Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From these discussions, it is apparent that: Alcoholic liver disease is increasing at a rapid rate in conjunction with an increase of annual gross and per capita consumption of alcohol. Alcoholic hepatitis and alcoholic hyaline are much less common in Japan compared to western countries. Alcoholic hepatic fibrosis and chronic hepatitis are the common types of alcoholic liver disease in Japan. Alcoholic hepatic fibrosis may be a pathological process or entity independent of fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. It is not clear at the present time whether heavy alcohol consumption per se or non-A, non-B hepatitis virus is the cause of chronic hepatitis seen in HBsAg negative alcoholics.
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PMID:Alcoholic liver disease in Japan. 302 74

A novel lymphokine, which we have designated as cholestatic factor (CF), was produced from peripheral blood lymphocytes of patients with drug-induced allergic intrahepatic cholestasis by stimulation with a causative drug in the presence of the liver soluble fraction containing liver-specific lipoprotein (LSP). Marked reductions in bile flow and bile acid excretion were induced in rats by injecting CF through a mesenteric vein. In order to confirm the presence of CF in the liver tissue of patients, we attempted to detect this lymphokine by using the enzyme-labelled antibody method. As a result, CF was found in the liver tissue of eleven out of thirty-eight patients with acute intrahepatic cholestasis including one with hepatitis A type, one with hepatitis B type, two with hepatitis non-A non-B type, five with drug-induced allergic hepatitis, one with alcoholic hepatitis and one with lupoid hepatitis. In contrast, CF was undetectable in the liver tissue of patients without intrahepatic cholestasis. These results may additionally support our assumption that CF plays an important role in the induction of intrahepatic cholestasis in various liver diseases.
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PMID:Detection of the cholestatic factor in the liver tissue of patients with acute intrahepatic cholestasis. 311 34

Elevated neopterin levels in blood or urine have been shown to be a marker for the activation of cell-mediated immunity in vitro and in vivo. To evaluate whether neopterin levels are elevated in patients with acute viral hepatitis, we measured urinary levels in 13 patients with hepatitis A, 26 with hepatitis B, 12 with non-A, non-B hepatitis, 8 with jaundice and/or cholestasis due to biliary and pancreatic disorders and 3 with alcoholic hepatitis and in 62 apparently healthy HBsAg carriers. Neopterin levels in patients with virus-induced hepatitis were significantly higher than those in patients with other diagnoses. Urinary neopterin levels were above normal in 49 of 51 patients with viral hepatitis and elevations during the course of hepatitis showed a pattern similar to that of the usual liver biochemical tests, suggesting that neopterin levels were related to the clinical activity of the viral disease. In patients with nonviral biliary and hepatic disorders, neopterin levels were usually normal and did not correlate with other liver biochemical tests. These findings suggest that cell-mediated immune mechanisms are activated during viral hepatitis and that neopterin measurement may be of value as an additional surrogate marker for non-A, non-B hepatitis.
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PMID:Urinary neopterin levels in acute viral hepatitis. 313 81

Liver biopsies from nine patients with maturity-onset diabetes and fatty liver hepatitis were semiquantitatively assessed, and the findings compared with those in alcoholic hepatitis. Overall appearances were similar, but the lesion in some diabetics was periportal rather than perivenular in location, and nuclear vacuolation of hepatocyte nuclei was always present. The inflammatory infiltrate often included neutrophil leucocytes, as in the alcoholic. In three patients with multiple biopsies, progression appeared to be slow, but one patient developed cirrhosis.
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PMID:The pathology of diabetic hepatitis. 263 85

The role of endotoxin in the pathogenesis of progressive liver disease is receiving increasing attention, but remains controversial. Similarly, although alcoholic hepatitis is now recognized as the transitional link between alcoholic fatty liver and advanced alcoholic liver disease, the aetiology of liver cell necrosis in alcoholic hepatitis is not known. Rats fed a nutritionally adequate liquid alcohol diet according to the formula of Lieber and DeCarli developed fatty livers. Littermates fed an identical diet and challenged with small IV doses (1 microgram/g body weight) of E. coli lipopolysaccharide endotoxin (LPS) developed focal necrotizing hepatitis. Control littermates fed an identical calorie balanced but alcohol free diet and challenged with identical doses of LPS did not develop any liver lesions. The hepatocyte necrosis with associated inflammatory changes induced by LPS in fatty livers has some features of early human alcoholic hepatitis and suggests that progressive alcohol induced damage may be multifactorial in origin.
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PMID:Endotoxin induced hepatic necrosis in rats on an alcohol diet. 330 47

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.
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PMID:Fatty liver disease in morbid obesity. 331 4

Patients suffering from rheumatoid arthritis, spondylosis, coxarthrosis, ankylosing spondylitis, chronic active and chronic alcoholic hepatitis were studied. The plasma vitamin E content remained unchanged. The TBA-reactive plasma substances (malondialdehyde) content of plasma increased in all patients except those with ankylosing spondylitis. Catalase activity of plasma increased in patients of both sexes suffering from rheumatoid arthritis and spondylosis and coxarthrosis, but decreased in the two hepatitis groups. The glutathione-peroxidase activity of RBC (1:9 haemolysate) increased in female rheumatoid arthritis patients and decreased in those suffering from chronic alcoholic hepatitis. The results showed that chronic inflammatory processes affect the rate of lipid peroxidation and the activity of the biological antioxidant mechanism.
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PMID:Vitamin E content and lipid peroxidation of blood in some chronic inflammatory diseases. 359 51

Patients with chronic heart failure (CHF) can often develop such diseases as hepatitis of viral etiology, alcoholic hepatitis, drug affection of the liver and other diseases masked as congestive liver. In most cases CHF concomitant liver diseases have an atypical course with a tendency to a chronic course. CHF is one of the important pathogenetic mechanisms lying in the basis of chronicity of concomitant liver diseases. Refractory CHF, inconsistency of the hemodynamic indices of persistent hepatomegaly must lead a physician to the detection of probable independent liver diseases complicating the syndrome of heart failure. CHF is a factor causing an enhanced fibrosing liver reaction. An important diagnostic test of fibrinogenesis lying in the basis of chronicity of liver diseases, is the determination of enzymatic markers reflecting synthesis and catabolism of the main substance of connective tissue. Change in the levels of haptoglobin, ceruloplasmin and glutamic acid dehydrogenase is an indirect sign of damage of the liver parenchymal endoplasmic reticulum. These indices can serve as differential criteria of the prevalence of cardiovascular disorders in the liver or concomitant independent liver diseases.
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PMID:[Pathogenetic mechanisms of chronicity in liver diseases in patients with circulatory failure]. 361 41

Defective regulation of neutrophil chemotaxis occurs in patients with alcoholic liver disease. One potent mediator of neutrophil chemotaxis is the complement-derived neutrophil chemoattractant, C5a, which can be inhibited by a serum protein, chemotactic factor inactivator. We hypothesized that chemotactic factor inactivator elevation might, in part, explain the defective neutrophil chemotaxis seen in patients with alcoholic hepatitis. To test this hypothesis, sera were collected from 22 patients with alcoholic hepatitis and 9 normal controls, and evaluated for the antigenic presence of chemotactic factor inactivator using an ELISA test. Chemotactic factor inactivator levels were found to be markedly elevated in patients with alcoholic hepatitis (162 +/- 24 micrograms per ml) compared to normals (60 +/- 3 micrograms per ml, p less than 0.01). Subdividing the hepatitis patients revealed that the elevation of chemotactic factor inactivator was found to be greatest in those patients with mild alcoholic hepatitis (prothrombin time within normal limits and bilirubin less than or equal to 5 mg per dl, 256 +/- 44 micrograms per ml, p less than 0.001), while the group with the severest hepatic dysfunction (prolonged prothrombin time and bilirubin greater than 5 mg per dl) did not differ significantly from controls (71 +/- 11 micrograms/ml, p less than 0.2). Importantly, the inhibition of C5a-induced chemotactic activity by partially purified chemotactic factor inactivator correlated with antigenic amounts of chemotactic factor inactivator in serum (r = 0.63, p less than 0.05). The C5a inhibitory activity in sera obtained from patients with alcoholic hepatitis coprecipitated with chemotactic factor inactivator when serum was precipitated by ammonium sulfate precipitation (45 to 64% saturation).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevation of chemotactic factor inactivator in alcoholic liver disease. 365 52

As free radicals and lipid peroxidation are involved in the pathogenesis of different inflammatory diseases of the liver, the blood malondialdehyde content, the activity or quantity of free radical eliminating enzymes and the natural antioxidant, vitamin E serum level has been studied in ten patients with chronic active hepatitis and in six subjects with alcoholic liver disease. Thirty healthy volunteers served as controls. The serum malondialdehyde/thiobarbituric acid reactive substance and its concentrations increased significantly in both hepatitis groups. The superoxide dismutase content was also raised in the patients' sera. The serum glutathione peroxidase (GSH-Px) activity was decreased in both groups, while the red blood cell GSH-Px showed a significantly lower activity in the alcoholic hepatitis patients. Serum catalase activity and vitamin E levels in both types of chronic hepatitis were not significantly different from the healthy controls.
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PMID:Studies of the blood lipid peroxide status and vitamin E levels in patients with chronic active hepatitis and alcoholic liver disease. 375 86


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