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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 76-year-old male was admitted to our hospital because of general fatigue in June 1987. He had received total gastrectomy against gastric carcinoma two years previously. The examinations revealed the elevation of GOT, GPT and gamma-GTP, and increased CT number of the liver. Specimen of the liver biopsy showed deposition of iron and slight fibrosis. He was diagnosed as idiopathic hemochromatosis. He was given deferoxamine, and his elevated GOT, GPT and gamma-GTP were normalized. Idiopathic hemochromatosis is frequently associated with various malignancies including hepatic carcinoma. However, only a few cases of idiopathic hemochromatosis associated with gastric carcinoma have been reported.
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PMID:[A case of idiopathic hemochromatosis associated with gastric cancer]. 142 60

To determine the frequency of liver profile abnormalities in hereditary hemochromatosis, we under took a retrospective survey in 100 patients, all of whom had undergone liver biopsy. Liver histology was compared with the biochemical profile, which included aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, bilirubin and albumin determinations. Mild abnormalities in the AST and ALT levels were seen in more than 65% of patients. Patients with cirrhosis had significantly greater elevations in AST, ALT, and alkaline phosphatase, and a significant decrease in albumin (p less than 0.05). Proband cases had more frequent abnormalities than discovered cases within families. Accordingly, we find that mild abnormalities in the biochemical liver profile are common in hemochromatosis and suggest that patients with an unexplained abnormality in the liver profile should be screened for hemochromatosis with a serum ferritin and transferrin saturation.
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PMID:Biochemical liver profile in hemochromatosis. A survey of 100 patients. 206 47

Treatment of rats with 100 mg kg-1 t-butyl hydroperoxide led to an enhanced ethane exhalation as a marker of in vivo lipid peroxidation, as well as a moderate hepatoxicity as evidenced by a rise in plasma activities of liver-specific enzymes (glutamate-pyruvate transaminase and sorbitol dehydrogenase) and an increase in hepatic calcium content. Furthermore, a depletion of hepatic glutathione by 17% was observed. Apart from the loss of glutathione, all these effects were antagonized by pretreatment of rats with the potent iron chelator deferrioxamine and potentiated by pretreatment with low concentrations of FeSO4 having no pro-oxidant activity per se; this was also the case in rats under conditions of iron overload (experimental haemochromatosis). These data indicate a close relationship between t-butyl hydroperoxide-induced lipid peroxidation and its hepatotoxicity, and point out the importance of iron in catalysing reinitiation (propagation) reactions of lipid peroxidation in vivo.
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PMID:The role of iron in t-butyl hydroperoxide-induced lipid peroxidation and hepatotoxicity in rats. 225 81

Iron overload is found clinically in such conditions as hemochromatosis and sideroblastic anemia, and after long term repeated transfusion in aplastic anemia. An animal model of iron overload was successfully developed in rats and rabbits by repeated intraperitoneal injections of ferric nitrilotriacetate (Fe3+-NTA). This procedure induced a diabetic state with hyperglycemia, ketonemia, glycosuria and ketonuria. Blood venesection on these rats reduced the iron load in the liver and pancreas, and ameliorated the general diabetic symptoms. A single injection of Fe3+-NTA in rats induced a temporary elevation in plasma iron concentration, lipid peroxidation in the perfused liver homogenate expressed by malondialdehyde (MDA) formation, blood GOT, GPT, ALP and gamma-GTP sequentially. Fe3+-NTA uptake in the liver caused membrane lipid peroxidation, and subsequently produced a transit liberation of liver cell enzymes, although the incorporated liver Fe3+-NTA was only 1% of the injected dosage (7.5 mg iron/kg BW) at 3 hr after injection. The direct toxic effect of Fe3+-NTA to living cells was examined using cultured normal rat liver parenchymal cells (RL-34). Marked cytolysis was found in cells exposed to more than 25 micrograms of iron through Fe3+-NTA/ml. At 50 micrograms iron of Fe3+-NTA/ml, most cells were lethally injured and the remaining cells were piled up and aggregated at 15 days. They grew on soft agar culture, and when inoculated subcutaneously to five newly born rats a subcutaneous tumor developed in all animals within three weeks. Lung metastases were found in three of five inoculated rats. A spin trapping technique with electron spin resonance (ESR) on Fe3+-NTA employing 5, 5-dimethyl-l-pyrroline-N-oxide (DMPO) yielded a spin adduct with three doublets (DMPO-Z) which corresponded to singlet oxygen. By ESR in the presence of H2O2, the Fe3+-NTA solution strongly generated hydroxyl radical. The production of active oxygen species by Fe3+-NTA solution may explain the toxicity and carcinogenicity of Fe3+-NTA. The majority of stainable iron in the iron overloaded tissue was hemosiderin (Hs). We tried to purify the Hs from multi-transfused human spleen by the method of Weir et al. The purified Hs did not show a DMPO-OH adducts in the presence of H2O2 and DMPO on ESR measurement. The Hs iron was solubilized with several biological ligands in an acidic state in the presence of a reducing reagent like glutathione. Solubilized Hs iron produced iron chelate complexes which resulted in OH radicals production in the presence of H2O2 in acidic conditions below pH 5.5.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathogenesis and mechanism of iron overload: ferric nitrilotriacetate, hemosiderin, active oxygen, and carcinogenesis]. 268 76

We evaluated 100 asymptomatic blood donors with serum alanine aminotransferase (ALT) levels exceeding 0.83 mu kat/L, for evidence of liver disease or risk factors for non-A, non-B hepatitis and followed serum ALT levels for another 6 months. In 92 donors completing the study, ALT elevations occurred once in 33%, intermittently in 36%, persistently in 28%. Twenty-two donors were obese, 5 had clinical and biochemical evidence of alcoholic liver disease, and 45 drank alcohol regularly; 1 had hemochromatosis, and another, myopathy. In 22 no cause for elevated serum ALT levels was found. The presence or absence of risk of acquiring hepatitis did not correlate with the pattern of ALT elevations or the identification of another cause for the elevated ALT levels. In 92 blood donors with an initially elevated ALT level, two-thirds have intermittent or persistent elevations; most approximately 20% have no apparent cause for the elevations other than possible non-A, non-B hepatitis. These findings may be helpful in counseling and following blood donors with elevated ALT levels.
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PMID:Evaluation of blood donors with elevated serum alanine aminotransferase levels. 311 21

Serum ferritin and hepatic enzyme concentrations were measured in 30 alcoholic subjects. Both the serum ferritin and gamma-glutamyltranspeptidase (GGT) values were raised in 23 subjects and a significant correlation was noted between the two measurements (r = 0,51; P less than 0,01). There was, however, no correlation between the initial serum ferritin concentration and the serum alanine transaminase and serum aspartate transaminase concentrations. The serum ferritin and GGT levels were followed serially during a period of abstinence in 9 subjects; values fell in parallel in all of them. The data indicate that a serum ferritin level above 300 micrograms/l is very unlikely to be the result of alcohol-induced liver damage if the serum GGT value is less than 50 U/l. The combined measurement of serum ferritin and GGT values should therefore prove useful in epidemiological studies concerned with defining the prevalence in different population groups of the HLA-linked iron-loading gene that leads to the clinical disorder of idiopathic haemochromatosis.
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PMID:Effects of heavy alcohol consumption on serum ferritin concentrations. 614 24

An experimental model of secondary hemochromatosis is described. Saccharated iron was administered i.v. to rats for 7 months in total doses in the range 1.0-1.7 g per kg body weight. After the completion of iron loading, the biochemical measurements revealed elevation of alanine aminotransferase (ALT), slight reduction of plasma glucose concentration, and significant reduction of both plasma and liver ascorbic-acid levels. The mean liver iron concentration was 50 times higher in iron-loaded animals than in controls. High concentrations of inorganic iron were also observed in spleen, pancreas, and heart. Histologic analysis revealed marked hepatic fibrosis in most animals in the experimental group. These results demonstrate this animal model presents some pathologic findings observed in human transfusional hemochromatosis. Additionally, hydroxyl free radicals were detected by electron paramagnetic resonance (EPR) spectroscopy in the iron-overloaded liver tissue processed at pH 5.0. No free radicals were detected at pH 7.4. These results suggest the possible participation of hydroxyl free radicals in the cellular toxicity of iron overload.
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PMID:Liver injury and generation of hydroxyl free radicals in experimental secondary hemochromatosis. 838 50

The aim of this study was to evaluate the diagnostic usefulness of percutaneous liver biopsy and screening for hepatitis C virus antibodies with 1st and 2nd generation ELISA in asymptomatic blood donors with persistent (> 1 year) and moderate elevation (> 1.5 times the upper limit of normal) of serum alanine aminotransferase. The diagnosis was established from clinical, biological and ultrasound data before biopsies were obtained, then compared to the histological diagnosis. Thirty one of 56 blood donors who satisfied the preceding criteria accepted liver biopsy and were subsequently included in the study. An accurate diagnosis was proposed before biopsy in 20 cases. This was in agreement with the histological results in 19 cases but in 2 of these, unexpected lobular hepatitis was associated with the expected steatosis. Positive hepatitis C virus tests corresponded to chronic hepatitis in all cases (n = 5). No accurate diagnosis could be proposed in the 11 remaining cases owing to the lack of evidence of any etiology (n = 4) or because several potential etiologies were possible for the same subject (n = 7). Histological diagnoses were: isolated steatosis (n = 12), steatosis associated with lobular hepatitis (n = 7) or with chronic persistent hepatitis (n = 1), chronic active (n = 2) or chronic persistent hepatitis (n = 3), alcoholic hepatitis (n = 2), hemochromatosis (n = 1), and normal liver (n = 3). Liver biopsy is essential to the accurate etiological diagnosis of persistent and moderate elevation of aminotransferases despite hepatitis virus C tests which are associated with the correct diagnosis of chronic hepatitis in 16% of cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Contribution of liver biopsy and serology of hepatitis C virus to the diagnosis of a moderate and prolonged elevation of aminotransferases]. 846 69

We describe three men and two women, aged 18-50, with an occasional finding of increased aspartate and alanine aminotransferase and gamma-glutamyl transpeptidase levels in the absence of any drug treatment and past or current alcohol abuse. Two patients were overweight (body mass index 29 and 32, respectively) and physical examination was normal in all but one case. Tests for hepatitis A, B and C, Epstein-Barr virus, cytomegalovirus, toxoplasma and autoimmune hepatitis were negative and metabolic diseases (Wilson's disease, haemochromatosis, alpha-l-antitrypsin deficiency) were excluded by specific tests. Ultrasound liver scan revealed massive steatosis in all patients. Liver histology showed diffuse steatosis and parenchymal inflammation in all cases, with concomitant fibrosis and Mallory bodies in three of them. Findings were consistent with non-alcoholic steatohepatitis, a rare condition with potential progression to cirrhosis in a minority of cases. This disease, for which no treatment is currently available, must be considered in all subjects with elevated aminotransferases, in the absence of known causes of liver damage.
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PMID:Non-alcoholic steatohepatitis. Report of five cases and review of the literature. 878 33

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23


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