Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The predictive value of 15 pre- and peroperative parameters upon survival after portacaval shunt was analyzed in a retrospective investigation of 134 elective operations. A multiple linear regression model was used. Survival was measured at three different points of time: one month, one year and five years after the operation. Survival at one month was influenced by the parameters bilirubin/s and ascites only. Survival at one year was influenced by albumin/s, sex, bilirubin/s, BSP, heart disease history and ascites Survival at five years was influenced by albumin/s, alkaline phosphatase/s, history of alcohol abuse, and globulin/s. These findings indicate that prediction of survival after portacaval shunt is an intricate process and that considerable improvement of the child criteria is possible.
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PMID:Factors predicing survival after portacaval shunt: a multiple linear regression analysis. 62 18

A 68-year-old man with a history of organic heart disease and marked weight loss was found to have apathetic thyrotoxicosis and hypercalcemia. Oral propranolol, 20.0 mg four times a day, provoked a gradual fall in serum calcium and alkaline phosphatase. It is concluded that relatively small doses of oral propranolol may be effective in the management of hypercalcemia accompanying thyrotoxicosis and that beta-blocking agents may not only inhibit the enhanced bone resorption caused by thyroid hormones but also block the stimulated osteoblastic activity.
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PMID:Oral propranolol in hypercalcemia associated with apathetic thyrotoxicosis. 66 23

Clinical and experimental heart irradiation can cause a variety of sequelae. A single dose of greater than or equal to 15 Gy leads to a reversible exudative pericarditis, occurring in dogs, rabbits or rats at around 100 days. Its time-course is very similar in all species investigated, but there are considerable species and strain differences in severity and incidence. After longer, dose-dependent latency times chronic congestive myocardial failure develops. At histological examination myocardial degeneration and necrosis is observed, which in some species is accompanied by a variable degree of interstitial fibrosis. In rabbits and rats, myocardial degeneration becomes apparent at around 70 days after 20 Gy and is preceded by a marked reduction in capillary density as well as ultrastructural endothelial cell degeneration. Simultaneously to structural capillary damage, a focal loss of the endothelial marker enzyme alkaline phosphatase was observed in rats in areas with subsequent myocardial degeneration. Cell kinetic studies in rabbits and rats revealed a radiation-induced wave of increased endothelial cell proliferation at 30-100 days postirradiation. In the rat it is exclusively seen in conjunction with alteration of endothelial cell marker enzymes. The temporal and spatial pattern of proliferative response exludes endothelial cell death in mitosis as the sole pathogenetic mechanism causing capillary loss and myocardial degeneration. Parallel to development of morphological damage, haemodynamic studies in various rats strains revealed a drop in cardiac output and left ventricular ejection fraction to about 64% of normal values after 20 Gy. In vivo, this slightly reduced cardiac function was then maintained in a steady state for many weeks, probably due to a compensatory up-regulation of cardiac beta-adrenergic receptors. In denervated working heart preparations in vitro, however, these compensatory mechanisms are not effective and stroke volume as well as cardiac contractility show a rapid and steady deterioration. In many respects radiation-induced heart disease conforms to radiobiological concepts of late-responding tissues, showing a chronic progressive time-course and a very pronounced fractionation effect. However, pathogenesis cannot be understood in terms of target cell depletion alone, and experimental evidence indicates the importance of alterations of regulatory mechanisms.
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PMID:Radiation-induced heart disease: review of experimental data on dose response and pathogenesis. 135 1

Growth failure is a major complication of chronic hypoxemia, as seen in infants and children with cyanotic congenital heart disease. To determine whether chronic hypoxemia during infancy affects the gastrointestinal tract, we examined small intestinal growth and digestive enzyme activities in chronically hypoxemic newborn lambs and in age-matched controls. Chronic hypoxemia was produced by placing an inflatable occluder around the main pulmonary artery and performing a balloon atrial septostomy. Aortic oxygen saturation was reduced to 60-74% for 2 wk, after which the small intestine was removed for analysis. During chronic hypoxemia, somatic growth rate was decreased to 60% of control (hypoxemic, 135 +/- 20 versus control, 216 +/- 26 g/d, p less than 0.02). No differences in caloric intake were found (hypoxemic, 129 +/- 4 versus control, 128 +/- 4 kcal/kg/d). Chronic hypoxemia did not alter small intestinal growth, as measured by jejuno-ileal weight, jejuno-ileal length, mucosal weight, or mucosal protein or DNA contents. However, sp act of lactase, the principal disaccharidase of the infant lamb intestine, were significantly decreased (hypoxemic, 0.08 +/- 0.01 versus control, 0.146 +/- 0.03 units of enzyme activity/mg DNA, p less than 0.05), as were the total small intestinal contents of lactase (hypoxemic, 61.7 +/- 7.0 versus control, 120.6 +/- 21.7 units of enzyme activity, p less than 0.01). There also were decreases in specific and total activities of other digestive enzymes such as maltase, amino-oligopeptidase, and alkaline phosphatase in hypoxemic intestine that did not achieve statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in postnatal intestinal function during chronic hypoxemia. 156 Oct 8

Radiation-induced myocardial degeneration in the rat is preceded by changes in capillary structure and function, which may be a major factor in the pathogenesis of radiation-induced heart disease. In order to investigate the mechanism of capillary damage we studied endothelial cell proliferation in untreated control rats and in rats at different times following local heart irradiation with 20 Gy using [3H]thymidine autoradiography. Since the latency times of myocardial degeneration as well as capillary damage are about twice as long in Sprague-Dawley rats as in Wistar rats, endothelial cell proliferation was studied in both strains. The percentage of labelled nuclei (LI) after repeated labelling over a period of 12 h was 0.32 +/- 0.06 in control animals of both strains. Therefore the turnover time of endothelial cells was estimated to be between 115 and 400 days. Following irradiation the LI increased above control levels. In both strains this was concurrent with the time of onset of capillary depletion and alkaline phosphatase loss, which occurred at around 23 days post-irradiation in Wistar rats and 58-74 days in Sprague-Dawley rats. In both strains the increase in LI was confined to alkaline-phosphatase-negative areas. In phosphatase-positive areas endothelial cell proliferation was unchanged in spite of the reduction in capillary density. Since, in general, the latency to post-irradiation death of a cell is closely related to its normal turnover time, the decrease in capillary density is not due to mitotic death of proliferating cells as is commonly seen in other tissues.
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PMID:Endothelial cell proliferation in the rat heart following local heart irradiation. 197 Sep 90

Alkaline phosphatase activity of capillary endothelial cells in the heart of Wistar and Sprague-Dawley rats was studied sequentially after single doses of 10, 15, 20, or 25 Gy. Following irradiation capillary density and alkaline phosphatase activity were focally lost before myocardial degeneration or clinical symptoms of heart disease developed. Recovery from both changes took place after doses of 10 or 15 Gy. The decrease in capillary density and enzyme activity showed the same strain difference in latency times and in the extent of the lesions as previously described for pathological and clinical signs of heart disease.
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PMID:Endothelial alkaline phosphatase activity loss as an early stage in the development of radiation-induced heart disease in rats. 356 89

A group of 71 chlorophenate-exposed sawmill workers were identified as part of a group undergoing an extensive health and environmental evaluation in a pulp mill. This group was compared with a group (N = 351) with no physical proximity to the area in which chlorophenates were used. Exposure was higher for those directly handling the wood and lower for those working in the area but not handling the wood. Those with chlorophenate exposure were not significantly more likely to report a history of jaundice or liver, kidney or heart disease. Moreover, the serum creatinine, bilirubin, glutamic oxaloacetic transaminase (GOT), and alkaline phosphatase values did not differ from those of the reference group. The hemoglobin level was similar in the three groups. But the peripheral blood leukocyte count was marginally lower in the exposed groups and their hematocrit was reduced, significantly so for the heavily exposed group. Urinalysis showed an increased prevalence of microscopic hematuria, especially with lower cell counts. No unequivocal explanation is available for the reduced hematocrit or the low level of hematuria.
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PMID:Occupational exposure to chlorophenates. Renal, hepatic and other health effects. 372 96

Among 2175 patients seen over the last three years in a non-specialized department of internal medicine with no intensive care unit, 100 had supranormal serum lactic dehydrogenase activities. These patients' case-reports have been analyzed. Nearly half the patients (47/100) had a malignant disease (cancer or hemopathy). Among the remaining patients, 19 had a hepatic disorder (alcohol hepatitis in 10, viral hepatitis in 8, and isoniazide hepatitis in 1), 7 had a heart disease (heart failure with hepatomegaly in 5, myocardial infarction in 2), and 27 had various other conditions (including hemolysis in 6 and polymyositis en 3). The value of serum LDH assay is obvious in situations other than acute conditions such as myocardial infarction of pulmonary embolism; these are better known and have not been studied here as their prevalence was low among the patients enlisted in our study. In comparison to other enzymes (alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), transaminases (GOT, GPT) that were also routinely assayed in our patients, abnormal serum LDH activities are much less common and their significance is quite different. An increase in serum and their significance is quite different. An increase in serum LDH activity indicates a serious condition, often with a fatal outcome. The "various other conditions" group includes patients with hemolysis, hepatitis and myositis; the other patients in this group either had severe infectious diseases or died suddenly in the first few days of their hospitalization before diagnosis had been established. Each etiologic group has been analyzed to asses the characteristics of patients with increased LDH activity according to each etiology. Analysis of coincident abnormalities of the other enzymes listed above shows marked differences between etiologic groups; diagnostic accuracy can thus be enhanced in certain conditions. Most patients with malignancies had poorly differentiated tumors, with metastases: 28 had an epithelial tumor, with hepatic and/or bone metastases in 23 cases, 5 had cancer of the liver, 10 had a malignant hemopathy (2 lymphomas, 5 myeloproliferative syndromes, 3 acute leukemias), and 4 had a sarcoma. Cancer of the lung is the most common malignancy (10 cases) and may be responsible for increased serum LDH activity even in patients without metastases. Serum LDH assay is of value for monitoring the course in patients with initially increased activities as it falls under effective therapy and rises during exacerbations.
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PMID:[Value and diagnostic significance of serum lactic dehydrogenase in internal medicine (author's transl)]. 628 24

Portacaval shunt was performed in ten patients with homozygous and two with heterozygous familial hypercholesterolemia (FH). Total serum cholesterol was lowered by 20% to 55.4% during follow-up periods of 14 months to almost 9 years, with commensurate decreases in LDL cholesterol. The effect on HDL cholesterol and triglyceride levels was variable. Tendinocutaneous xanthomas diminished or disappeared. Growth and development in children proceeded or accelerated. There was no detectable emotional or intellectual deterioration. Hepatic failure did not occur, although blood ammonia concentrations and serum alkaline phosphatase levels increased relative to preoperative values. Cardiac symptoms were often improved, but evidence of reversal of cardiovascular lesions was inconclusive. Three patients with pre-existing heart disease died of cardiac complications after 4 months, 18 1/2 months, and 30 months. Portacaval shunt has been effective therapy for patients with FH who were refractory or intolerant to medical treatment; it should be performed before the development of irreversible cardiovascular damage.
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PMID:Portacaval shunt in patients with familial hypercholesterolemia. 661 51

We describe here an easy method of determining prolidase (EC 3.4.13.9) in plasma after preincubation with Mn2+ for 24 h at 37 degrees C to maximize prolidase activity. The mean activity in 338 patients who were either in hospital or outpatients was 900 U/L +/- 520 (2 SD), unrelated to sex or age. In 25 of these 338 samples tested, prolidase activity was between 1500 and 2000 U/L. It exceeded 2000 U/L in eight, all of whom were patients with chronic liver disease. Plasma prolidase activity was normal in cytolytic syndromes such as liver or heart disease. Of the 27 patients with cirrhosis, only five exhibited prolidase activity greater than 2000 U/L. Plasma prolidase activity was uncorrelated with six biochemical indexes to liver function (the aminotransferases, alkaline phosphatase, glutamyltransferase, total bilirubin, and serum albumin) or with the degree of cirrhotic fibrosis. We believe that plasma prolidase activity may be high only in the early stage of fibrosis. This hypothesis would be consistent with the data on rat-liver collagenolytic activities during CCl4 administration. Monitoring of plasma prolidase activity might be useful in evaluating fibrotic processes in chronic liver disease in the human.
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PMID:Plasma prolidase activity: a possible index of collagen catabolism in chronic liver disease. 669 25


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