Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of cycloheximide (CHM) and chloramphenicol (CAP) on rat serum proteins and on their electrophoretic patterns have been investigated. It has been shown that total serum protein is decreased by both treatments. CHM causes a fall in transferrin and alpha2(3-8) globulin content, while CAP reduces only alpha2(3-8) globulins. Different microscopic features of hepatic steatosis are described with both drugs. The results are briefly discussed.
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PMID:The influence of cycloheximide and chloramphenicol on rat serum proteins. 118 96

Two brothers presented with olivopontocerebellar atrophy of neonatal onset. The clinical features (failure to thrive, hypotonia, liver disease, effusions, and visual inattention) were similar to those of the four cases already reported, as were the necropsy findings of olivopontocerebellar atrophy, hepatic steatosis and fibrosis, and microcystic renal changes. The clinical similarities between this and the disialotransferrin developmental deficiency syndrome were noted. The characteristic abnormality of serum transferrin found in the latter syndrome was also found in the two cases reported here. We suggest that both syndromes are caused by the same, or related, defects in glycoprotein metabolism.
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PMID:Olivopontocerebellar atrophy of neonatal onset and disialotransferrin developmental deficiency syndrome. 192 7

We assessed the prevalence of previously unrecognized hemochromatosis among patients in whom diabetes mellitus was diagnosed after the age of 30 yr, and we evaluated the positive predictive value of biochemical screening tests for hemochromatosis in diabetic subjects. Thirty-eight of 572 patients screened (6.6%) had a serum ferritin level greater than 324 micrograms/L; 16 patients had normal levels on repeat testing. Four patients' serum ferritin levels fell to less than 400 micrograms/L. Seven of 18 patients with a persistently elevated serum ferritin level did not undergo a liver biopsy because of a recognized cause of hyperferritenemia (carcinoma, alcoholism, or systemic lupus erythematosus). The diagnosis of hemochromatosis seemed certain in 1 of 3 patients who were not biopsied for technical reasons. Of 8 patients biopsied, 2 had hemochromatosis, 4 had fatty liver, 1 had hemosiderosis, and 1 had a chronic inflammatory cell infiltrate with no iron deposition. Of 4 patients with a raised transferrin saturation level, 2 had raised serum ferritin levels and hemochromatosis, 1 had raised serum ferritin and hemosiderosis on liver biopsy, and 1 had a normal transferrin saturation level on repeat testing. Two of 3 cases of hemochromatosis had other clinical markers of the condition. Therefore, routine screening of diabetic patients for hemochromatosis is not necessary, because patients with hemochromatosis will often have other clinical features of the disease. When screening diabetic patients for hemochromatosis, it should be remembered that a persistently raised serum ferritin level has a low positive predictive value (16.6%) and that a normal transferrin saturation level does not exclude the diagnosis.
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PMID:Usefulness of biochemical screening of diabetic patients for hemochromatosis. 235 Oct 33

The metabolism of transferrin was studied using purified 125I-labeled transferrin in 11 alcoholic patients; six with fatty liver and five with cirrhosis. Six healthy subjects whose alcohol intake was les than 40 gm daily were studied as a control group. There were no significant differences in the mean fractional catabolic rate and plasma volume in the alcoholic groups when compared with control subjects. A significantly decreased mean serum transferrin concentration was found in the alcoholic cirrhotic patients (1.8 +/- 0.3 gm per liter vs. 2.9 +/- 0.2; p less than 0.01), resulting from diminished total body synthesis (0.9 +/- 0.2 mg per kg per hr vs. 1.8 +/- 0.2; p less than 0.01). In contrast, in the patients with alcoholic fatty liver, the mean total body transferrin synthesis (2.4 +/- 0.3 mg per kg per hr) was significantly increased when compared with controls (p less than 0.05). For all the alcoholic patients, the serum transferrin correlated with transferrin synthesis (r = + 0.70; p less than 0.01) but the serum iron did not. These results suggest that, in alcoholic cirrhosis, transferrin synthesis is decreased, probably reflecting diminished synthetic capacity by the liver. In contrast, in patients with alcoholic fatty liver, transferrin turnover is accelerated.
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PMID:Transferrin metabolism in alcoholic liver disease. 402 86

This study was performed to determine the effects of different amounts of lipid in enteral diets during the postburn period. Forty-five guinea pigs with catheter gastrostomy received a 30% total body surface area full thickness flame burn. After burn they were given intragastric tube feedings using five diets at different dietary lipid composition: 0, 5, 15, 30, and 50% of nonprotein calories. Total calories administered (175 kcal/kg/day), protein content and composition (20% of total calories), total volume, and vitamin and mineral content were constant in all animals. At postburn day 14, body weight, carcass weight, and muscle weight were the greatest in 0 and 5% lipid groups, and the least in 30 and 50% lipid groups. Serum transferrin was highest in the 5 and 15% lipid groups, and lowest in the 30 and 50% lipid groups. Total nitrogen content in muscle and cumulative nitrogen balance were best in the 15% lipid group. Liver fatty infiltration, caused from a larger proportion of carbohydrate administration, was greater in the 0 and 5% lipid groups and less in 15 and 30% groups. It is concluded that dietary lipid levels between 5 and 15% of nonprotein calories are optimal for nutritional support after burn injury. The nutritional management of postburn patients with higher levels of dietary lipid should be reconsidered.
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PMID:Optimal lipid content for enteral diets following thermal injury. 644 Oct 4

The serum concentrations of prealbumin, transferrin and immunoglobulins, as well as their concentration ratios, were determined in patients with fatty liver, alcoholic cirrhosis and primary biliary cirrhosis to evaluate the usefulness of these measurements in the differentiation between these diseases, and in the evaluation of the severity of the liver injury. Alcoholic cirrhosis was characterized by high IgA/prealbumin and IgG/prealbumin ratios, whereas in fatty liver these ratios remained normal or close to normal. The IgG concentration and the ratio of IgG/prealbumin were markedly higher in advanced than in early alcoholic cirrhosis, IgG/prealbumin being the most sensitive indicator. None of the assays reflected the degree of fatty degeneration. In primary biliary cirrhosis the mean IgG concentration was 93% higher than in alcoholic cirrhosis. One of ten patients with primary biliary cirrhosis had a normal IgM level, whereas 2 of 10 patients with alcoholic cirrhosis had a value above normal (greater than 2.9 g/l). IgM alone did not differentiate between alcoholic and primary biliary cirrhosis, while the ratio of IgA/IgM seems useful: a value over 2.0 was found in all patients with alcoholic cirrhosis but in none of those with primary biliary cirrhosis.
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PMID:Serum prealbumin, transferrin and immunoglobulins in fatty liver, alcoholic cirrhosis and primary biliary cirrhosis. 685 Nov 68

The exact differential diagnosis of iron overload syndromes is mandatory as important therapeutic consequences may derive from a correct diagnosis, especially when hemochromatosis is present. To facilitate diagnostic and therapeutic decisions algorithms and probabilistic calculations based on different frequencies of clinical symptoms and typical laboratory findings of the diseases in question have been proposed. Overestimation and/or underestimation of clinical symptoms and/or laboratory findings in using such calculations, however, may lead to incorrect diagnosis and therapy as demonstrated in this case. We report on a 62-year-old patient with arthralgia, pathologic glucose metabolism, brown skin pigmentation and excessively elevated ferritin and transferrin saturation levels, which initially were interpreted as signs of the assumed underlying disease (hemo-chromatosis) based on a high initial suspicion level and further corroborated by Bayesian probability analysis yielding a probability 99.0 % for the presence of hemochromatosis. Because of this high probability and the patient's wish for treatment phlebotomy was started, but stopped after having obtained negative results of genetic testing and normal quantitative liver iron values. The diagnosis of hemochromatosis had to be revised and symptoms and laboratory findings of this patient were found to be compatible with chronic fatty liver and pathologically altered iron metabolism due to chronic alcohol intake which the patient has initially concealed. The joint pain was explained in terms of chronic degenerative bone destruction, the impaired glucose tolerance seen as the consequence of obesity and the skin pigmentation was ascribed to sun exposure due to the patient's outdoor activities as a hobby farmer not evaluated during initial presentation. The implications and importance of unbiased history taking, critical interpretation of clinical symptoms and laboratory findings in using probabilistic calculations and diagnostic decision analysis are emphasized and the different mechanisms of iron metabolism in hemochromatosis and hemosiderosis are discussed.
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PMID:[Hemochromatosis or hemosiderosis? Initial misinterpretation of clinical symptoms and laboratory findings in a 62-year-old patient]. 1196 34

Chronic liver disease is a major cause of morbidity and mortality in the United States. Although often used to detect liver disease, the prevalence and etiology of elevated aminotransferases are unknown. We analyzed data on adults ages 17 yr and older (N = 15,676) from the Third National Health and Nutrition Examination Survey (1988-1994). Participants were classified as having elevated aminotransferase levels if either aspartate aminotransferase or alanine aminotransferase was elevated above normal. Aminotransferase elevation was classified as "explained" if there was laboratory evidence of hepatitis B or C infection, iron overload, or if there was a history of alcohol consumption. Analyses were weighted to provide national estimates. The prevalence of aminotransferase elevation in the United States was 7.9%. Aminotransferase elevation was more common in men compared to women (9.3% vs 6.6%, p = 0.002), in Mexican Americans (14.9%) and non-Hispanic blacks (8.1%) compared to non-Hispanic whites (7.1%, p < 0.001). High alcohol consumption, hepatitis B or C infection and high transferrin saturation were found in only 31.0% of cases. Aminotransferase elevation was unexplained in the majority (69.0%). In both men and women, unexplained aminotransferase elevation was significantly associated with higher body mass index, waist circumference, triglycerides, fasting insulin, and lower HDL; and with type 2 diabetes and hypertension in women (all p < 0.05). Aminotransferase elevation was common in the United States, and the majority could not be unexplained by alcohol consumption, viral hepatitis or hemochromatosis. Unexplained aminotransferase elevation was strongly associated with adiposity and other features of the metabolic syndrome, and thus may represent nonalcoholic fatty liver disease.
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PMID:The prevalence and etiology of elevated aminotransferase levels in the United States. 1280 14

Three patients are reported with a prior history of alcohol misuse accompanied by abnormal liver toxicity tests and other indices of alcohol misuse. A decreased but persistently raised serum gamma-glutamyl transferase activity during subsequent abstinence or controlled drinking was interpreted incorrectly as due to continued alcohol misuse whereas obesity-related fatty liver was the probable cause. The value of serum carbohydrate deficient transferrin assays in the differential diagnosis of abnormal liver toxicity tests is emphasized.
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PMID:Obesity as a cause of "false-positive" alcohol misuse laboratory investigations. 1457 22

A 32-year-old man presented with increases in serum alanine aminotransferase activity, iron concentration, and transferrin saturation, suggestive of hepatic dysfunction and iron overload. In addition, he had unusually low plasma concentrations of LDL-cholesterol and apolipoprotein (apo) B. Hepatic ultrasonography was consistent with fatty liver. On liver biopsy, marked steatosis and moderate to marked iron deposition were observed. The patient was found to carry the HFE C282Y and H63D mutations, which are associated with hereditary hemochromatosis, and the alpha(1)-antitrypsin PiZ variant. An immunoblot of plasma for apoB showed the presence of a truncated apoB species, indicative of familial hypobetalipoproteinemia. DNA sequence analysis revealed that the patient was heterozygous for the apoB-80.5 (c.11040T>G) mutation. This unique case shows an unusual combination of underlying disorders that could all be contributing to liver dysfunction and fatty liver.
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PMID:Liver dysfunction and steatosis in familial hypobetalipoproteinemia. 1551 99


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