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)

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

To determine whether physicians in an academic medical center excluded hemochromatosis as a diagnosis in a population of patients with mildly elevated liver enzyme values, we reviewed 100 charts of patients with both aspartate aminotransferase and alkaline phosphatase levels that were less than twice the upper limit of normal. We analyzed each chart to determine if hemochromatosis would have been excluded by a subsequent workup. Those patients who did not have a complete workup were assigned to one of three categories: (1) no mention was made of abnormal liver enzyme values; (2) liver enzyme values were ascribed to some condition other then hemochromatosis and no definitive workup was done; and (3) the condition of the patient was so poor that assessment did not seem indicated. Ninety of 100 patients were not given a workup to exclude hemochromatosis. Physicians often ignore mild elevations in liver enzyme values.
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PMID:Pursuing mild elevations of liver enzyme values to exclude hemochromatosis. 223 55

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

Tissue iron loading in hypotransferrinaemic (hpx/hpx) mice was investigated as a model for genetic (primary) haemochromatosis. Iron loading of liver preceded that in the pancreas and heart. One-year-old hpx/hpx mice showed iron staining in exocrine pancreas, liver parenchymal cells, and cardiac and intestinal smooth muscle cells. Iron-loaded macrophages were observed in all these tissues. Islets of Langerhans, biliary epithelial cells, and spleen were iron-free. The pancreas was fibrotic with massive macrophage infiltration and loss of secretory epithelium. Liver showed evidence of chronic inflammatory infiltration with increased collagen fibres in the parenchymal region but no cirrhosis. Serum aspartate aminotransferase activity and plasma glucose were increased in hpx/hpx compared with wild-type mice. Heavy iron loading with haemosiderin deposition in the liver could be demonstrated in hpx/hpx mice from 6 weeks of age. Heterozygous hypotransferrinaemic mice showed minor increases in liver iron stores at 6-12 weeks, but not at 1 year of age. Serum ferritin levels in heterozygous mice were also increased at 6-8 weeks of age. It was concluded that 1-year-old hpx/hpx mice showed evidence of liver and pancreatic damage secondary to tissue iron overload. The iron loading pattern and tissue damage showed some features which were distinct from those observed in haemochromatosis.
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PMID:Tissue iron loading and histopathological changes in hypotransferrinaemic mice. 827 72

Iron overload is a major cause of morbidity and mortality in thalassemia major patients. All chronic liver diseases may be associated with such endocrine symptoms as diabetes mellitus, testicular failure or hypothyroidism. We studied 15 thalassemic patients (12 men and 3 women; age range: 10-50 years, mean: 22.5 years). All patients received blood transfusions, but only some were treated with iron chelation. Seven patients were splenectomized. MRI was performed with an 0.5 T superconducting magnet, using SE T1- and T2-weighted and IR sequences. We used these data with Bloch's equation to calculate T1 and T2 values. Quantitative analysis was made by calculating signal intensity and relaxation times in 8 hepatic regions of interest: marked reduction in hepatic signal intensity and a negative relationship between T1 and serum ferritin (r = 0.646, p < 0.01) and between T2 and serum ferritin (r = 0.688, p < 0.01) were observed. Moreover, a negative relationship was found between hepatic signal intensity and aspartic aminotransferase (r = 0.524, p < 0.05). Our results confirm the value of MRI in the diagnosis and evaluation of hepatic iron overload but an accurate quantitative analysis can be made only when hepatic iron levels are between 1 and 2 mg/g of liver. Even though it is below statistical significance, the negative relationship between signal intensity and aspartic aminotransferase suggests that hepatic hemochromatosis can influence pituitary-thyroid axis and interfere with peripheral hormone metabolism.
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PMID:[Secondary hepatic hemochromatosis: diagnosis and quantification with 0.5 T magnetic resonance. Value and limitations]. 829 5

Biochemical evidence of iron overload (transferrin saturation greater than 60% and/or serum ferritin concentration greater than 1000 micrograms/L) was observed in 16% of patients admitted to an alcohol withdrawal unit. No subjects in an age and sex matched control group showed such biochemical changes. Whilst changes in serum ferritin concentration closely correlated with aspartate aminotransferase activity and could be explained by alcohol induced liver damage, the increased transferrin saturation was not similarly explained. In nine patients withdrawal of alcohol resulted in a decrease in transferrin saturation and serum ferritin, the former due to a reduction in serum iron concentration. In patients with high alcohol intake biochemical measures of iron status may be misleading and a decrease in both transferrin saturation and serum ferritin concentration after withdrawal of alcohol may help to rule out the possible diagnosis of hereditary haemochromatosis.
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PMID:Assessment of iron status in association with excess alcohol consumption. 857 83

The purpose of this study was to evaluate the distribution of haemosiderin iron in various regions of the liver (central, intermediary and peripheral hepatocytes, Kupffer cells, portal macrophages and bile duct epithelial cells) in 174 patients with different hepatic diseases (alcoholic cirrhosis (n = 49), alcoholic steatosis (n = 60), non-alcoholic cirrhosis (n = 16), acute hepatitis (n = 20), clinically overt untreated hereditary haemochromatosis (n = 3), miscellaneous disorders (n = 26)), and in 13 subjects with a normal liver biopsy. Furthermore, the relationship between liver haemosiderin iron, biochemical iron status markers and biochemical liver tests was investigated. In haemochromatosis iron was consistently present in all examined regions of the liver, and in 43% of patients with alcoholic liver disease haemosiderin was present in at least one region of the liver lobule. In 65% of patients with acute hepatitis, haemosiderin was present in macrophages and Kupffer cells. In other hepatic diseases and in normal livers, haemosiderin was rarely seen. Regression analyses showed a correlation between iron status markers in most patients, except in those with high serum aspartate aminotransferase levels. In conclusion, haemosiderin iron is distributed in a typical pattern in haemochromatosis, alcoholic liver disease and acute hepatitis. Both histochemical liver iron and serum ferritin are of value as indirect markers of liver iron stores in patients with moderate hepatocellular damage.
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PMID:Distribution of liver haemosiderin iron in 187 patients with various types of hepatic diseases. 861 Nov 97

The aetiology, biochemistry, clinical features and complications of histologically confirmed hepatic cirrhosis in 45 patients (26 females, 19 males) seen at the University Hospital of the West Indies, Jamaica, between 1984 and 1994 are presented. The age range was 1 to 72 years (mean 48 years). Abdominal swelling and weight loss were the commonest symptoms, occurring in 51% and 47% of patients, respectively. Jaundice was a presenting feature in 44%. Hepatomegaly was present in 71% of patients and splenomegaly in 33%. The aetiological factors were: alcohol (36%), bush tea (18%), chronic active hepatitis (11%), drugs (7%), and haemochromatosis (2%). Hepatitis B surface antigen was detected in 2 of 20 patients tested. 24% of the patients also had diabetes mellitus., 29% were anaemic, 29% were thrombocytopenic, 4% were leukopenic, and the prothrombin time was prolonged in 22%. The albumin/globulin ratio was reversed in 71% of the patients. The alkaline phosphatase was elevated in 56%, the aspartate aminotransferase was increased in 58% and the gamma glutamyl transpeptidase in 56%. 56% of the patients had macronodular cirrhosis; the liver showed a micronodular pattern in 18%; 7% had biliary cirrhosis; 7% chronic active hepatitis with cirrhosis; and 13% showed a mixed macro-micronodular pattern. Ascites and fluid overload developed in 44% of the patients. Hepatic encephalopathy occurred in 18% and upper gastrointestinal bleeding in 18%.
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PMID:Hepatic cirrhosis in Jamaica. 926 May 37

At routine determination of serum activities of transaminases (aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) increased levels are frequently found. An algorithm may be used in the analysis of elevated transaminase levels: after elimination of the most frequent causes of hepatitis (alcoholic hepatitis, chronic hepatitis B and C) and some rare conditions (autoimmune hepatitis, alpha 1-antitrypsin deficiency, haemochromatosis and Wilson's disease), the diagnosis will often be nonalcoholic steatohepatitis. Although nonalcoholic steatohepatitis is considered a stable disease, recent literature shows a progression to cirrhosis in 8-17%. So far, no effective therapeutic strategies are available for nonalcoholic steatohepatitis.
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PMID:[Management of asymptomatic elevated serum aminotransferase levels, particularly in nonalcoholic steatohepatitis]. 1032 Dec 58

It has been proposed that iron overload may adversely affect liver disease outcome. The recent identification of 2 mutations in the HFE gene related to hereditary haemochromatosis (Cys282Tyr and His63Asp) provided an opportunity to test whether they are associated with hepatic iron accumulation and the activity and severity of liver disease in hepatitis C virus (HCV) infection. We investigated the prevalence of HFE mutations in 135 male patients with chronic HCV hepatitis, and correlated genotype distribution with different parameters of iron status and the activity and severity of liver disease. Of these 135 patients, 6 (4.4%) carried Cys282Tyr and 32 (23.7%) carried His63Asp, frequencies which were similar to those observed in healthy controls. Serum iron levels and transferrin saturation (but not ferritin levels or liver iron content) were significantly higher in carriers than in non-carriers of HFE mutations. No difference was observed in serum ALT, AST and GGT levels between carriers and non-carriers. Finally, scores for necroinflammatory activity and fibrosis in the liver were significantly higher in HFE carriers than in non-carriers. Patients with chronic HCV infection carrying HFE mutations tend to present more evident body iron accumulation and a higher degree of necroinflammatory activity and fibrosis in the liver. HFE gene mutations might be an additional factor to be considered among those implicated in the determination of a worse prognosis of the liver disease in chronic HCV infection.
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PMID:Are haemochromatosis mutations related to the severity of liver disease in hepatitis C virus infection? 1069 80


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