Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic alcohol consumption results in early biochemical and ultrastructural alterations of the hepatocyte which in turn may lead to alcoholic fatty liver as well as alcoholic hepatitis and via the central hyaline sclerosis to fibrosis and cirrhosis of the liver. Already at the stage of the alcoholic fatty liver an isolated increase of serum gamma-glutamyltransferase activity can often be observed; it results from hepatic microsomal enzyme induction and may facilitate early recognition of alcoholic liver injury. To establish the diagnosis, however, a histological examination of the liver is necessary. The therapy of alcohol-induced liver injury is based upon an absolute alcohol abstinence since alcohol itself or one of its metabolites are hepatotoxic.
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PMID:[Clinical aspects of alcohol induced liver injury (author's transl)]. 35 67

Alcoholic steatosis was associated with sclerosis around the terminal hepatic venules in liver biopsies of 40% of chronic alcoholics but not in those of moderate drinkers. To determine whether this sclerosis could be a precursor lesion of cirrhosis, controlled studies were performed in animal models. In the alcohol-fed baboons that developed fibrosis or cirrhosis, progressive perivenular sclerosis invariably started at the fatty liver stage before or even more commonly in the absence of alcoholic hepatitis. No sclerosis occurred in controls or in alcohol-fed baboons and rats that did not progress beyond the fatty liver stage. The clinical and experimental data indicate that sclerosis around the terminal venules, a common but often overlooked complication of alcoholic fatty liver, reflects heavy prolonged drinking, and may identify those patients who are susceptible to develop the more advanced lesions of alcoholic liver injury upon continued drinking.
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PMID:Early perivenular sclerosis in alcoholic fatty liver: an index of progressive liver injury. 40 18

Consecutive liver biopsies from alcoholic, diabetic and overweight patients are compared morphologically and in addition a comparison is made between groups with a combination of two or three of the above conditions. Both fatty change and morphological activity are greater in the groups with alcoholism, and this gives good reason to believe that the activity in the form of alcoholic hepatitis is the cause for the more common development of cirrhosis in alcoholic fatty liver than in fatty liver with other aetiology.
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PMID:Morphological features in non-cirrhotic livers from patients with chronic alcoholism, diabetes mellitus or adipositas. A comparative study. 71 11

Alcoholic liver damage is only produced by constant alcohol intake. Close dose and time relationships are apparent. For many years, alcoholic fatty liver is the only noticeable alteration. It is completely reversible in 2-4 weeks when ethanol intake is stopped. After about 6 years of chronic abuse alcoholic hepatitis may develop. Once established it progresses within weeks or months to cirrhosis if ethanol intake is not discontinued. On the other hand, alcoholic hepatitis heals under complete abstenence from alcohol with unimportant fibrosis. After over-indulgence in alcohol over a period of 22 years, there is a 50% probability of cirrhosis. This shows clearly that the resistance of the liver to alcohol varies considerably in different individuals. Even in early stages of alcoholic cirrhosis the prognosis is reasonable. If these patients observe complete abstenence from ethanol, their life expectation is only slightly different from the average of the population. The extent of the consumption of alcohol is of decisive importance for the development of cirrhosis. New and very careful investigations reveal that the susceptibility to alcohol is different in both sexes. For men the danger level would thus appear to be around 60 g and for women around 20 g of pure alcohol a day. Beyond these critical levels the morbidity of cirrhosis multiplies almost in geometric progression with increasing amounts of ethanol.
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PMID:Alcohol consumption and diseases of the liver. 91 49

Alcoholism is the most common form of drug abuse and alcoholic liver disease is a major health problem which in terms of increasing incidence is only rivaled by viral hepatitis. Cirrhosis of the liver, most of which is probably alcoholic, is among the leading causes of morbidity and mortality between the ages of 25 to 65 in Western countries. Alcoholic liver disease includes adaptive and toxic ultrastructural alterations, alcoholic fatty liver, alcoholic hepatitis and alcoholic cirrhosis, later accompanied by hepatoma.
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PMID:[Biochemical and clinical aspects of alcoholic liver damage]. 100 21

To assess whether the hepatitis C virus plays an important role in Chinese patients with acute and chronic liver disease, antibodies to HCV (anti-HCV) were measured by enzyme immunoassay in 67 patients with type A and B acute viral hepatitis, 165 patients with non-A, non-B (NANB) hepatitis, 438 patients with chronic hepatitis, 200 patients with postnecrotic liver cirrhosis, 72 patients with alcoholic liver disease, 55 patients with non-alcoholic fatty liver, 24 patients with toxic and drug-induced hepatitis, and 20 patients with other chronic liver diseases. Anti-HCV was not detected in sera from patients with type A and B acute viral hepatitis, toxic and drug-induced hepatitis, primary biliary cirrhosis, Wilson's disease, or lupoid hepatitis. The anti-HCV prevalence was found to be highest in patients with NANB hepatitis (59% in sporadic and 73.2% in transfusion-associated), 16.4% in non-alcoholic fatty liver, 5.6% in alcoholic liver disease, 6.8% in chronic hepatitis, and 16% in postnecrotic liver cirrhosis. In patients with chronic hepatitis, the anti-HCV prevalence was significantly higher in HBsAg-negative (15/34, 44.1%) than in HBsAg-positive cases (15/404, 3.7%; P less than 0.0001). The results indicate that HCV is a major agent of NANB hepatitis and plays an important role in HBsAg-negative chronic liver disease in Taiwan.
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PMID:Prevalence of anti-HCV among Chinese patients with acute and chronic liver disease. 131 64

The pharmacokinetics of trapidil (Rocornal, Deutsches Hydrierwerk Rodleben GmbH) were studied in 15 patients with chronic liver disease (12 patients with hepatic cirrhosis, 2 patients with alcoholic fatty liver, one patient with liver fibrosis). Trapidil was given orally (200 mg, Rocornal dragees 100 mg) as well as intravenously (100 mg) in random order. Serum samples were analyzed for trapidil by HPLC. The pharmacokinetic parameters were compared with the parameters of 12 healthy volunteers, investigated by Weiss [1991]. Total plasma clearance was decreased significantly in patients with hepatic cirrhosis (99.6 ml/min vs 273.1 ml/min in controls and 255.3 ml/min in patients with non cirrhotic liver disease). However, there was no difference in clearance between patients with compensated and patients with decompensated cirrhosis. Clearance and aspartate aminotransferase activity correlated inversely. In addition, in some of the patients suffering from portal hypertension delayed absorption was observed, but the difference did not reach statistical significance. The volumes of distribution were significantly lower in patients with non alcoholic cirrhosis (19.9 l vs 36.8 l in controls and 41.0 l in patients with alcoholic cirrhosis). It might be concluded from this study, that dosage adjustments are necessary in treatment of patients with cirrhosis. In patients suffering from portal hypertension an intravenous administration should be prefered.
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PMID:Pharmacokinetics of trapidil (Rocornal) in patients with chronic liver disease. 149 Aug 1

Malondialdehyde (MDA) level was determined spectrophotometrically with thiobarbituric acid method on 50 healthy persons and 160 patients with alcoholic and nonalcoholic liver diseases. Alcoholics without liver damage show normal plasma MDA values. Alcoholic fatty liver, alcoholic hepatitis and alcoholic liver cirrhosis cause an increase of MDA values. The highest concentrations of MDA were found on patients with acute virus hepatitis. Also noninfectional hepatitis and nonalcoholic liver cirrhosis showed an elevated MDA-Level. Liver damage and lipid peroxidation are considered as closely connected processes.
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PMID:[Malondialdehyde concentration in blood plasma of patients with liver diseases]. 164 26

Hepatic glutathione (GSH) S-transferase (GST) activity and the tissue distribution of a cationic GST were investigated in biopsy liver samples obtained from patients with alcoholic liver diseases. GST activities in alcoholic fatty liver were significantly high, whereas those in cirrhosis were significantly low compared with normal liver. In fatty liver, immunohistochemically, the staining of the enzyme was strongly positive in hepatocytes around intensive fatty metamorphosis. Then, using experimental chronic alcohol-fed rats, the changes in hepatic GST and GSH peroxidase (GPx) activities and lipid peroxide (LPO) and GSH contents in alcoholic fatty liver were evaluated. Hepatic GST isoenzymes were analyzed and tissue distribution of cationic and neutral GSTs was also investigated. Liver GSH content decreased at two weeks and increased at six weeks. Liver LPO content was elevated at four and six weeks and cytosolic GPx activity was enhanced at four weeks. Cytosolic GST activity was enhanced at six weeks. The cationic and neutral GST isoenzyme pattern was unchanged compared with normal liver. Immunohistochemically, the distribution and intensity of the staining of GSTs were essentially unchanged. There was no evidence of an increase in the GST isoenzyme with selen-independent GPx activity. However, GSTs were strongly stained in the hepatocytes with fatty droplets. Thus, in alcoholic fatty liver, hepatic GST and GPx activities are thought to be enhanced by different mechanisms. The elevated GPx activity may relate to the production of LPO. However, the enhancement of GST activity may result from some other causes which include the enzyme induction.
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PMID:Glutathione S-transferase in alcoholic fatty liver. 177 80

Aggregation and derangement of cytokeratin intermediate filaments are thought to be the key mechanism in the formation of Mallory bodies in alcoholic liver disease (ALD). To study the incidence and patterns of intracellular distribution of aggregated cytokeratin and to determine its utility as a diagnostic marker of ALD, 108 liver biopsy specimens from patients with various liver abnormalities were examined by an avidin--biotin peroxidase complex technique on paraffin section using a monoclonal antibody to cytokeratins (Hybritech). In normal liver (n = 11), only bile duct epithelium was positive. Both bile ducts and hepatocytes were positive in pathologic livers (n = 97). In ALD, 82 per cent of cases (42 of 51) showed cytokeratin positivity versus 15 per cent (seven of 46) in nonalcoholic liver disease (e.g., chronic hepatitis, nonalcoholic cirrhosis, cholestasis, and primary biliary cirrhosis). The highest incidence (100 per cent, 37 of 37) of positivity was obtained in cases with alcoholic hepatitis and cirrhosis compared with only 36 per cent (five of 14) in alcoholic fatty liver. Mallory bodies were found by the immunoperoxidase method in 71 per cent of cases (30 of 42) versus in 40 per cent (17 cases) by hematoxylin--eosin stain. In alcoholic fatty liver and alcoholic hepatitis, centrilobular hepatocytes showed cytokeratin positivity, whereas such reactivity was seen predominantly at the periphery of the regenerative nodules in alcoholic cirrhosis. A rare periportal hepatocyte was positive in the nonalcoholic group. These findings suggest that the differential distribution patterns of aggregated cytokeratin may be helpful in differentiating alcoholic from nonalcoholic liver diseases.
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PMID:Distribution patterns of cytokeratin antigen determinants in alcoholic and nonalcoholic liver diseases. 243 6


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