Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
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Gene/Protein
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Target Concepts:
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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)
Albert (Clin Chem 1982;28:1113-9) has proposed estimation of likelihood ratios by logistic regression analysis. The usual likelihood-ratio approach for estimation of post-test probability of disease from sensitivity and specificity data of a diagnostic test has been extended by Birkett (J Clin Epidemiol 1988; 41:491-4) for situations with more than two diagnostic categories. We suggest here a combination of these ideas, demonstrating this by a re-evaluation of previously published data on the validity of neopterin as a tool for differential diagnosis between chronic non-A, non-B hepatitis and
fatty liver
. Analysis of neopterin data in combination with the ratio between serum concentrations of aspartate aminotransferase and of
alanine aminotransferase
yielded a good discrimination between three mutually exclusive diagnostic categories, namely,
fatty liver
and chronic persistent and chronic aggressive non-A, non-B hepatitis. The approach is flexibly applicable to situations with different pre-test probabilities. The sum of estimated post-test probabilities deviates slightly from the sum of pre-test probabilities. This deviation is a function of the coefficients obtained in logistic regression, and an analytical expression for the deviation is given. The generalized likelihood-ratio approach appears promising in complex diagnostic situations when multiple diagnostic tests are available.
...
PMID:Generalized likelihood ratio concept and logistic regression analysis for multiple diagnostic categories. 249 33
In order to investigate the reason for the elevation of serum gamma-glutamyltranspeptidase (GGT) after chronic alcohol consumption, the activity of this enzyme, together with the activities of aspartate aminotransferase,
alanine aminotransferase
and alkaline phosphatase in serum (parameters of liver cell damage) and the excretion of D-glucaric acid (D-GA) in urine (parameter of microsomal enzymatic induction) were determined in 72 chronic alcoholics. Of these, 32 had no significant liver disease (1st group) and 40 had an overt liver disease varying from
fatty liver
to liver cirrhosis (2nd group). The GGT was elevated in only 62% of the patients of the first group, but in 95% of the second group. Of the latter group, patients with cirrhosis had significantly higher GGT mean levels than the patients with
fatty liver
. On the other hand, increased D-GA excretion was only found in 23% of the group 1 patients and in 44% of the group 2 patients. Moreover, in all patients there was a significant correlation between the values of GGT and aspartate aminotransferase, but not between GGT and D-GA. From these results, the GGT increase in chronic alcoholics, would seem to be better related to cellular damage than to enzymatic induction assessed on the basis of D-GA urinary excretion.
...
PMID:Abnormal serum gamma-glutamyltranspeptidase in alcoholics. Clues to its explanation. 256 72
At routine blood donation, a 37-yr-old man with an elevated serum
alanine aminotransferase
was found to have primary sclerosing cholangitis. The majority of asymptomatic blood donors with elevated aminotransferase levels are presumed to have
fatty liver
or chronic non-A, non-B hepatitis. However, a substantial number of blood donors with elevated aminotransferase levels will have other hepatobiliary diseases, including primary sclerosing cholangitis. The implementation of aminotransferase screening of blood donors should result in earlier diagnosis, better understanding of natural history, and occasionally, earlier treatment of a number of hepatobiliary diseases.
...
PMID:Diagnosis of primary sclerosing cholangitis in a blood donor with elevated serum alanine aminotransferase. 270 21
The identification and clinical significance of light microscopic giant mitochondria (GM) were investigated in liver biopsy specimens of 60 alcoholics. By light microscopic examinations using the same section and neighboring sections, we suggest that light microscopic GM correspond to the crystalloid bodies (CB) detected on ultrastructural observation. The reasons are as follows: (1) difference in stainability between eosinophilic light microscopic GM and acidbasophilic mitochondria; (2) similarity in morphological features and density of the round- and cigar-shaped types at the light microscopic level to those of CB at the electron microscopic level; (3) similarity of the area occupied in the hepatic cytoplasm at both light and electron microscopic levels; (4) the crystalline structure of CB in compatible with the subtype of Mallory body (MB); (5) a description of CB has been made at the electron microscopic level, although not yet at the light microscopic level. Moreover, we clinically observed that light microscopic GM seldom appeared either in early
fatty liver
of cases aged 35 or less or the late macronodular liver cirrhosis stage of alcoholic liver injuries while they were frequently recognized during the acute aggravation phase of the chronic stage (
GPT
: p less than 0.05). Furthermore, if one was to assume that MB is a change accompanying necrosis of the liver cells, the light microscopic GM might be a change accompanying degeneration of the cytoplasmic organelles.
...
PMID:Ultrastructural identification and clinical significance of light microscopic giant mitochondria in alcoholic liver injuries. 270 52
We had previously hypothesized that linoleic acid (LA) was essential for development of alcoholic induced liver injury in our rat model. Male Wistar rats were fed a nutritionally adequate diet (25% calories as fat) with ethanol (8-17 g/kg/day). The source of fat was tallow (0.7% LA), lard (2.5% LA) or tallow supplemented with linoleic acid (2.5%). Liver damage was followed monthly by obtaining blood for
alanine aminotransferase
assay and liver biopsy for assessment of morphologic changes. Enzyme and histologic changes (
fatty liver
, necrosis and inflammation) in the tallow-linoleic acid-ethanol fed animals were more severe than in the lard-ethanol group. The tallow ethanol group did not show any evidence of liver injury. Our results strongly support our hypothesis that LA is essential for development of alcoholic liver disease in our rat model.
...
PMID:Dietary linoleic acid is required for development of experimentally induced alcoholic liver injury. 291
The prevalence of
fatty liver
disease at autopsy ranges from 40% to 80% in Europe and North America, and liver injury tests are abnormal in up to 8% of healthy populations. Liver injury tests were therefore examined in a group of 325 workers without exposure to hepatotoxins to identify the influence of obesity and gender. Obesity was a strong predictor of the degree of abnormality for serum levels of arginine and
alanine aminotransferase
and of alkaline phosphatase, even in the normal range. Women generally demonstrated lower levels of these enzymes. Workers with morbid obesity were substantially more likely to have abnormal liver injury tests. Obesity and gender must be considered in the interpretation of abnormal liver injury tests in hazardous waste workers.
...
PMID:Liver injury tests in hazardous waste workers: the role of obesity. 291 8
An unresolved controversy is whether exposure to organic solvents in the workplace causes hepatotoxicity. From a medical surveillance study of 289 printing factory employees who were exposed primarily to toluene, we identified eight workers who had persistently abnormal serum transaminase and/or alkaline phosphatase values. The eight men were generally healthy and gave no history of taking medications or of drinking ethanol to excess. None was obese or diabetic. Six patients had hepatomegaly based on physical examination. All eight had mild elevations (less than 2 to 3 times the upper value of normal) of serum transaminases [alanine (
ALT
) and aspartate aminotransferase (AST)]. However, there was a marked increase in the ratio of
ALT
/AST (mean = 1.61). In each case, liver biopsy revealed mild, pericentral fatty change. Our results, consistent with those previously published by some others, suggest that pericentral
fatty liver
with mild "reactive hepatitis" is the most likely diagnosis in workers exposed to solvents for whom common causes of mild liver test abnormalities have been excluded. An increased
ALT
/AST ratio may represent a convenient, previously unrecognized indicator of this condition.
...
PMID:Liver structure and function in print workers exposed to toluene. 261 34
About 90 per cent of morbidly obese patients show histological abnormalities of the liver. One third of patients have fatty change involving more than 50 per cent of hepatocytes.
Fatty liver
disease can be divided into four histological groups:
Fatty liver
, fatty hepatitis,
fatty liver
with portal fibrosis, and cirrhosis. Most patients show only fatty change. Alcohol, drugs, diabetes, poor nutrition, and weight-reducing surgery contribute to progressive liver damage, but morbid obesity alone may lead to severe disease showing all the features of alcoholic hepatitis and may end in cirrhosis and liver failure. The accumulation of fat alone is unlikely to be the stimulus to inflammation and fibrosis. Only one fifth of patients have complaints that arise from the liver. The development of severe
fatty liver
disease may also be asymptomatic and rarely shows the florid picture associated with alcoholic hepatitis. There is poor correlation of liver function test results with morphology in obesity.
ALT
levels exceeding twice the normal limit have some predictive value for histological grades of severity, but they are present in few patients. Pericentral and pericellular fibrosis in prebypass liver biopsies may be an important prognostic lesion for the development of fatty hepatitis and cirrhosis. In contrast with the frequent progression to massive fatty change, inflammation and fibrosis after bypass surgery, weight loss by low-calorie dieting, or starvation is accompanied by improvement in fatty change and return of liver function tests to normal.
...
PMID:Fatty liver disease in morbid obesity. 331 4
We evaluated the change in serum
alanine aminotransferase
(
ALT
;
EC 2.6.1.2
) to serum aspartate aminotransferase (AST; EC 2.6.1.;
ALT
/AST) ratio with the degree of
fatty liver
in morbidly obese patients. A total of 31 patients were included in the study.
Fatty liver
was graded as 0 to 4+. The mean and SD of AST and
ALT
were not significantly different between groups of patients with various grades of
fatty liver
. There was, however, a significant correlation between the
ALT
/AST ratio and the degree of fatty infiltration of the liver. This, we believe, implies damage mainly to the plasma membrane allowing loss of cytoplasmic enzymes rather than loss of mitochondrial enzymes.
...
PMID:Serum alanine aminotransferase to aspartate aminotransferase ratio and degree of fatty liver in morbidly obese patients. 356 88
Protection against the toxic effects of chronic alcohol consumption was observed in male guinea pigs maintained on a high-ascorbic-acid diet (vitamin C-deficient chow plus 2.0 mg ascorbic acid/ml drinking water) as compared to animals on a low-ascorbic-acid diet (vitamin C-deficient chow and from 0.025 to 0.050 mg ascorbic acid/ml drinking water). Alcohol was orally administered to the guinea pigs at a dose of 2.5 g/kg for up to 14 weeks. Levels of serum aspartate aminotransferase and serum
alanine aminotransferase
were significantly elevated in animals on the low-ascorbic-acid diet that received alcohol, 120 and 250%, respectively. In contrast, in animals on the high-ascorbic-acid diet that received alcohol, levels of
alanine aminotransferase
were not significantly elevated and levels of aspartate aminotransferase were elevated 50%. In addition, some of the animals on the low-ascorbic-acid diet that received alcohol for 12 to 14 weeks developed
hepatic steatosis
and necrosis, whereas none of the animals on the high-ascorbic-acid diet that received alcohol for the same length of time manifested these changes.
...
PMID:Ascorbic acid chronic alcohol consumption in the guinea pig. 371 80
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