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)

In a group of 34 chronic alcohol addicts with neuropsychic manifestations--alcoholic encephalopathy (AE)--and 9 subjects with chronic non-alcoholic liver diseases, biochemical (ammonemia, pyruvicemia, lactacidemia), enzymatic (gamma-glutamyltranspeptidase (gamma-GPT)) and morphological assays were carried out comparatively with conventional liver investigations. Alcoholic liver disease was found present in 16 patients (47%). A peculiar biochemical profile was observed in subjects with hepato-alcoholic encephalopathy: ammonemia 191.3 +/- 70.3 gamma %, pyruvicemia 2.7 +/- 0.82 mg %, lactacidemia 15.76 mg % and gamma-GPT 80.5 U/l, as compared with ammonemia 121 +/- 33.5 gamma %, pyruvicemia 2.74 +/- 1.2 mg %, lactacidemia 16.65 mg % and gamma-GPT 42.6 U/l in AE without hepatic disease, and in non-alcoholic liver diseases in which ammonemia was 88.6 gamma % (in chronic hepatitis) and 126.3 gamma % (in hepatic cirrhosis). Thus, coexisting involvement of the liver and presence of portal-systemic shunts in AE can be estimated by the assay of certain biochemical and enzymatic parameters.
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PMID:The hepatic component in alcoholic encephalopathy. 712 7

Alcoholic liver disease represents about 15% of all indications for liver transplantation. Patient selection is difficult, and must be rigorous. Peri-operative risks are evaluated on the same basis as for other chronic liver diseases, with special attention for alcoholic extra-hepatic morbidity and nutritional status. Definite withdrawal from alcohol is mandatory. Predictive factors of long-term abstinence are the absence of psychopathologic state, an adequate social and affective situation, the possibilities of professional reinsertion, and a strong motivation of the patient towards liver transplantation. A six-month period of complete abstinence before registration on a liver transplantation waiting list is not mandatory, although intermittent alcoholic abuse before transplantation should be an exclusion factor. Liver transplantation must be proposed based on the severity of liver failure, as assessed by pronostic scores. It must be rapidly discussed following an acute episode of decompensation, in the absence of a significant improvement despite adequate medical therapy. It must also be discussed for long-term abstinent patients, with an apparently stabilized cirrhosis, but with an important decrease of the functional liver mass. The evaluation of the functional liver mass is based upon the Child-Pugh score, associated with the results of metabolic liver function tests, the measurement of the hepatic volume and the severity of portal hypertension.
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PMID:[Liver transplantation for alcoholic liver disease. Selective indications]. 763 19

Morphological changes in liver biopsies from 40 alcoholic patients were studied, 20 of which being ordinary alcoholics (40-80g ethanol/day) and the other 20 being heavy drinkers (above 80g ethanol/day for over 20 years). All being male who have neither type B nor type C hepatitis. The basic morphological changes observed being: 1. Liver cell degeneration including fatty degeneration & focal ballooning, decrease in liver cell size, occasional giant mitochondrion and Mallory's body formation. 2. Focal necrosis with neutrophil infiltration. 3. Pericellular fibrosis of liver cells, hepatic fibrosis and early cirrhosis. Alcoholic liver disease can be divided into 5 types: I. alcoholic fatty liver (AFL), II. alcoholic hepatitis (AH), III. alcoholic hepatic fibrosis (AHF), IV. alcoholic liver cirrhosis (ALC), V. slight alcoholic liver disease (SALD). The degree of liver damage (liver cell necrosis and hepatic fibrosis) is closely related to the amount of daily ethanol intake. The progression of liver damage observed in our study is much milder than reports from Europe, the U.S. and Japan.
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PMID:[Morphological study on 40 cases of alcoholic liver disease]. 804 54

While there are no liver diseases specific to advanced age, the presentation, clinical course and management of liver diseases in the elderly may differ in important respects from younger individuals. The management of older patients with specific liver diseases should be informed by these differences. Alcoholic liver disease presents at a more advanced stage, drug induced liver disease and viral hepatitis may also be more severe. It is increasingly recognised that primary hepatocellular cancer arises in elderly cirrhotics regardless of the etiology of the cirrhosis, the risk highest in hemochromatosis and cirrhosis arising from hepatitis B and C.
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PMID:Liver disease in the elderly. 807 21

Alcoholic liver disease (ALD) is one the most serious consequences of chronic alcohol abuse. Liver cirrhosis, the culmination of the illness, is one of the leading causes of death in Western countries. Mitochondria are a target of ethanol intoxication mainly due to the toxic effects of acetaldehyde, a byproduct of ethanol metabolism. Morphological and functional changes in mitochondria are one of the key hallmarks of chronic ethanol exposure in both chronic alcoholics and experimental models of alcoholism. The functional changes observed in mitochondria from ethanol-treated animals are translated in an overall decrease in ATP levels resulting from a lower rate of ATP synthesis as a consequence of impaired processing at the translational level of some components of oxidative phosphorylation encoded by mitochondrial DNA genome. Mitochondrial glutathione (GSH) plays a critical role in the maintenance of cell functions and viability and in mitochondrial physiology by metabolism of oxygen free radicals generated in the respiratory chain. GSH in mitochondria originates from cytosol by a transport system which translocates GSH into the matrix. This transport system is impaired in chronic ethanol-fed rats, which translates in a selective and significant depletion of the mitochondrial GSH content resulting in the development of an increased susceptibility to oxidant stress. Using the intragastric infusion model of experimental ALD in rats, the profound and selective mitochondrial GSH depletion precedes the onset of alcoholic liver disease, mitochondrial lipid peroxidation, and progression of liver damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial glutathione depletion in alcoholic liver disease. 812 2

The aim of our work was to study the prevalence of HBV markers in Alcoholic Liver Disease (ALD) by evaluating clinical and biochemical parameters that could further characterize the association. A prospective and sequential study of 107 patients with ALD was performed, including 83 cases of cirrhosis and 24 cases of alcoholic hepatitis. Daily ingestion of pure ethanol was of at least 70 gm for seven years or more and always associated with hepatocellular disfunction. According to the serological profile for HBV markers the patients were allocated to one of four groups: group I infected (positivity of HBsAg and anti-HBc); group II immunized (positivity of anti-HBs and anti-HBc); group III without HBV markers (negativity of HBsAg, anti-HBc and anti-HBs); group IV isolated anti-HBc. The prevalence of HBsAg positivity in ALD was high: 15.89% whereas immunity was low: 26.17% suggesting a great exposure to the virus and a deficient immunological response. No significant statistical differences were found among the three groups when clinical and biochemical parameters were individually considered. Nevertheless, when a Child/Campbell classification was applied, patients with ALD associated with HBV (group I) showed a significant difference, presenting a predominance of child C, with a bad prognosis.
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PMID:[The hepatitis B virus in alcoholic liver disease: its clinical and biochemical assessment]. 815 19

Many of the extrahepatic manifestations of alcoholic liver disease are not specific and can be seen in other forms of cirrhosis and with alcohol abuse. Features that are more common or more florid in patients with alcoholic liver disease have been discussed in this chapter. Alcoholic liver disease results in changes in many systems in the body and it is important that these are recognized and treated where appropriate.
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PMID:Extrahepatic manifestations of alcoholic liver disease. 821 6

Alcoholic liver disease is a major cause of liver disease and has become an ever-increasing indication for liver transplantation (LTx). Follow-up studies have reported a higher rate of alcohol recidivism in patients transplanted for alcoholic hepatitis, compared with those transplanted for endstage alcohol-associated cirrhosis. It is assumed widely that recurrent alcohol use is associated with reduced compliance with immune suppression and, as a result, an increased risk of graft rejection and loss. To assess this question, 209 alcoholic patients transplanted for either alcoholic hepatitis with cirrhosis or cirrhosis alone between January 1, 1986 and December 31, 1991 were followed, with a mean follow-up of 4.4 +/- 0.6 years. There were 175 episodes of acute cellular rejection (ACR) that occurred in 137 patients, for an overall rejection rate of 83.7% or at a rate of 1.25 episodes/patient with rejection. The rate of ACR was three times as great in those who remained alcohol-abstinent (2.24 episodes/patient), compared with those who admitted to continued alcohol use (0.75 episodes/patient) (p < 0.01). A total of 33 episodes of chronic rejection occurred in 26 patients, for an overall rate of 12.4%. As was the case for ACR, the chronic rejection rate was greater among those who were continuously alcohol-abstinent, compared with those who intermittently used alcohol after successful LTx. There were no differences in the mean FK 506 or cyclosporin A levels in the groups with and without a rejection episode at the time the rejection episode was documented by liver biopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of alcohol use on allograft rejection rates after liver transplantation for alcoholic liver disease. 856 Dec 84

Alcoholic liver disease encompasses three main forms of liver injury: fatty change, alcoholic hepatitis and cirrhosis. However, there are many other types of injury, including perivenular fibrosis, venous occlusive lesions, microscopic cholangitis and chronic active hepatitis. The pathological spectrum is reviewed in this paper, and the contribution of other injurious agents to the pathological features is identified. Alcoholic liver disease can be mimicked by a variety of non-alcoholic liver diseases. However, features such as fatty liver with perivenular fibrosis, giant mitochondria, spotty hepatocyte necrosis, Mallory bodies, a micronodular pattern of cirrhosis, and iron deposition are strongly suggestive of an alcoholic aetiology. Correlation of clinical findings, and especially the alcohol history, and histopathological factors is necessary for the definitive diagnosis.
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PMID:Pathological spectrum of alcoholic liver disease. 897 50

Alcoholic liver disease evolves from fatty change through alcoholic hepatitis to alcoholic cirrhosis. Its development is associated with an excess mortality both in relation to the presence of liver disease and to other complications of alcohol abuse. In the majority of patients fatty liver is a benign lesion which will reverse completely following abstinence from alcohol. Continued drinking is associated with the eventual development of cirrhosis in approximately 20% of individuals. Survival rates of 70% are reported both at 2 years and at 10 years. Alcoholic hepatitis is a precirrhotic lesion; progression to cirrhosis is observed more commonly in women, in individuals with severe disease and in those who continue to drink. Thirty-day mortality rates of less than 20% are observed in patients with mild to moderate disease but exceed 40% in individuals with severe liver injury. Corticosteroids may improve short term survival in a small subgroup of patients with severe alcoholic hepatitis. Survival rates of 55 to 60% are reported both at 2 years and at 10 years. Survival is significantly reduced in women and in the elderly and is adversely affected by the presence of severe liver injury, evolution to cirrhosis and continued drinking. Two-thirds of patients with alcoholic cirrhosis present with decompensated disease; 15% will develop hepatocellular carcinoma. Survival rates at 5 years vary from zero to 80%; 60 to 90% of individuals die of their liver disease. Survival is adversely affected by the presence of decompensated disease, superimposed alcoholic hepatitis, continued drinking and the development of hepatocellular carcinoma. The advent of hepatic transplantation, which has a 5-year survival rate in excess of 70%, will influence these survival figures.
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PMID:The prognosis and outcome of alcoholic liver disease. 897 53


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