Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of an intrinsic inhibitor of ACE in blood of approximately 25% of sera submitted for serum ACE assay in the diagnosis and evaluation of patients with sarcoidosis, and the common use of ACE inhibitors (captopril and enalapril) in the treatment of hypertension and congestive heart failure, stimulated these studies to compare the effects of the intrinsic and medicinal inhibitors upon serum ACE activity. Since the intrinsic ACE inhibitor in man is affected by serum dilution (inhibition is reversed) and by dialysis (inhibition becomes irreversible), these manipulations were also studied with medicinal inhibitors to provide guidelines for suspecting their presence in submitted serum samples without an accompanying history. Enalapril was found to have delayed onset of action after oral administration (1-2 hours), and was even further delayed (4 hours) when the intrinsic inhibitor also happened to be present. Inhibition by enalapril was not attenuated with refrigerated storage, with dilution or with dialysis of the serum. Captopril had a more rapid time of onset of ACE inhibition, but its inhibitory activity was markedly reduced with refrigerated storage of the serum; patients showed either a short half-life for the effect (1-4 days) or a prolonged half-life (10-17 days). Inhibitory activity of captopril was reversed following dilution of serum or following dialysis. The reversal of inhibition by captopril following dialysis, therefore, differed from the effect of dialysis on the intrinsic ACE inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
Sarcoidosis 1989 Sep
PMID:Effect of captopril and enalapril medication on the serum ACE test for sarcoidosis. 255 60

In the polymorphous picture of roentgenological shifts in disseminated tuberculosis and sarcoidosis of the lungs the authors mark out x-ray symptom complexes of differential diagnosis value. The complexes are based on predominating affection of the bronchopulmonary structures, x-ray characteristics of granulomas, nature and extent of the affections of the lymph nodes of the lung roots and mediastinum and the type of hypertension development in pulmonary circulation.
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PMID:[Differential x-ray diagnosis of disseminated tuberculosis and sarcoidosis of the lungs]. 271 85

Cardiac manifestations of sarcoidosis reflect the presence of granulomata in the myocardium or pulmonary arterial hypertension due to the advanced pulmonary form of the disease. Electrocardiographic changes may point to the form of the underlying pathology. The electrocardiograms of 150 newly diagnosed, untreated sarcoid patients, of whom no one had cardiac symptoms were analysed. Pathologic ECG changes indicative of myocardial sarcoidosis and/or pulmonary arterial hypertension were found in 20 (13.3%) patients. In cases with pathologic changes the ECG following the corticosteroid therapy was examined to test the stability or transitoriness of these changes. Two thirds of them disappeared following the corticosteroid therapy. Patients with the pathologic ECG, compared to the group as a whole, had a significantly more frequent pulmonary form of sarcoidosis and more severe restrictive and obstructive ventilatory changes.
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PMID:[Changes in the electrocardiogram in patients with sarcoidosis]. 274 17

Measurement of plasma angiotensin-converting enzyme (ACE) is of value in sarcoidosis and, when specific inhibitors are prescribed therapeutically, in hypertension and heart failure. In this study a rapid kinetic assay for estimation of plasma ACE is described and assessed. In particular the effects of zinc ion have been studied. In contrast to previous reports, a marked potentiation of ACE activity by micromolar concentrations of zinc was noted. The relationship between plasma zinc concentration and ACE activity in vivo was also investigated and related to albumin concentration. The findings may have implications for interpretation of plasma ACE activity in patients with low plasma zinc levels.
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PMID:Studies with an automated kinetic assay for plasma angiotensin-converting enzyme activity and its potentiation by zinc ion. 282 96

The study population comprises 28 patients with sarcoidosis who all had repolarization disturbances in their exercise ECGs. None of the patients had hypertension or known cardiovascular disease, and all but two were non-smokers. The mean age was 45 years. Exercise test with beta-adrenergic blockade was performed within one month of the first examination. Persisting abnormal ST-T changes in exercise ECGs after beta-blockade were seen in 12 (43%) patients. No significant relationship was found between persisting ST-T changes and age, sex, chest X-ray stage, lung function or working capacity. In an earlier study, we found ST-T abnormalities in exercise ECG in 56 of 127 individuals (44%) in a consecutive 5-year study of patients with newly detected sarcoidosis. From this and the present report we postulate that, in our region, as much as 20% of the patients with newly detected sarcoidosis might have organic myocardial disease, possibly of sarcoid origin, as shown by repolarization disturbances in exercise ECG. If ECG abnormalities in the ST-T region are present in patients with sarcoidosis, exercise ECG with beta-blockade is a simple way of establishing suspicion of organic myocardial lesions. If exercise ECG abnormalities in the ST-T region persist after beta-blockade, careful clinical follow-up is recommended, and, in some patients early steroid therapy should be considered.
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PMID:Exercise test in patients with sarcoidosis. The importance of repolarization disturbances. 334 4

Using the formulae of Fazio and coworkers, the regional extravascular lung water per blood volume and flow was calculated in normal volunteers, in patients with left heart failure, sarcoidosis, allergic alveolitis and pneumonia. The double-isotope technique was used. 113mIn-chloride was intravascular tracer and 123I-antipyrine extravascular tracer. They were injected intravenously as rapid bolus. The activity in the lungs was detected with gamma camera and the time-activity curves were generated with PDP-Gamma-11 computer system. Mean transit times were calculated using two different mathematical handlings of the dilution curves, with gamma fitting parameters and by the area-per-height method. The latter method gave mean transit times about double those calculated with gamma fitting parameters, because the peripheral injection decreased the peak height. Therefore, the area per height method to calculate mean transit times by peripheral injection was found to be inaccurate. The control group consisted of 16 healthy adults. In two subjects repeated studies were made in one week. Their individual, regional extravascular lung water values varied somewhat, but were on second examination found to be between the range of the values found from the first examination. The regional extravascular lung water values in patient groups were correlated with corresponding clinical, laboratory and roentgenographic findings. The values for extravascular water discussed on the next page are calculated only by means of transit times with gamma fitting parameters, although the extravascular water values determined by the area-per-height method also significantly increased in patients compared to the control group. The cardiac group consisted of 52 patients, of whom 23 had clinically compensated and 29 decompensated left heart failure. Regional extravascular lung water significantly increased in patients with decompensated heart failure when compared to patients with compensated heart failure. The cardiac group was also divided into three subgroups after radiological grading of pulmonary venous hypertension. Between GR I (n = 17) without signs of venous hypertension and GR II (n = 18) with signs of venous congestion no significant differences in regional extravascular lung water were found. However, in GR I and GR II the values for regional extravascular water increased when compared to the control group, which is probably due to increased perfusion of vessels or increased blood volume in these cardiac patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Measurement of regional extravascular lung water using the double indicator-dilution isotope technique. 391 68

Clinical findings and structural alterations in the kidneys of 6 patients with sarcoidosis and an associated glomerulonephritis are described. Five of the 6 patients manifested the nephrotic syndrome during some phase of their illness. Additional clinical evidence of renal disease included persistent microscopic hematuria (5 patients), hypertension (4 patients) and progressive renal failure (3 patients). Glomerular pathology varied and included proliferative glomerulonephritis (3 patients), membranous glomerulonephritis (1 patient), and chronic glomerulonephritis (2 patients). In 2 patients sequential examination of the kidney was possible, with renal biopsies preceding autopsy examination by 3 and 6 years, respectively. Glomerular pathology had progressed in severity in each case. Immunofluorescent studies in 2 patients revealed patterns of glomerular antibody localization consistent with immune complex disease. Electron microscopic studies of 1 revealed membranous changes characterized by electron-dense subepithelial and intramembranous deposits. Totally unexpected were virus-like intraendothelial structures in the glomeruli identical to those previously reported in systemic lupus erythematosus. Since current evidence suggests that the pathogenesis of both membranous and proliferative types of glomerulonephritis is immunologic, it should not be surprising that sarcoidosis, a disease which quite possibly results from an immune response to a disseminated antigen(s), should occasionally include glomerulonephritis as a part of its histologic expression.
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PMID:Glomerulonephritis associated with sarcoidosis. 455 25

Angiotensin-converting enzyme activity is present in human sarcoid as well as murine schistosome granulomas. Inhibition of angiotensin-converting enzyme by captopril results in decreased granuloma size in animals. Since captopril is used clinically to treat hypertension, its effect on human lymphocyte thymidine incorporation was determined. It was found that 5 X 10(-5) M and 10(-4) M captopril enhances lymphocyte thymidine uptake induced by 25 micrograms/ml phytohaemagglutinin-P. This suggests that captopril can alter immunological reactivity in man and that angiotensin-converting enzyme may have an immunological function.
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PMID:Captopril enhances in vitro human lymphocyte thymidine incorporation. 639 83

Pulmonary hypertension is an uncommon complication of sarcoidosis and is usually related to the development of end-stage, interstitial fibrosis or honeycomb lung. We describe a patient with sarcoidosis who developed pulmonary hypertension in the absence of significant parenchymal fibrosis. The pulmonary hypertension in this case was caused by granulomatous destruction of arteries and veins, as documented by an open-lung biopsy and autopsy. Clinical features, including pulmonary function tests, are presented which suggested that end-stage interstitial lung disease was not causing the hypertension. Recognition of this complication of sarcoidosis is important if effective therapy is to be found.
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PMID:Vascular sarcoidosis: a rare cause of pulmonary hypertension. 682 15

A 27-year-old patient, originally from Martinique, presented with a progressive hepatic granulomatosis with hepatomegaly, splenomegaly, and non-icteric cholestasis, associated with bronchial granulomatosis lesions. The sarcoidosis regressed rapidly after high doses (60 mg/day) of prednisone. Portal hypertension developed later and provoked a severe hematemesis from rupture of esophageal varices. Signs of pulmonary arterial hypertension were then observed, and the diagnosis confirmed by pressure tests after catheterization, and angiography. A portocaval shunt caused the esophageal varices to subside, but the pulmonary arterial hypertension, resistant to corticotherapy, was rapidly fatal. In the case reported, the pulmonary arterial hypertension, independent of any parenchymatous lesion, was attributed to fibrosis of the arterial walls. The association of portal and pulmonary arterial hypertension with sarcoidosis is a very rare occurrence, and the pathogenesis of this association remains a debatable subject.
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PMID:[Sarcoidosis and portal and pulmonary arterial hypertension: a case report (author's transl)]. 722 52


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