Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Detection of alcohol abuse is of utmost importance in the diagnosis and management of alcoholic cardiomyopathy. The ability of laboratory tests and clinical signs to detect alcohol abuse was compared in 31 patients with severe heart failure due to underlying dilated cardiomyopathy. Alcoholic cardiomyopathy was diagnosed in 13 patients and a variety of nonalcoholic cardiomyopathies were diagnosed in the remaining 18 patients. At the time of hospital admission, all patients received a complete cardiovascular examination as well as routine hematologic and biochemical tests. Details concerning past and recent alcohol intake were obtained by an individual who was unaware of the diagnostic status of the patients. The two groups of patients did not differ with respect to clinical presentation, self-report of recent drinking patterns, or clinical signs and medical history items that have been found to be associated with chronic alcohol abuse. However, the group with alcoholic cardiomyopathy had significantly higher values for mean corpuscular volume and gamma-glutamyltranspeptidase. Our results suggest that a combination of routine laboratory tests may be effective in the detection of alcohol abuse in patients with dilated cardiomyopathy.
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PMID:Alcohol abuse in patients with dilated cardiomyopathy. Laboratory vs clinical detection. 197 Apr 74

48 asymptomatic alcoholics (mean age 31.2 years) with an average daily alcohol consumption of 287 g were studied about 45 h (mean) after the last ingestion of alcohol. M-mode echocardiography and 24-h long-term ECG recordings were performed. 24 of these patients were restudied after a mean of 12 days of abstinence using long-term ECG recording. All patients were in sinus rhythm. 44 of 48 patients demonstrated supraventricular premature beats. In three patients, there were ventricular pairs (1/24 h). Two further patients had ventricular triplets (1/24 h). Echocardiography demonstrated a significant enlargement of left atrial dimensions (LA: 39 +/- 3.8 mm), of the diameter of the left ventricular posterior wall (10 +/- 4.1 mm), and of the interventricular septum (12 +/- 1.7 mm) compared to control data in 24 'normals'. In addition, there was a significant increase in the derived left ventricular mass index (292 +/- 48.2 g). Left ventricular enddiastolic diameter was not significantly different. Laboratory tests showed pathologically elevated values of SGOT, SGPT, and gamma-GT whereas serum potassium was normal. During restudy of the long-term ECG after 12 days, complex ventricular arrhythmias were no longer detectable. In six patients, echocardiography was repeated after a mean of 110 days of abstinence. Three of these patients had had marginal left ventricular fractional shortening during the first study which was normalized at the repeat study. Our results show some degree of left ventricular dysfunction in some chronic alcoholics without clinical overt heart failure.
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PMID:[The effect of alcohol on the heart in chronic alcoholics]. 323 42

To characterize the incidence and severity of liver function abnormalities in patients with congestive heart failure, we analyzed systemic hemodynamics and biochemical profiles in 133 patients with stable chronic congestive heart failure, secondary to a dilated cardiomyopathy. The patients were divided into three groups, based on the severity of the reduction in cardiac index (CI). The mean values of all liver function tests in groups 1 (n = 43; CI greater than or equal to 2.0 L/min/m2) and 2 (n = 48; CI greater than 1.5 and less than 2.0 L/min/m2) were essentially normal, except for minimally elevated alkaline phosphatase levels and slightly decreased albumin levels in both groups, and slight increases in levels of gamma-glutamyl transpeptidase and total bilirubin in group 2. In contrast, group 3 patients (n = 42; CI less than or equal to 1.5 L/min/m2) had the most severe heart failure, as assessed by the lowest CI and highest cardiac filling pressures, and significantly higher levels of aspartate aminotransferase (65 +/- 82 U/L), alanine aminotransferase (77 +/- 102 U/L), lactate dehydrogenase (282 +/- 91 U/L), and total bilirubin (29 +/- 14 mumol/L [1.7 +/- 0.8 mg/dL]). The percentage of patients in group 3 with these abnormalities ranged between 27% and 80%. Although linear regression analysis showed that the elevations in right atrial and pulmonary wedge pressures, and the decreases in CI, were significantly correlated with liver function abnormalities, the correlation coefficients were small. Thus, liver function abnormalities remain common in patients with congestive heart failure but are generally small in magnitude and not associated with clinically apparent hepatic disease. It is likely that reduced forward flow and passive backward congestion are both contributing factors in the pathogenesis of these biochemical abnormalities, although nonhemodynamic factors may also be important.
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PMID:Liver function abnormalities in chronic heart failure. Influence of systemic hemodynamics. 360 80

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

An evaluation is made of liver malfunctions in patients receiving TPN over a period of > or = 15 days between 1989 and 1991. Use was made of the monitoring records on patients undergoing TPN and, subsequently, of clinical records, with analysis of diagnoses and type of intervention, the biochemical parameters (SGOT, SGPT, GGT, FA, LDH, and total and direct bilirubin), and the type and degree of malnutrition, nutritional backup, associated medication, etc. A group of patients was excluded from the study on the basis of the following criteria: liver-biliary disease, cardiac insufficiency, liver metastasis, sepsis, kidney insufficiency and hepatotoxic drugs. Of 237 patients, 75 (31.64%) had liver alterations: following application of the exclusion criteria, 24 patients (10.12%) were taken with liver alterations attributable to the TPN. Macro- and micronutrients were included in the TPN. We found no relation between the kcal/kg of weight, nor with the quantity of glucose and fats nor of nitrogen, calculated according to individual requirements: they remained within the limits established. No serious case of cholestatic jaundice was encountered. Moderate to severe malnutrition was found in 50% of patients, so that this must be treated as a risk factor. GGT is the first enzyme to alter; this occurred in the largest proportion of patients (91.66%), followed by SGPT. FA and GOT are altered in the same percentage of patients. Biochemical parameter monitoring is essential in patients undergoing TPN, not only for appraisal of the nutritional state but also to prevent or correct potential serious metabolic complications.
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PMID:[Liver dysfunction associated with total parenteral nutrition]. 844 68

A number of simple clinical and laboratory variables were analysed in a group of patients with chronic heart failure to evaluate their prognostic significance. Five hundred and fifty-two patients were followed for a maximum of 13 years with a total exposure time to death or censored survival of 1148 years. Of the clinical variables, diuretic dose and NYHA class were related to mortality (P < 0.01), and ischaemic heart disease was associated with a worse prognosis than other aetiologies (P < 0.05). Of the laboratory variables, abnormalities of liver function tests including bilirubin (P < 0.01), aspartate transaminase (P < 0.005), gamma glutamyl transpeptidase (P < 0.005) and alkaline phosphatase (P < 0.01) were all related to mortality as was plasma urate (P < 0.01). Multivariate survival analysis of all variables showed aspartate transaminase (chi 2 17.36, P < 0.001) accounted for the greatest variance followed by serum bilirubin (chi 2 14.35, P < 0.005). Thus, abnormalities in liver function tests have prognostic importance in chronic heart failure.
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PMID:The importance of abnormalities of liver function tests in predicting mortality in chronic heart failure. 888 55

Abnormal liver function in thyroid disorders may be secondary to thyrotoxicosis or to autoimmune injury to the liver. We report the case of a 36-year-old female who developed jaundice and pruritus with mild cholestasis and moderately elevated transaminase levels. The diagnosis of Graves' disease was made shortly thereafter. Laboratory findings were: alanine and aspartate aminotransferase 219 (IU/I (N: 9-50) and 102 IU/I (N: 10-15) respectively, alkaline phosphatase 336 IU/I (N: 40-135), bilirubin 24 micromol/I (N: 2-23), and gamma-glutamyl transpeptidase 232 IU/I (N: 9-43). Abdominal ultrasonography showed normal bile ducts; echocardiography ruled out heart failure; viral and autoimmune markers for hepatitis and cirrhosis were negative. Percutaneous liver biopsy showed moderate intrahepatic steatosis, anisokaryosis, lymphocyte infiltration in the portal areas, and Kupffer cell hyperplasia. Outcome was favorable after seven months of iodine therapy, confirming the diagnosis of thyrotoxicosis hepatitis.
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PMID:[Thyrotoxicosis hepatitis: a case report]. 1145 76

Seven related Quarter Horse foals that died by 7 weeks of age were examined for glycogen branching enzyme (GBE) deficiency. Clinical signs varied from stillbirth, transient flexural limb deformities, seizures, and respiratory or cardiac failure to persistent recumbency. Leukopenia (5 of 5 foals) as well as high serum creatine kinase (CK; 5 of 5), aspartate transaminase (AST; 4 of 4), and gamma glutamyl transferase (GGT; 5 of 5) activities were present in most foals, and intermittent hypoglycemia was present in 2 foals. Gross postmortem lesions were minor, except for pulmonary edema in 2 foals. Muscle, heart, or liver samples from the foals contained abnormal periodic acid Schiff's (PAS)-positive globular or crystalline intracellular inclusions in amounts proportional to the foal's age at death. Accumulation of an unbranched polysaccharide in tissues was suggested by a shift in the iodine absorption spectra of polysaccharide isolated from the liver and muscle of affected foals. Skeletal muscle total polysaccharide concentrations were reduced by 30%, but liver and cardiac muscle glycogen concentrations were normal. Several glycolytic enzyme activities were normal, whereas GBE activity was virtually absent in cardiac and skeletal muscle, as well as in liver and peripheral blood cells of affected foals. GBE activities in peripheral blood cells of dams of affected foals and several of their half-siblings or full siblings were approximately 50% of controls. GBE protein in liver determined by Western blot was markedly reduced to absent in affected foals, and in a half-sibling of an affected foal, it was approximately one-half the amount of normal controls. Pedigree analysis also supported an autosomal recessive mode of inheritance. The affected foals have at least 2,600 half-siblings. Consequently, GBE deficiency may be a common cause of neonatal mortality in Quarter Horses that is obscured by the variety of clinical signs that resemble other equine neonatal diseases.
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PMID:Glycogen branching enzyme deficiency in quarter horse foals. 1181 63

An autopsy case with a widespread mucosal carcinoma of the biliary tree was reported. A biochemical profile of the bile duct damage was noticed in a woman in her seventies during a gastric examination. Imaging procedures depicted irregular dilatations of intrahepatic bile ducts with a bead-like appearance. Elevated levels of serum alkaline phosphatase and gamma-glutamyltransferase with a negative antimitochondrial antibody persisted. The patient was diagnosed as primary sclerosing cholangitis, she was followed up for 4 years under preservative therapies, and died of anasarca and heart failure. Post-mortem examination showed a diffuse mucosal carcinoma of both intrahepatic and extrahepatic biliary passages including the gallbladder with a minimal invasion and scattered foci of adenoma-like area in part. There was no evidence of gallstones or pre-existing sclerosing cholangitis. The striking features of the tumor were extensive papillary growth, mucus secretion and irregular dilatation of bile ducts. The tumor may bear biological and morphological homology with intraductal papillary mucinous tumor of the pancreas.
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PMID:Diffuse mucosal carcinoma of intrahepatic and extrahepatic bile ducts including gallbladder. 1258 48

Besides other organic nitrates, nitroglycerin (glyceryl trinitrate; GTN) has been used to treat acute heart failure particularly due to ischemic heart disease. However, one of serious clinical problems of the GTN therapy, particularly a long-standing medication, is hemodynamic tolerance to GTN, manifested by the decreased therapeutic efficacy of the drug. The most recent studies have suggested that mitochondrial lipoate/dihydrolipoate system-dependent aldehyde dehydrogenase-2 plays a key role in nitric oxide release from GTN. The aldehyde dehydrogenase-2 performs three enzymatic activities of dehydrogenase, esterase and reductase. The reductase activity is responsible for bioactivation of organic nitrates, such as GTN yielding nitrite and dinitrate (1,2-GDN/1,3-GDN, approximately 8:1). In view of a large contribution of dihydrolipoic acid to stabilization and regeneration of thiol groups, necessary for the reductase activity of aldehyde dehydrogenase-2, we conducted studies aimed to determine whether lipoic acid administration to rats is able to prevent GTN tolerance. The studies were conducted on 4 groups of animals: control saline-treated, model GTN-tolerant, GTN + lipoic acid-treated, lipoic acid alone-administered groups. On the 9th day of experiment animals were given i.v. therapeutic dose of GTN. We measured in all animals systolic and diastolic blood pressure before injection of therapeutic dose of GTN into the cadual vein and during 20 min thereafter. Levels of nitric oxide and reactive oxygen species and activities of glutathione peroxidase and superoxide dismutase were assayed in the aorta, plasma and heart of all animals. In addition, levels of malondialdehyde, and non-protein thiols, and activities of glutathione S-transferase and gamma-glutamyl transpeptidase were evaluated in the heart and plasma. The obtained results indicate that treatment of rats with a combination of lipoic acid and GTN can efficiently counteract GTN tolerance.
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PMID:The role of lipoic acid in prevention of nitroglycerin tolerance. 1861 39


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