopril in a dose of 1200 mg/kg. At an injection site, a necrotic ulcer was noted in the skin of rats and mice which received subcutaneously captopril in a dose of 1600 mg/kg or more and 1200 mg/kg, respectively.
...
PMID:[Acute toxicological studies of captopril in rats and mice]. 627 82

A 29-year-old man was referred to our hospital because of exertional dyspnea and progressive eruption on the buttocks and the lower extremities. Chest roentgenograms and computed tomograms taken at that time revealed diffuse fibrotic changes accompanied by multiple cavities and bullae in the lungs. There were no signs of mediastinal or hilar lymphadenopathy. A chest roentgenogram taken 7 years before admission showed no abnormalities. Serum ACE and lysozyme levels were high: 29.9 IU/l and 14.1 micrograms/ml, respectively. 67Ga scintigraphy showed diffuse uptake in both lung fields. The PPD skin test was negative, and repeated sputum smears and cultures were negative for pyogenic bacteria and acid-fast bacilli. Examination of transbronchial lung biopsy and skin biopsy specimens confirmed the diagnosis--they showed noncaseating epithelioid granulomas with giant cells and a negative reaction of the stain to acid-fast bacilli, which are compatible with sarcoidosis. The patient was given 30 mg/d of prednisone orally. The dyspnea and eruption were clearly alleviated, although there was little roentgenographic regression of cystic or fibrotic changes. There have been only a few reports of cystic and fibrotic changes early in the course of sarcoidosis. The cystic lesions in this case were probably secondary pulmonary cavities caused by the contracting and obstructive changes related to pulmonary fibrosis.
...
PMID:[A case of sarcoidosis with advanced cystic and fibrotic changes in a young patient]. 773 83

Cough is known to be the major respiratory side effect of treatment with angiotensin converting enzyme inhibitors (ACEI). Recently, ACEI have been implicated in drug-induced lung disease. We report a new case of diffuse pneumonitis which occurred during treatment with ACEI. A 73-year-old man was admitted for cough, dyspnea at rest, fever and weight loss. The patient had been treated with the ACEI pirindopril during 6 months for systemic hypertension. Chest radiographs showed reticular infiltrates in the upper lung fields. A CT scan confirmed the infiltrates and showed pleural thickening and airspace opacities. White blood cell counts showed 15,700/mm3 leucocytes with 940 eosinophils/mm3. Transbronchial biopsy was consistent with infiltration of the lung with eosinophils. There was no evidence for another etiology. Once the drug was withdrawn, clinical and radiological abnormalities improved but steroids were required to control symptoms. This report suggests that pirindopril, as captopril, can induce the picture of drug-induced pulmonary disease.
...
PMID:[Pneumopathy induced by pirindopril. A case report]. 804 99

A 57-year-old man with a cough and increasing exertional dyspnoea for the past 6 weeks was found on examination to have a loud systolic murmur and cardiomegaly with pulmonary congestion. Echocardiography revealed congenitally corrected transposition of the great arteries (cTGA: atrioventricular and ventriculoarterial discordance): a morphologically right ventricle with a tricuspid valve on the left, a morphologically left ventricle with bicuspid a-v valve on the right, the aorta arising ventrally from the left-sided (morphologically right) ventricle. The tricuspid valve showed an Ebstein-like anomaly with obvious regurgitation. Transoesophageal and contrast echocardiography defined valvar anatomy, attachment of the great arteries and cardiac chambers to the venous and arterial circulations, as well as absence of a left to right shunt. Angiography revealed a coronary anatomy typical for cTGA. The exertional dyspnoea responded to diuretics and low doses of ACE inhibitor. Follow-up monitoring of the valvar regurgitation and appropriate endocarditis prophylaxis were recommended. As the haemodynamics in cTGA is normal, in the absence of additional anomalies, it is a congenital cardiac defect which can, though rarely, present first in adulthood. Life expectancy depends on the nature of any additional defects and the degree of commonly associated tricuspid valve regurgitation. As this case demonstrates, echocardiography can largely define the anomalies.
...
PMID:[Congenitally corrected transposition of the great vessels in adulthood. The value of noninvasive study methods]. 807 3


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---