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)

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

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

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 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

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin--lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although these agents have been proven safe in clinical trials, like any drug, they carry the risk for adverse effects. The bile-acid sequestrants may cause constipation, reflux oesophagitis, and dyspepsia, and may bind coadministered medications such as digitalis glycosides, beta blockers, warfarin, and exogenous thyroid hormone. Nicotinic acid use is commonly associated with flushing and pruritus and may also cause non-specific gastrointestinal complaints, hepatotoxicity (hepatic necrosis, hepatitis, or elevated liver enzymes), gout, myolysis, decreased glucose tolerance and increased fasting glucose levels, and ophthalmological complications including decreased visual acuity, toxic amblyopia, and cystic maculopathy. The HMG-CoA reductase inhibitors may produce liver enzyme elevations, creatine kinase elevations and rhabdomyolysis. The combination of a reductase inhibitor and a fibrate increases the risk for rhabdomyolysis. Possible adverse effects of the fibric-acid derivatives include abdominal discomfort, nausea, flatulence, increased lithogenicity of bile, liver enzyme elevations and creatine kinase elevations. Probucol may increase the QTc interval and may cause non-specific gastrointestinal complaints.
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PMID:Currently available hypolipidaemic drugs and future therapeutic developments. 859 27

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 test for hepatitis, retrovirus, tumor markers, fertility markers, thyroid functions, and therapeutic drugs. The time to first result is 15 approximately 25 min for most routine assay 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 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:[Fluorescence polarization immunoassay and microparticle enzyme immunoassay]. 895 38

Signalment, clinical signs, and physical examination and clinicopathologic findings in dogs diagnosed with Hepatozoon canis parasitemia (n = 100) were compared with those in Hepatozoon-negative dogs (n = 180). A subset (n = 15) of Hepatozoon-positive dogs with unusually high (> 800 H canis gametocytes/microL of whole blood) parasitemia was compared with dogs that had low parasitemia (n = 85) and with Hepatozoon-negative dogs (n = 180). Hepatozoon-positive dogs significantly differed from Hepatozoon-negative dogs in body temperature, total red blood cell count, hemoglobin concentration, hematocrit, and platelet count. Dogs with high H canis parasitemia significantly differed from those with low parasitemia in hemoglobin concentration, hematocrit, and total neutrophil count. Clinical findings from dogs with high H canis parasitemia included emaciation, lethargy, hyperglobulinemia, hypoalbuminemia, and increased serum alkaline phosphatase and creatine kinase activities. Findings at necropsy included hepatitis, pneumonia, and glomerulonephritis associated with H canis schizonts and extensive parasitism of bone marrow, spleen, and lymph nodes. Low hemoglobin concentration, low platelet count, and concurrent parvovirus infection together represented the best predictor variables for Hepatozoon positivity in dogs presenting to the hospital.
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PMID:Retrospective case-control study of hepatozoonosis in dogs in Israel. 947 Jan 63

Acute quadriplegic myopathy is a rare condition associated with the use of nondepolarizing muscle-blocking agents and corticosteroids in the course of severe systemic illness. A 17-month-old boy underwent liver transplantation for fulminant hepatitis. He was intubated for 24 days and treated with vecuronium bromide and high-dose methylprednisolone. The child was weaned from the ventilator and presented extreme weakness in the upper limbs and total paralysis of the lower limbs. Serum creatine kinase level was normal and electromyography showed myopathic abnormalities. Muscle biopsy showed severe type-1 fiber atrophy and selective loss of myosin thick filaments was seen on electron microscopy. Scattered regenerating fetal myosin-positive fibers were present, mu calpain was absent, while m calpain was diffusely expressed. Physical therapy was immediately started and the child recovered even though corticosteroids were not discontinued. The pathogenesis of acute quadriplegic myopathy is still unknown. We suggest that it could be due to abnormal protein turnover in the muscle. Several independent factors, such as corticosteroid treatment, immobilization, or cytokines, could take part in a cascade of events that leads to an excessive yet selective degradation of proteins involving myosin thick filaments and possibly components of sarcolemma, causing muscle inexcitability.
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PMID:Acute quadriplegic myopathy in a 17-month-old boy. 1064 15

We describe a 61-year-old man presenting with necrotizing myopathy associated with chronic active hepatitis due to hepatitis C virus (HCV) infection. Thirteen patients with HCV-associated myopathy have been reported previously. In most of these cases, varying degrees of inflammatory changes were observed in the muscle tissue. In 2 patients, myopathy developed after initiation of interferon therapy for chronic HCV hepatitis. Our case was unusual due to long-standing elevation of creatine kinase values which improved following interferon therapy and the non-inflammatory features of the muscle tissue where the HCV RNA minus strand, a marker for replicative intermediates of the virus, was undetectable. The association of myopathy with HCV infection might represent a unique clinical entity, although the underlying pathological mechanisms remain unknown.
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PMID:Necrotizing myopathy in a patient with chronic hepatitis C virus infection: a case report and a review of the literature. 1073 41

A 68-year old Japanese male with alcohol related rhabdomyolysis, hepatitis, and hematological disorders is presented. Biochemical data showed markedly elevated levels of serum hepatobiliary enzymes, lactate dehydrogenase and myoglobin, and decreased levels of serum sodium and phosphate. The serum creatine kinase level was approximately 40 times higher than the normal upper limit with 97% of MM fraction. Clinical manifestations of rhabdomyolysis, such as myalgia, muscle weakness and acute renal failure, were not recognized. Hematological examinations revealed mild neutropenia, lymphopenia, monocytopenia and thrombocytopenia but no anemia or macrocytosis. Initial treatment of an intravenous infusion of saline (30 mL/Kg body weight) and subsequent low sodium diet was successfully completed without severe complications. All the abnormal laboratory data were normalized within three weeks of his hospitalization. We suggest that hyponatremia and hypophosphatemia may be involved in the development of rhabdomyolysis, hepatitis and hematological disorders.
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PMID:Rhabdomyolysis, hepatitis and multiple hematological disorders associated with alcohol abuse: a case report. 1293 2


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