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 clinical significance of hepatocellular lipolysosomes in patients with various liver diseases was investigated. Of the 102 cases studied, lipolysosomes were found in 78 cases or 76%. In patients with fatty change of the liver, hepatocellular lipolysosomes were found in 62 of 68 or 91%. In patients without fatty change, lipolysosomes were found in 16 of 34 or 47%. The lipolysosome:lipid ratio in the hepatocytes ranged from 0 to 10%. No differences were found in the lipolysosome:lipid ratios of patients with acute hepatitis, cholestasis, fatty liver, chronic hepatitis, or cirrhosis. In chronic hepatitis and cirrhosis with associated fatty change, the ratio was correlated with the serum level of cholesterol, whereas in fatty liver the ratio was not correlated with any parameters of patient's age, etiologic factors, or serum level of cholesterol. The findings suggest that lysosomal function is less significant as a pathogenesis of fat infiltration but lipolysosomes increase in number as a sequence of cholesterol overload to the liver.
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PMID:Lipolysosomes in human hepatocytes: their increase in number associated with serum level of cholesterol in chronic liver diseases. 683 12

We measured the concentration in plasma of fibronectin, a recently characterized high molecular weight glycoprotein, in patients with various liver diseases. We found that it was significantly increased in acute hepatitis, fatty liver, all types of chronic hepatitis and liver cirrhosis without clinical evidence of ascites. Only in patients at the decompensated stage of liver cirrhosis, i.e. patients with clinical evidence of the presence of ascites, was it significantly reduced. Based on the immunohistochemical study on biopsy specimens of the liver using anti-human fibronectin antiserum, we suggest a possible correlation of the elevated plasma fibronectin to the wide distribution of specific fluorescence associated with the fibrillar structures in necrotic areas, expanded portal areas or thick fibrous septa in the liver diseases. Accelerated catabolism of plasma fibronectin mediated by increased fibrinolytic activity may contribute to the decrease in the level of plasma fibronectin in severe liver cirrhosis.
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PMID:Distribution of fibronectin in plasma and liver in liver diseases. 703 11

To test whether reduced hepatic uroporphyrinogen decarboxylase activity is a specific and intrinsic defect in porphyria cutanea tarda, we measured enzymatic activity in the livers of 17 patients with porphyria cutanea tarda, 12 "normal" control patients without liver disease, and 41 patients with other forms of porphyria, alcoholic liver disease, hemochromatosis, or chronic hepatitis. Enzyme activity in all the patients with porphyria cutanea tarda was lower than in the patients without this disease, except for one patient with alcohol-induced fatty liver. Reduction of hepatic iron stores by phlebotomy did not alter the enzymatic activity in porphyria cutanea tarda. We conclude that reduced hepatic uroporphyrinogen decarboxylase activity is a specific and intrinsic hepatic defect in porphyria cutanea tarda, but modulation of uroporphyrinogen synthesis by extrinsic factors is required for the full biochemical expression of the disease.
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PMID:Decreased hepatic uroporphyrinogen decarboxylase activity in porphyria cutanea tarda. 706 51

A 41/2-year-old asymptomatic girl with persistent elevated serum transaminase levels for eight months was found to have Wilson's disease. The diagnosis was suspected by the presence of fatty liver and nonspecific chronic hepatitis on liver biopsy and was proved by studies of copper metabolism, including determinations of serum ceruloplasmin and hepatic copper concentrations. Unexplained persistent transaminase elevation in children demand investigation by needle liver biopsy. Th presence of fatty liver and hepatitis should raise the possibility of Wilson's disease, which may then be confirmed by more specific tests. Advantages to early diagnosis include the institution of specific therapy and prevention of progressive liver disease.
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PMID:Persistent transaminasemia and fatty liver. Their use in the diagnosis of presymptomatic Wilson's disease. 706 50

Fifty-three histologically proved cases of various diffuse liver disease were studied for their computed tomography numbers (CTN). The machine used was Ohio Nuclear's Delta Scanner 50FS type and CTN was expressed by the Hounsfield unit (H). Mean CTN in each group was as follows: 66.6 +/- 2.6 H in normal control (N), 63.3 +/- 6.0 H in chronic hepatitis (CH). 61.8 +/- 7.0 H in liver cirrhosis (LC), and 44.4 +/- 10.6 H in fatty infiltration (FI). There were no significant differences among them except FI group. As N group were all above 60 H and CH and LC groups were all above 50 H, CTN below 60 H suggests chronic liver disease or fatty infiltration and CTN below 50 H strongly suggests fatty infiltration. In eleven cases where total lipid content of the liver could be be biochemically determined by the sulfo-phospho-vanillin reagent, a relation of total lipid content to CTN was studied. As a result, a significant correlation existed between them (r = -0.89; p less than 0.001). If the diagnostic criterion of fatty liver was set at total lipid content above 100 mg/g wet liver, CT criterion was estimated at CTN below 48 H from the regression formula.
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PMID:Computed tomography in the diagnosis of fatty liver: total lipid content and computed tomography number. 707 50

Serum concentrations of conjugated cholic acid determined radioimmunologically were investigated for 3 hours after a test meal in 62 patients with fatty liver, 70 patients with chronic hepatitis and 30 patients with liver cirrhosis. Values were compared with results of further data from chemical pathology. Increased fasting bile acid values were found in 18% of patients with fatty liver, 13% with chronic hepatitis and in 70% with cirrhosis. Following the test meal maximum concentration increase of cholic acid conjugates was obtained after one hour. 70.5% of patients with fatty liver, 80% of patients with chronic hepatitis and 97% of patients with cirrhosis were identifiable by increased bile acid levels. Postprandial serum bile acid levels therefore have a higher sensitivity for diagnosis of liver disease than bilirubin, glutamic-oxaloacetic transaminase, alkaline phosphatase or gamma-glutamyl transferase.
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PMID:[Value of serum levels of conjugated cholic acid in the diagnosis of liver disease (author's transl)]. 710 4

Percutaneous transhepatic portal catheterization was performed in 68 cases of liver diseases in the 2 year period from 1978 to 1980. The Chiba University method was modified. Portal vein catheterization was successful in 61 cases (90%). Selective splenic vein catheterization was successful in 55 of the 61 cases (90%) and selective superior mesenteric vein catheterization in 59 cases (97%). The liver was punctured an average of 4.6 times in order to successfully insert the catheter into the main portal vein, and the number of punctures was less than 10 in 57 of the 61 cases (93%). The portal vein pressure was 310+/-67 mm H2O in idiopathic portal hypertension (8 cases), 290+/-83 in liver cirrhosis (33 cases), 193+/-71 in chronic hepatitis (7 cases) and 166+/-50 in fatty liver (4 cases). Portal vein pressure rose from 205+/-75 to 380+/-55 mm H2O in 11 cases after forced Valsalva maneuver. No major complications were encountered.
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PMID:Percutaneous transhepatic portal catheterization-modification of Chiba method and portal vein pressure in liver diseases. 713 52

Size of gallbladder after overnight fasting and the kinetics of gallbladder contraction following i.v. injection of 1 I. U. of CCK was investigated in patients with chronic liver disease (liver cirrhosis: n = 26; chronic hepatitis: = 12; fatty liver: n = 5). The results were compared with those obtained in an age and sex matched control group of subjects without symptoms of diseases of the liver or gastrointestinal tract (n = 15). Ultrasound was used for continuous monitoring of gallbladder emptying. In the cirrhotics the cartographically determined initial area of the gallbladder was significantly greater than in the controls (p less than 0,01). The kinetic of gallbladder emptying following CCK-pancreozymin stimulation was similar in the groups of patients with liver diseases to that of the control subjects. However, the residual area of the gallbladder following maximal contraction was again significantly greater in the cirrhotics when compared to the control group (p less than 0.05). The area of the gallbladder in patients with chronic hepatitis exhibited similar changes of the values in the fasting state and after maximal contraction as seen in the patients with liver cirrhosis, although the differences when compared to the control group were not significant. The results show that in spite of distinct signs of a hypotonic state of the unstimulated gallbladder in patients with chronic liver disease the kinetic of contraction following an exogenous stimulus with CCK remains normal.
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PMID:[Ultrasound measurement of gallbladder response to cholecystokinin in patients with chronic liver disease (author's transl)]. 731 56

Expert judgement of selected gastro-intestinal disorders, as well as of pancreatic and liver disease and of the status after gastric surgery is discussed. The group of liver disease commented upon includes virus hepatitis as a disease caused by professional activity, fatty liver, chronic hepatitis and cirrhosis of the liver. A causal relationship between progressive liver disease and peptic ulcer has to be accepted; a causal relationship between most types of liver disease and cholelithiasis however has not yet been established. In conclusion, the advantages are stressed of an early mobilisation of patients with chronic liver disease as well as the positive effects of physical therapy upon the course of the disease, the psychological and general status of the patient.
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PMID:[Expert judgement of gastro-intestinal disease in Austrian social medicine (author's transl)]. 743 75

Several antibiotics can cause severe hepatic injury. It is the purpose of this paper to review the main antibiotics that can cause hepatic injury and discuss the presentation, pattern, and outcome of hepatic injury. In the case of the penicillins, the combination amoxycillin-clavulanate and the penicillinase-resistant penicillins oxacillin, (di-)cloxacillin, and flucloxacillin can cause (mainly cholestatic) hepatitis. Cephalosporins have little hepatotoxicity; ceftriaxone can cause drug-induced gallstones. The potential of erythromycin and several other macrolides to cause (usually cholestatic) hepatitis is well established. Tetracyclines can cause a syndrome mimicking acute fatty liver of pregnancy, but this complication has virtually disappeared. Quinolones seem to be able to cause cholestasis. Sulfamethoxazole/trimethoprim can cause severe hepatotoxicity, especially in patients with acquired immunodeficiency syndrome (AIDS). Finally, nitrofurantoin can cause acute cholestatic and hepatocellular reactions as well as chronic hepatitis mimicking chronic auto-immune hepatitis.
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PMID:Hepatotoxicity of antibiotics. 749 42


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