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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe pregnancy-induced hypertension and markedly elevated levels of serum alkaline phosphatase developed in a 29-year-old-woman in whom one pregnancy resulted in intrauterine death. Acute fatty liver of pregnancy developed with good fetal outcome in the next pregnancy. This case suggests that pregnancy-induced hypertension and acute fatty liver of pregnancy are part of a clinical spectrum. Moreover, classic abnormalities of liver function tests need not be present in acute fatty liver of pregnancy.
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PMID:Pregnancy-induced hypertension and acute fatty liver of pregnancy: atypical presentations. 222 Sep 20

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.
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PMID:Abnormal serum gamma-glutamyltranspeptidase in alcoholics. Clues to its explanation. 256 72

Purpose of this study was to elucidate the difference in severity of alcoholic liver diseases (ALD), especially of alcoholic hepatitis (AH) between female and male. We have experienced 15 female and 113 male patients with ALD laparoscopically and histologically proved during the past 10 years. In female patients, histological analysis revealed 8 cases of cirrhosis, 2 each cases of AH, fibrosis and chronic hepatitis, and 1 case of fatty liver. Occurrence of AH in female (13%) was significantly higher than male in which AH was seen in 3 cases (3%) (p less than 0.05). Duration of alcoholic abuse in female AH patients was shorter than male AH patients (5.5 +/- 0.5 years vs 24.0 +/- 2.9 years). Total alcohol consumed in female AH patients was less than male AH patients (256 +/- 52 kg vs 1560 +/- 703 kg). Abnormality in liver function tests including hepaplastin test, serum bilirubin, transaminases, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyltranspeptidase, immunoglobulins was outstanding in female patients compared with male patients. Histological findings such as hepatocellular ballooning, neutrophilic infiltration, fatty change and wiremesh fibrosis were intensive in female patients compared with male patients. In conclusion, there were much more severe ALD like AH or cirrhosis in female than male patients. In female AH patients duration of alcoholic abuse was shorter and total alcohol consumed was less than male AH patients. And it was suggested that female AH is clinically and pathologically getting severe compared with male AH.
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PMID:[Sex difference in alcoholic liver disease: with special reference to the severity of alcoholic hepatitis]. 280 7

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.
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PMID:Liver injury tests in hazardous waste workers: the role of obesity. 291 8

Persistent abnormalities of liver function tests occur in approximately 15% of home parenteral nutrition (HPN) patients and are associated with steatosis, steatohepatitis, and, rarely, fibrosis or cirrhosis. Approximately one-third of patients with gut failure on long-term HPN have low total and free plasma carnitine concentrations, and it has been suggested that a deficiency of L-carnitine may be responsible for the steatosis and steatohepatitis in HPN patients. To determine whether administration of L-carnitine is capable of reversing steatosis in HPN patients, 4 adult women on HPN for a mean of 53 mo (range 21-80 mo) were studied before and after 1 mo of intravenous L-carnitine supplementation (1 g/day). All patients had abnormalities in standard liver function tests and low total and free plasma carnitine values. The mean total and free plasma carnitine concentrations and the mean total hepatic carnitine concentration were reduced before supplementation and rose to normal values after treatment (27.4 +/- 2.3 to 35.5 +/- 3.1 nmol/ml, 19.4 +/- 2.8 to 25.7 +/- 2.5 nmol/ml, and 3.5 +/- 0.65 to 6.5 +/- 1.2 nmol/mg of noncollagen protein, respectively). However, there were no significant changes in mean serum aspartate aminotransferase and alkaline phosphatase levels (65 +/- 21 vs. 54 +/- 12 IU and 429 +/- 220 vs. 472 +/- 224 IU, respectively), plasma free fatty acids, plasma triglycerides, hepatic free fatty acid and triglyceride concentrations, or the grade of hepatic steatosis on light microscopy. These results suggest that carnitine deficiency is not a major cause of steatosis and steatohepatitis in patients receiving HPN.
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PMID:L-carnitine therapy in home parenteral nutrition patients with abnormal liver tests and low plasma carnitine concentrations. 312 32

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.
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PMID:Liver structure and function in print workers exposed to toluene. 261 34

The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by several nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending whether or not glycogen stores are adequate, inhibits protein synthesis, and results in a fatty liver and elevations in serum triglyceride levels. Increases in serum lactate, results from the increased reduced nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide + (NADH/NAD+) ratio, and hyperuricemia probably occurs owing to the increased turnover of adenine nucleotides after ethanol ingestion. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde, the major metabolite of ethanol, increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Chronic ethanol administration also results in decreased vitamin A stores and reduced bone mass and blood levels of 25-hydroxyvitamin D. The mechanism whereby ethanol affects these vitamins and their associated enzymes is unknown.
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PMID:The effect of ethanol and its metabolites on carbohydrate, protein, and lipid metabolism. 329 39

There were significant changes in enzyme activities and concentrations of metabolites in the blood and liver of cows with fatty livers when compared to normal cows. Blood and liver samples were taken from cows at the abattoir immediately after slaughter. The liver was checked for pathological signs and the samples were divided according to the degree of fatty changes. Three groups were studied: controls showing no gross pathological signs, mild fatty infiltration and severe infiltration. In cows with fatty liver, there were significant increases in the serum activities of isocitric dehydrogenase (ICDH), glucose-6-phosphate dehydrogenase (G6PDH), glutamic dehydrogenase (GLDH), lactic dehydrogenase (LDH), malic dehydrogenase (MDH), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and acid phosphatase (ACP). In the fatty liver, the activities of the enzymes, ICDH, G6PDH, LDH, MDH, ALP and malic enzyme (ME) were significantly higher, while sorbitol dehydrogenase (SDH) was significantly lower. While serum total lipid decreased, the opposite was seen in the liver with higher lipid content, mainly due to triglycerides and cholesterol esters. The significant increases in the NADPH generating enzymes ME, ICDH, G6PDH and MDH, which are required for fatty acid synthesis, suggest that the lipids accumulated in the liver are not only of extrahepatic origin, mobilized into the liver, but also arise from increased lipid synthesis in the liver which is induced during the laying down of fat in the liver. Measurement of the serum NADPH generating enzymes may serve as a useful biochemical test specific for fatty liver in cows.
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PMID:Biochemical changes associated with the fatty liver syndrome in cows. 339 48

Excessive fat accumulation in the liver is a common metabolic disorder seen in humans and animals. Fatty liver was induced in the rat by feeding the animals with a sucrose rich diet containing 1% orotic acid for 2-3 weeks. In the sera from fatty liver rats there were significant changes in the level of alanine aminotransferase (+ 68.7%), malic dehydrogenase (+ 77.8%), gamma-glutamyl transpeptidase (- 53.4%) and total lipids (+ 26.6%). There were small to no changes in the levels of aspartate aminotransferase, glucose-6-phosphate dehydrogenase, lactic dehydrogenase, aldolase, malic enzyme, 6-phosphogluconic acid dehydrogenase, alkaline phosphatase and albumin. In fatty liver, significant differences were seen in the levels of glucose 6-phosphate dehydrogenase (+ 235%), malic enzyme (+ 170%), gamma-glutamyl transpeptidase (+ 113%), 6-phosphogluconate dehydrogenase (+ 63%), aspartate aminotransferase (+ 35.6%), malic dehydrogenase (+ 38%), lactic dehydrogenase (+ 37%), and alanine aminotransferase (- 23%). Comparison of the non-fatty part with the fatty part of the fatty liver showed larger changes in the non-fatty part of the liver, suggesting that during the fattening process, there is an induction of enzymes in the liver reaching a peak prior to lipid accumulation, declining thereafter during liver fattening. The increase in NADPH-generating lipogenic enzymes suggests that accumulated fat in the liver is at least partially from de-novo increased synthesis in the liver.
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PMID:Biochemical changes in liver and blood during liver fattening in rats. 377 7

The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending on whether glycogen stores are adequate, inhibits protein synthesis, and results in fatty liver and in elevations in serum triglyceride levels. Increases in high-density lipoprotein cholesterol after ethanol ingestion may explain the lower risk of myocardial infarction and death from coronary disease after moderate drinking. Increases in serum lactate, resulting from the increased NADH/NAD+ ratio, and hyperuricemia, most likely the result of increased turnover of adenine nucleotides, are common transient effects of ethanol ingestion. Causes of vitamin deficiencies in alcoholism are decreased dietary intake, decreased intestinal absorption, and alterations in vitamin metabolism. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Ethanol decreases hepatic vitamin A concentration and its conversion to active retinal, and modifies renal metabolism of vitamin D.
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PMID:Metabolic effects of alcohol. 388 Dec 85


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