Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The impact of dengue on liver function was studied by biochemical tests on 125 male and 145 female patients diagnosed with this disease during an outbreak that extended from November 1987 to December 1988. Abnormal levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase (G-GT) were observed in 93.3%, 82.2%, 7.2%, 16.3% and 83.0% of the patients, respectively. The elevation of transaminases was mild to moderate in most cases, but was 10-fold greater than the normal upper limit for AST and ALT in 11.1% and 7.4% of the patients, respectively. Initially, the level of AST was greater than that of ALT, increasing to maximum levels nine days after the onset of symptoms, then decreasing to normal levels within two weeks. Results of the biochemical tests did not differ significantly between the cases with and without hepatitis B or hepatitis C virus infection, but significantly higher elevations of AST, ALT, and G-GT were observed in patients with episodes of bleeding. Liver biopsies of two patients showed features of lobular hepatitis. Of the five fatal cases, three died of hepatic failure. It is concluded that dengue fever may cause hepatic injury and transaminase elevation similar to that in patients with conventional viral hepatitis. In epidemic or endemic areas, dengue fever infection should be considered in the differential diagnosis of hepatitis.
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PMID:Liver biochemical tests and dengue fever. 135 50

The recent cloning of the genome of hepatitis C virus (HCV) has allowed the detection of antibodies to HCV (anti-HCV) in human serum. The presence of serum antibodies to HCV often indicates active infection with HCV. We have assessed the serological and histological features in a group of alcoholic patients with chronic liver disease and have evaluated the possible etiologic role of HCV infection in the development of liver damage. Serum samples and liver biopsy specimens were obtained from 41 consecutive patients, all having a definite history of alcohol abuse and evidence of chronic hypertransaminasemia. Fifteen patients (37%) were positive for anti-HCV by ELISA, and 13 (86.6%) of them were also positive by RIBA. Eleven of these patients had histologic features of chronic active hepatitis (CAH), a lesion which is not known to be induced by excessive alcohol intake. No other possible causes of CAH were found, and CAH was not present in any of the anti-HCV negative patients. In patients with CAH, mean AST to ALT ratio was less than 1 (0.6), a finding which is characteristic of viral rather than alcoholic chronic liver disease. In conclusion, our study suggests that sporadic hepatitis C virus infection plays an etiologic role in the development of chronic active liver disease in a subgroup of alcoholic patients.
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PMID:Serological and histological aspects of hepatitis C virus infection in alcoholic patients. 166 17

During the last week of December 1989, an outbreak of respiratory system infection involved 32 hospital personnel and 2 patients was detected in Gazi University Medical Faculty Hospital. White blood cells count of the patients were either normal or there were a slight leucopenia. Throat cultures of the most patients were normal. Serum ASO, CRP, bilirubin, AST and ALT were usually within normal limits. According to symptoms, signs and laboratory data we considered a viral disease, especially influenza. All patients recovered without any sequelae. Of 34 in-patients, 8 paired sera, 2 acute phase sera, and 10 convalescent phase sera were tested for the presence of Hemagglutination Inhibition (HI) antibody to three influenza virus strains recommended by WHO in the 1989-1990 season: Influenza A/Taiwan/1/86 (H1 N1), Influenza A/Shanghai/11/87 (H3 N2), Influenza B/Victoria/2/87. All of the sera were negative for Influenza B/Victoria/2/87. There were no significant rises in HT antibody titer for Influenza A/Taiwan/1/86 (H1 N1). The sera for 4 of 8 patients examined both acute and convalescent phase sera had fourfold or greater rise in HI antibody for Influenza A/Shanghai/11/87 (H3 N2). Four patients examined only convalescent sera had 1/40 or greater rises in HI antibody for this influenza subtype. It was considered that this influenza outbreak was probably caused by Influenza A/Shanghai/11/87 (H3 N2).
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PMID:[An outbreak of influenza in hospital personnel]. 228 92

As part of a study of the pathology and pathogenesis of bovine ephemeral fever virus infection 44 cattle were infected by the intravenous injection of virulent virus. Thirty-eight animals responded clinically and detailed haematological and serological data were obtained from 10 of them. Inappetence was the only clinical sign observed before the onset of fever. The temperature response was characteristically biphasic, with the second peak occurring 12 to 24 hours after the first. The only consistent haematological response was an increase in the numbers of circulating neutrophils with a concurrent decline in the numbers of mononuclear leucocytes. There were no detectable changes in plasma or blood volume, packed cell volume, red cell count, haemoglobin concentration, serum calcium, magnesium, phosphorus and creatinine concentrations, or aspartate aminotransferase activity. Viraemia was demonstrated on either the first or second day of clinical disease and lasted for at most 48 hours. Low levels of neutralising antibody could be detected within one or two days after the cessation of viraemia. Six antibody-free animals did not respond clinically to injection with virulent virus, and did not develop detectable viraemia or a serum neutralising antibody response.
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PMID:Clinical response of cattle to experimental infection with bovine ephemeral fever virus. 230 90

The effect of PG on patients with fulminant and subfulminant viral hepatitis (FHF) was studied. 17 patients presented with FHF secondary to hepatitis A (n = 3), hepatitis B (n = 6), and non-A, non-B (NANB) hepatitis (n = 8). 14 of the 17 patients had stage III or IV hepatic encephalopathy (HE). At presentation the mean aspartate transaminase (AST) was 1,844 +/- 1,246 U/liter, bilirubin 232 +/- 135 mumol/liter, prothrombin time (PT) 34 +/- 18, partial thromboplastin time (PTT) 73 +/- 26 s, and coagulation Factors V and VII 8 +/- 4 and 9 +/- 5%, respectively. Intravenous PGE1 was initiated 24-48 h later after a rise in AST (2,195 +/- 1,810), bilirubin (341 +/- 148), PT (36 +/- 15), and PTT (75 +/- 18). 12 of 17 responded rapidly with a decrease in AST from 1,540 +/- 833 to 188 +/- 324 U/liter. Improvement in hepatic synthetic function was indicated by a decrease in PT from 27 +/- 7 to 12 +/- 1 s and PTT from 61 +/- 10 to 31 +/- 2 s, and an increase in Factor V from 9 +/- 4 to 69 +/- 18% and Factor VII from 11 +/- 5 to 71 +/- 20%. Five responders with NANB hepatitis relapsed upon discontinuation of therapy, with recurrence of HE and increases in AST and PT, and improvement was observed upon retreatment. After 4 wk of intravenous therapy oral PGE2 was substituted. Two patients with NANB hepatitis recovered completely and remained in remission 6 and 12 mo after cessation of therapy. Two additional patients continued in remission after 2 and 6 mo of PGE2. No relapses were seen in the patients with hepatitis A virus and hepatitis B virus infection. Liver biopsies in all 12 surviving patients returned to normal. In the five nonresponders an improvement in hepatic function was indicated by a fall in AST (3,767 +/- 2,611 to 2,142 +/- 2,040 U/liter), PT (52 +/- 25 to 33 +/- 18 s), and PTT (103 +/- 29 to 77 +/- 44 s), but all deteriorated and died of cerebral edema (n = 3) or underwent liver transplantation (n = 2). These results suggest efficacy of PGE for FHF, and further investigation is warranted.
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PMID:Biochemical and clinical response of fulminant viral hepatitis to administration of prostaglandin E. A preliminary report. 279 44

Ten yearling white-tailed deer (Odocoileus virginianus) were inoculated with bluetongue virus serotype 17. Two yearling white-tailed deer were inoculated with sonicated heparinized noninfected blood and served as controls. Clinical signs of bluetongue virus infection included increased rectal temperature, erythema, facial edema, coronitis, and stomatitis. By postinoculation day (PID) 8, excessive bleeding and hematoma formation at venipuncture sites, dehydration, and diarrhea developed. At necropsy, the most consistent findings were oral lesions and widespread hemorrhage, which ranged from petechia to massive hematoma formation. Bluetongue virus caused progressive prolongation of activated partial thromboplastin time and prothrombin time, and progressive reduction of Factors VIII and XII plasma activities beginning on PID 6. A progressive decrease in platelet numbers also developed on PID 6. Changes in platelet size were not detected. Mean thrombin time was shortened, but prolongation developed in 1 deer. Mean fibrinogen concentration and Factor V plasma activity initially increased and then decreased, but remained above preinoculation values. Factor V activity was low in a few deer. Results of screening tests for inhibitors of the intrinsic coagulation system were positive in 2 deer. High concentrations of fibrin(ogen) degradation products were first detected between PID 3 and 6. Hematologic changes included leukopenia, lymphopenia, neutrophilia, and low total plasma protein concentration. Differences in PCV, hemoglobin concentration, or RBC counts were not detected between infected and control deer. Serum total bilirubin concentration increased by PID 6, primarily because of increased unconjugated bilirubin concentration. Mild to severe increases in serum aspartate transaminase activity were accompanied by more marked increases in creatine kinase activity. Indirect Coombs test results were negative in all deer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimentally induced bluetongue virus infection in white-tailed deer: coagulation, clinical pathologic, and gross pathologic changes. 285 9

The term chronic active hepatitis covers aetiologically different conditions with similar histological features. Autoimmune chronic active hepatitis - the type that was described originally - is the only type which responds well to prednisolone therapy. Autoimmune chronic active hepatitis can be differentiated from other types by serological and other markers. Treatment with prednisolone should be given for at least two years, with adjustment of dosage according to the serum levels of aspartate transaminase; maintenance does should be 8-12 mg a day. Azathioprine (50-100 mg a day) may be given concurrently as a corticosteroid-sparing agent. Prednisolone therapy in patients with autoimmune chronic active hepatitis enhances the quality of life and survival is prolonged greatly; currently the survival rate after 10 years for prednisolone-treated cases is at least 70%. Prednisolone is not effective in hepatitis B-associated chronic active hepatitis and may be deleterious. In cryptogenic chronic active hepatitis, in which markers of autoimmunity or hepatitis B viral infection are lacking, a trial of prednisolone therapy may be given for three months, and continued only if the indices of disease activity indicate a response. Corticosteroid agents have not proved of benefit in other liver diseases, including alcoholic hepatitis and acute liver failure, and a beneficial effect in primary biliary cirrhosis is yet to be established.
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PMID:Treatment of chronic active hepatitis and other liver diseases with corticosteroid agents. 356 Dec 94

We measured levels of virus in sequential specimens from 137 patients with Lassa fever. The probability of fatal disease increased significantly with the level of viremia measured either on admission or during the course of illness. The odds ratio of death in patients with viremia greater than 10 TCID50/ml was 3.7 (90% confidence interval, 1.9-7.2). The same ratio in patients with viremia greater than 10 TCID50/ml and with levels of aspartate aminotransferase greater than or equal to 150 IU/liter was 21.5 (95% confidence interval, 5.2-99.0). Virus was found in throat cultures from 39% of viremic patients, compared with 14% of nonviremic patients (P less than .002); however, the level of virus was usually less than or equal to TCID50/ml. Fewer than 3% of patients were viruric during acute illness, and virus was isolated from three of three samples of cerebrospinal fluid. On admission, 53% of patients had IgG antibodies, and 67% had IgM antibodies. Recovery was not associated with the presence of either IgG or IgM. Virus was isolated from greater than 100 serum specimens that also contained high titers of IgG. Clinical Lassa fever was shown to be a disseminated systemic, primary viral infection, with an outcome highly associated with viremia but not with development of antibody.
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PMID:Clinical virology of Lassa fever in hospitalized patients. 380 73

Virus isolation and titration, electrocardiography, enzyme assays and light and electron microscopic studies were undertaken in male turkeys infected with influenza A/turkey/Ontario/7732/66 virus to determine its potential role in the genesis of heart disease. Virus was isolated from the heart initially before a demonstrable viremia and terminally in declining serum viral titer. Virus was isolated from the heart muscle as early as 1 day postinoculation. Highest viral titers were found in the heart at 6 days postinoculation and coincided with maximum elevations of serum glutamic-oxalacetic transaminase and lactic acid dehydrogenase, microscopic lesions in the heart and cardiac arrhythmias. Microscopic lesions in the heart were first detected at 4 days postinoculation and consisted of disseminated areas of necrosis, focal myocarditis, pericarditis and endocarditis. Alterations in myocardial ultrastructure which followed viral infection included fragmentation and dissolution of myofibrils, dilation of the sarcotubular system, increase in membrane vesicle formation in the region of the endoplasmic reticulum, discontinuity of the sarcolemma, proliferation of mitochondrial population, swelling of mitochondria with separation and disruption of the cristae, and the presence of intramitochondrial and perinuclear densities.
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PMID:Light and electron microscopic changes in the myocardium of influenza-infected turkeys. 463 35

Heroin abusers are frequently found to have abnormal liver function tests and hepatic histology. Hepatitis viruses A, B, and NANB, other drugs or drug contaminants and excessive alcohol consumption are factors thought to contribute. One hundred and sixteen heroin abusers attending a London treatment centre were studied. Sixty two (53%) had a raised aspartate transaminase. This was not explained by current infection with hepatitis A and B, cytomegalo or Epstein-Barr viruses, excessive alcohol consumption (greater than 80 g/day) or concomitant drug taking. Abnormal liver function tests were as frequent in those with markers of current or past HBV infection as those without and there was evidence that both HBV infection and the cause of the abnormal liver function tests were acquired in the first few years of intravenous drug abuse. Liver biopsies from eight patients showed chronic hepatitis with a mild lobular and portal inflammatory infiltrate, fatty change and prominent sinusoidal cells. Electron microscopy showed cytoplasmic trilaminar tubular structures and dense fused membranes in dilated endoplasmic reticulum. These clinical, biochemical, serological, and histological features would suggest a major role for NANB virus infection in the aetiology of hepatitis in heroin abusers.
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PMID:Clinical, biochemical, serological, histological and ultrastructural features of liver disease in drug abusers. 642 58


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