Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum creatine phosphokinase (CPK) and serum glutamic oxaloacetic and pyruvic transaminase (SGOT, SGPT) levels were determined in 61 patients with leptospirosis and 16 with viral hepatitis during the acute phase of illness. The CPK value was elevated in 29 leptospirosis patients and normal in all 16 hepatitis patients. Conversely, mean SGOT and SGPT levels were lower in leptospirosis patients. The CPK determination is a simple test that may provide diagnostic information in a jaundiced patient, particularly when characteristic manifestations of leptospirosis are absent. The pattern of greatly elevated CPK levels with only modest elevations in transaminase values in an acutely jaundiced patient should strongly suggest a diagnosis of leptospirosis.
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PMID:Serum creatine phosphokinase in leptospirosis. 117 21

The increase of serum ASTm activity might reflect the severity of damage at the subcellular level of the myocardium. 50 patients with acute myocardial infarction (AMI) were observed. The mean peak ASTm activity was 34.34 +/- 34.60 IU/L and 48 patients (96%) greater than or equal to 9 IU/L (two times median value of normal subject). The peak time (36 h) came later and the duration (120 h) was longer than that of CK-MB. ASTm/ASTt ratio in groups of AMI, non-AMI heart failure and acute ictero-hepatitis was 0.25 +/- 0.10, 0.02 +/- 0.05 and 0.05 +/- 0.02 respectively. The former was significantly greater than other two groups (P less than 0.01). The activity of ASTm in AMI cases with heart function at I, II and III + IV (Killip classification) was 21.8, 40.2 and 76.2 IU/L respectively (F = 8.407 P less than 0.01) and it was 84.9 and 24.7 IU/L in the death and surviving groups (P less than 0.01). The result showed that the estimation of serum ASTm level was helpful to the establishment of diagnosis in the patients with AMI who were sent delayed to the hospital. It held special significance in evaluating the severity of myocardial damage, heart function and in predicting the prognosis of AMI.
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PMID:[Serum mitochondrial aspartate aminotransferase (ASTm) in acute myocardial infarction]. 191 59

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

Fenofibrate is a lipid-regulating drug which is structurally related to other fibric acid derivatives, such as clofibrate. At the recommended dosage of 200 to 400 mg daily, it produces substantial reductions in plasma triglyceride levels in hypertriglyceridaemic patients and in plasma total cholesterol levels in hypercholesterolaemic patients. High density lipoprotein (HDL)-cholesterol levels are generally increased in patients with low pretreatment values. Fenofibrate appears to be equally effective in diabetic patients with hyperlipoproteinaemia without adversely affecting glycaemic control. The influence of fenofibrate on the plasma lipid profile is sustained during long term (2 to 7 years) treatment. Comparative studies conducted to date have involved only small groups of patients--in overall terms fenofibrate was at least as effective as other fibrates, but larger comparative studies are needed before valid conclusions on its relative efficacy compared with nonfibrate lipid-lowering drugs can be drawn. The influence of fenofibrate on morbidity and mortality from cardiovascular disease has not been studied. Clinical adverse reactions to fenofibrate have mainly consisted of gastrointestinal disturbances, headache and muscle cramps. Transient elevations in transaminase and creatine phosphokinase levels commonly occur. Isolated cases of hepatitis with substantially elevated transaminase levels have been reported. Fenofibrate induces hepatomegaly, peroxisome proliferation and hepatic carcinomas in rodents, but this type of hepatotoxicity has not been observed in humans. The biliary lithogenic index is increased by fenofibrate, but this has not been shown to have increased the incidence of gallstones in treated patients. Thus, fenofibrate offers an effective and well tolerated alternative to clofibrate or other fibric acid derivatives, but its relative efficacy and tolerability compared with other types of lipid-lowering drugs, and its effect on cardiovascular morbidity and mortality, remain to be clarified.
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PMID:Fenofibrate. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in dyslipidaemia. 222 16

A 19-year-old man with a generalized seizure disorder was treated with phenytoin. A hypersensitivity reaction was marked by hepatitis, severe myalgia, proximal arm weakness, and high serum creatine kinase. Biopsy was diagnostic of myopathy. Patients demonstrating abnormalities of immune responsiveness may best be managed by use of an alternative anticonvulsant.
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PMID:Myopathy and hypersensitivity to phenytoin. 668 25

Low values of serum creatine phosphokinase (CPK) were found in a group of 27 patients suffering from acute viral hepatitis. The values were significantly lower than CPK values in a group of 25 patients with extra hepatic obstructive jaundice (23.3 +/- 32.1 versus 163 +/- 43 U/L, p less than 0.001). CPK values in the hepatitis group when recovered (6 months after hospitalization) were much higher than the mean CPK levels in the same group during the acute illness (178 +/- 28 versus 23.3 +/- 32.1 U/L, p less than 0.001) and were the same as a control group of 26 healthy volunteers (179 +/- 28 versus 179 +/- 20.9 U/L). Similar results were found when the groups were divided into separate male and female groups. Serum CPK values, thus, were found to be a useful diagnostic tool to distinguish between patients with intrahepatic jaundice due to acute viral hepatitis and patients with extra hepatic obstructive jaundice.
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PMID:Low serum creatine phosphokinase values in patients with acute viral hepatitis. 671 30

A 22-year-old man with Marfan's syndrome and a history of antinuclear antibody-positive hepatitis died 25 days after undergoing cardiac valve replacement surgery for mitral valve prolapse. Giant cell myocarditis was found at autopsy. The multinucleated giant cells were shown by immunoperoxidase techniques to contain lysozyme, but not myosin or creatine phosphokinase, suggesting that they were derived from macrophage, rather than myocyte, precursors.
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PMID:Giant cell myocarditis after mitral valve replacement: case report and studies of the nature of giant cells. 672 75

Serum creatine kinase isoenzymes were determined in 24 patients with hepatic failure. Hepatic failure was due to severe acute and chronic liver disease. The 24 patients presented different degrees of coma. Nineteen cases (seven hepatitis and 12 cirrhosis) in coma grades III and IV showed the presence in serum of BB, brain and MB, myocardial isoenzymes. Follow up in six of these cases demonstrated that worsening or improvement was accompanied by an increase or decrease of this brain isoenzyme concentration. The leakage from their respective tissues of the brain and myocardial creatine kinase isoenzymes is probably due to the toxic and surface activity properties of serum free fatty acids, bile salts, and bilirrubin, which increase, among other factors, in these pathological entities.
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PMID:Serum creatine kinase isoenzymes behavior in hepatic failure with encephalopathy. 728 32

We report the occurrence of rhabdomyolysis and hepatitis in a 17-year-old girl after the ingestion of up to 10.8 g of isoniazid. The initial isoniazid concentration in the blood was 1,230 mmol/L. There were no findings indicating the ingestion of other substances known to be associated with rhabdomyolysis. In addition to rhabdomyolysis (peak creatine phosphokinase 88,000 U/L), the patient had a significant elevation of her liver enzymes (peak aspartate aminotransferase 1,980 U/L). She recovered completely without evidence of liver or renal damage. Rhabdomyolysis and isoniazid-induced hepatitis are complications that should be considered when caring for patients with acute isoniazid ingestion.
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PMID:Isoniazid-associated rhabdomyolysis. 766 61

We describe a new clinical laboratory instrument, the Abbott AxSYM, which provides random- and continuous-access testing for immunoassays, 20 onboard reagents, primary tube sampling, and a throughput of 80 to 120 tests per hour. The AxSYM incorporates three separate analytical technologies for processing immunoassays: microparticle enzyme immunoassay, fluorescence polarization immunoassay, and a novel technology known as ion-capture immunoassay. The system incorporates both common and technology-specific subsystems controlled by a real-time software scheduling processor. Tests can be processed in one- or two-step sandwich or competitive formats, with variable pipetting steps, incubation periods, optical read formats, and wash sequences. Menu capabilities include tests for hepatitis, retrovirus, tumor markers, fertility markers, thyroid functions, and therapeutic drugs. The time to first result is approximately 15-25 min for most routine assays and < or = 15 min for stat assays (i.e., creatine kinase MB isoenzyme, human chorionic gonadotropin beta subunit, and therapeutic drugs). AxSYM assay performance for 23 assays was comparable with that of the Abbott IMx and TDx analyzers; specimen correlation data had correlation coefficients ranging from 0.97 to 0.99 and slopes ranging from 0.99 to 1.10. Within-run imprecision (CV) was 1.5% to 11.4%, with most assays (19 of 23) demonstrating CVs < or = 8.0%.
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PMID:Abbott AxSYM random and continuous access immunoassay system for improved workflow in the clinical laboratory. 769 38


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