Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma lipid and lipoprotein profile was determined in 12 cirrhotics, 15 patients with cirrhosis and hepatocellular carcinoma (HCC) and 20 healthy volunteers. When compared with controls plasma total cholesterol (TC), high density lipoprotein cholesterol (HDLC), high density lipoprotein phospholipids (HDLPL), HDLPL/PL levels were low, phospholipid (PL) was normal and HDLC/TC and PL/TC were high in cirrhosis. In cirrhotics with HCC, TC, PL, PL/TC levels were elevated while HDLC, HDPL, HDLC/TC and HDLPL/PL were normal. A comparison within the patient groups showed that in cirrhosis alone, the levels of TC, HDLC, PL, HDLPL and HDLPL/PL were lower and PL/TC level was higher than in cirrhotics with HCC. Plasma albumin levels showed a negative correlation with PL/TC and a positive correlation with HDL-cholesterol in cirrhosis. In cirrhosis with HCC plasma, phospholipid levels showed a significant negative correlation with total bilirubin and alanine aminotransferase. The variations in the level of plasma lipids and lipoproteins may assist in describing the nature of these two forms of liver disease.
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PMID:Abnormal lipid and lipoprotein patterns in liver cirrhosis with and without hepatocellular carcinoma. 133 73

In compliance with the mandatory medical surveillance of workers exposed to tetrachloroethylene (PCE) in Italy, isoenzyme fractioning of serum gamma-glutamyltransferase (GGT) was performed on 141 workers of both sexes and on 130 control subjects. None of the workers showed any clinical symptoms of liver disease and their enzymatic profiles, including AST, ALT, 5'-NU, ALP, and GGT, were within the normal reference limits. A statistically significant increase in total GGT serum level was found in the exposed subjects, which was associated with an increase in one of the two fractions normally present in healthy individuals (GGT-2), as well as with the appearance and progressive increase of the level of a fraction (GGT-4) considered to be an expression of hepato-biliary impairment. Further research is ongoing among these workers, which will clarify whether or not electrophoretic GGT tests may be useful in detecting liver function changes due to occupational exposure to PCE.
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PMID:gamma-Glutamyltransferase isoenzyme pattern in workers exposed to tetrachloroethylene. 135 99

The transaminases, alkaline phosphatase (AP) and gamma-glutamyl transferase (G-GT) are most widely used as indicators of hepatobiliary disease. Elevated serum levels of transaminases (AST and ALT) usually indicate hepatocellular damage. ALT elevations, however, can also be of extrahepatic origin (muscle). The ratio of the transaminases in serum (AST/ALT) and the mitochondrial isoenzyme of AST are frequently higher in alcoholic than in non-alcoholic liver diseases. Serum activities of AP and G-GT are elevated in cholestasis: Both enzymes, however, are not liver-specific and G-GT activity is induced by alcohol and certain drugs. A hepatic enzyme pattern (predominant transaminase elevation) should be discriminated from a cholestatic pattern (predominant AP and G-GT elevation). The most frequent diagnoses in asymptomatic patients with accidentally detected, mostly mild to moderate transaminase elevations are: alcoholic liver disease, (mostly chronic) viral hepatitis, and already much less frequently, drug induced liver disease and non-alcoholic steatosis. Solely if the respective investigations are negative or/and the transaminases stay elevated for greater than or equal to 6 months despite strict alcohol abstinence, omission of any potentially hepatotoxic drug or weight reduction are further steps justified.
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PMID:[Increased liver enzymes: what should be done?]. 135 16

Intercellular adhesion molecule-1, an immunoglobulin supergene family member, is known to account for important steps in cell activation and the immune response. By a non-isotopic slot-dot immunoblotting assay, we measured circulating levels of intercellular adhesion molecule-1 in 26 patients with hepatitis C virus-associated chronic active liver disease before and after beta-interferon therapy, in 6 patients with non-A, non-B acute self-limiting hepatitis and in 13 healthy subjects. Circulating intercellular adhesion molecule-1 was found in 10 of 13 (77%) normal controls at low concentrations which were not statistically different from those measured in patients with hepatitis C virus-associated chronic active liver disease responsive to beta-interferon, whereas significantly higher levels were found in unresponsive patients. Higher serum intercellular adhesion molecule-1 levels were found in 4 of 10 (40%) beta-interferon-responsive patients compared with 13 of 16 (18%) unresponsive patients. Intercellular adhesion molecule-1 levels persisted after discontinuation of beta-interferon treatment and did not correlate with hepatocytolysis (as indicated by alanine aminotransferase serum activity) either in chronic active liver disease or acute hepatitis. However, a good correlation was found between intercellular adhesion molecule-1 and its expression on liver cells, thus emphasizing that induced circulating levels may reflect the state of activation at the sites of the inflammatory process. These data strongly support the view that intercellular adhesion molecule-1 plays an important role in liver cell damage in hepatitis C virus-associated acute and chronic liver disease, and that its circulating levels may be a good prognostic parameter of responsiveness to beta-interferon therapy.
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PMID:Circulating levels and liver tissue distribution of intercellular adhesion molecule-1 during beta-interferon therapy of hepatitis C virus-associated chronic active liver disease. 135 8

There is controversy about clinical management of patients who persistently have antibodies to hepatitis C virus (anti-HCV) but who have no symptoms and signs of liver disease. We have taken liver biopsy samples from 23 such patients (16 of whom had normal alanine aminotransferase [ALT] values) to assess prevalence of liver disease and to see whether anti-HCV and HCV-RNA correlated with histological findings. 16 patients had histological evidence of chronic hepatitis, which was not predicted by serum ALT or by the pattern of specificity of anti-HCV. All 16 cases with hepatitis C viraemia (HCV-RNA detected by polymerase chain reaction), including 9 with normal ALT, had chronic hepatitis on biopsy (p less than 0.001), whereas 7 HCV-RNA-negative cases had normal liver histology. These findings indicate that serum HCV-RNA is a sensitive and specific marker of liver disease in anti-HCV-positive subjects, independent of ALT values, and challenge the idea of the existence of "true" healthy carriers of HCV.
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PMID:Hepatitis C viraemia and liver disease in symptom-free individuals with anti-HCV. 135 32

The localization of hepatitis C virus-infected hepatocytes in the human liver remains unclear despite the development of a serological assay for the antibody to hepatitis C virus. We studied their localization immunohistochemically with monoclonal antibodies to core, envelope and NS3 antigens of hepatitis C virus. We examined 48 liver biopsy samples from C100-3 antibody-positive patients with chronic liver disease (chronic persistent hepatitis, 5 cases; chronic active hepatitis, 41 cases; cirrhosis, 2 cases) and 12 liver biopsy samples from C100-3 antibody-negative patients with chronic liver disease (type B chronic hepatitis, 8 cases; alcoholic liver disease, 4 cases). In the C100-3 antibody-positive group, positive immunostaining for core antigen, envelope antigen and NS3 antigen was found in 23% (11 of 48), 24% (11 of 45) and 24% (11 of 46), respectively. Negative results were obtained in the C100-3 antibody-negative group. Hepatocytes with positive staining were scattered in the lobules, and they were found in the same regions irrespective of whether the antibody to core antigen, to envelope antigen or to NS3 antigen was used. Each positive cell was strongly stained in the cytoplasm; these decorations disappeared after absorption of the primary antibody with purified antigen. mean ALT levels in the patients with positive immunostaining for core, envelope or NS3 antigen (174.8 +/- 105.7 U/L) tended to be higher than in those with negative immunostaining (142.0 +/- 93.8 U/L). On histological evaluation of liver specimens with a scoring system of the histological activity index, intralobular inflammation and fibrosis had higher scores for samples with positive rather than negative immunostaining (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunohistochemical detection of hepatitis C virus-infected hepatocytes in chronic liver disease with monoclonal antibodies to core, envelope and NS3 regions of the hepatitis C virus genome. 137 9

Hepatitis C virus (HCV) is the most important cause of transfusion-related non-A, non-B hepatitis. It is also thought to be the prime cause of non-transfusion-related or sporadic chronic liver disease. To assess the extent of HCV infection and its significance in this last form, we evaluated the clinical, serological and histological features of 84 consecutive HCV-related patients without a history of blood or blood products transfusion, alcohol or intravenous drug abuse or other known risk factors. Our results indicate that 68 patients (81%) had signs of chronicity, and 33 (39.2%) had superimposed cirrhosis. Serum abnormal alanine aminotransferase and gamma-glutamyltransferase activities represented good predictive markers of liver histological signs of chronicity. The levels of serum gammaglobulins were found to parallel histological severity of liver disease. One or more hepatitis B virus (HBV)-associated markers were present in 52 patients (61.9%). Only 6 (7.1%) were chronic HBV carriers, and 3 of them had signs of active virus replication. These data indicate that HCV plays a major role in the etiology of sporadic chronic liver disease. Its presence is associated with histological forms of chronic liver disease in most patients, who likely represent chronic HCV carriers.
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PMID:Hepatitis-C-virus-related chronic liver disease of sporadic type: clinical, serological and histological features. 137 48

A prospective study of liver disease has been conducted among patients entering our Dialysis Unit between 1987 and 1990. On entry, 7 patients had a history of blood transfusions but none had clinical or biochemical features of liver disease. During follow-up, 13 further patients were transfused; 1 case developed acute resolving hepatitis B and another acute non-A, non-B hepatitis progressing to chronicity. Eleven other cases showed transient or fluctuating ALT abnormalities. On entry, anti-HCV was negative by both 1st and 2nd generation ELISA assays (Ortho-Diagnostic Systems) in all cases. During follow-up, a positive reaction was detected in 17 cases: 4 patients were positive by both assays and 13 only by 2nd generation test (p less than 0.01). HCV was implicated in 66% of cases with liver disease of the non-A, non-B type and in 50% of transfused as compared to 23% of nontransfused cases (p = n.s.). These findings suggest that HCV could play a major etiological role in liver disease of hemodialysis patients and that anti-C100 reactivity is more affected by immunosuppression associated with chronic uremia.
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PMID:Hepatitis C virus infection in hemodialyzed patients detected by first and second generation assays. 138 Jan 33

The authors evaluated the clinical significance of anti-C100, anti-GOR and anti-CP9 in hepatitis C virus (HCV)-related liver disease in two populations: 459 healthy subjects and 385 patients with chronic liver disease (CLD). Previously we reported high rates of mortality and morbidity (5.3%) of CLD in subjects in Saga, Japan. This was ascribed to the high prevalence (10.8%) of anti-HCV among randomized populations, as detected by the C100 ELISA test system, as compared with a finding of 2-3% in Japanese blood donors in the same decade. The incidence of anti-C100, anti-GOR and anti-CP9 detected by ELISA test system in the healthy population currently surveyed was 17.0%, 19.2% and 32.0% respectively, as compared with 75.3%, 60.3% and 73.0% respectively, in those with CLD. The incidence of positivity for at least one of the three antibodies was high (36.4%) among healthy subjects, and even higher (86.5%) among the patients with CLD. In the healthy subjects, incidence of positivity increased with age. The healthy and CLD populations differed in the proportion of cases positive for all three antibodies vs. those positive for at least one antibody: healthy subjects, 52/167, 31.1%, vs. CLD patients, 197/333, 59.2%; P less than 0.01. Among the anti-C100-positive healthy cases, these was a significantly high level of AST, ALT, ZTT and gamma GTP compared with negative cases, with or without anti-GOR and anti-CP9 (P less than 0.01-0.05). These observations suggest that the presence of anti-C100 may be related to the active state of HCV-related liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Overlap and discrepancy between tests for anti-C100, anti-GOR and anti-CP9 in patients with chronic liver disease and inhabitants in Saga, Japan. 138 31

Long-term ethanol feeding has been shown to selectively reduce hepatic mitochondrial glutathione content by impairing mitochondrial uptake of this thiol. In this study, we assessed the role of this defect in evolution of alcoholic liver disease by examining the mitochondrial glutathione pool and lipid peroxidation during progression of experimental alcoholic liver disease to centrilobular liver necrosis and fibrosis. Male Wistar rats were intragastrically infused with a high-fat diet plus ethanol for 3, 6 or 16 wk (the duration that resulted in induction of liver steatosis, necrosis and fibrosis, respectively). During this feeding period, the cytosolic pool of glutathione remained unchanged in the ethanol-fed animals compared with that in pair-fed controls. In contrast, the mitochondrial pool of glutathione selectively and progressively decreased in rats infused with ethanol for 3, 6 or 16 wk, by 39%, 61% and 85%, respectively. Renal mitochondrial glutathione level remained unaffected throughout the experiment. Serum ALT levels increased significantly in the ethanol-fed rats at 6 wk and remained elevated at 16 wk. In the mitochondria with severely depleted glutathione levels at 16 wk, enhanced lipid peroxidation was evidenced by increased malondialdehyde levels. Thus a progressive and selective depletion of mitochondrial glutathione is demonstrated in the liver in this experimental model of alcoholic liver disease and associated with mitochondrial lipid peroxidation and progression of liver damage.
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PMID:Hepatic mitochondrial glutathione depletion and progression of experimental alcoholic liver disease in rats. 144 96


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