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)

16 patients (14 males, 2 females, mean age: 59.2 years) underwent sonographic-guided ethanol injections as treatment for 23 hepatocellular carcinomas (HCC) complicating cirrhosis. All lesions were pathologically proven by sonographic-guided cytology. Tumor sizes ranged from 9 to 66 mm. Sterile 96% alcohol was injected with a 17.7 cm-long 22 gauge spinal needle at one week intervals. At each session, 8-50 ml was injected depending on the diameter of the tumor. We regarded as a "success" the negativation of the cytologies one, two and three months after the end of the treatment associated with normalization of alpha-fetoprotein levels and typical echographic and tomodensitometric changes. No serious complication was associated with the procedure. In the "Child A" group1, 6 of 7 tumors have been successfully treated, the largest measuring 66 mm. The seventh lesion is currently being treated. In the "Child B" group1 3 of 6 lesions have been successfully treated. No success has been obtained in the "Child C" group. Volumes of alcohol greater than previously reported may be useful for lesions larger than 40 mm. Percutaneous alcohol injections can be considered as an alternative to surgery even for lesions larger than 50 mm. Among 4 patients presenting with 11 liver metastases of colic and gastric adenocarcinoma and 1 patient with a small bowel carcinoid tumor, one remission with a follow-up of 5 months was observed.
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PMID:[Percutaneous ethanol injection of malignant liver tumors under ultrasonographic guidance]. 165 40

The serum activity of alcohol dehydrogenase was determined in healthy controls and in patients with liver diseases. The mean activity in hepatoma (6.4 +/- 1.0U/L) was significantly higher (P less than 0.05) than the mean values in liver cirrhosis (2.7 +/- 0.5U/L); hepatitis (4.3 +/- 1.0U/L), obstructive jaundice (2.9 +/- 0.5U/L) and healthy controls (0.7 +/- 0.1U/L). Alcohol dehydrogenase purified by CM-cellulose chromatography from the sera of patients with hepatoma had a higher affinity for butanol long chain saturated and unsaturated alcohols than the purified enzyme from healthy controls. Similarly, hepatoma alcohol dehydrogenase oxidized ethanol very poorly (KM = 154 microM) when compared with that from healthy controls (KM = 40.2 microM). Hepatoma alcohol dehydrogenase was inhibited by pyrazole while those of other liver diseases and the healthy controls were not. These properties of serum alcohol dehydrogenase may prove useful in the early diagnosis of hepatoma since biochemical changes occur before morphological changes in the development of cancer.
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PMID:Properties of serum alcohol dehydrogenase in Nigerians with primary hepatoma. 166 17

Neuropsychological deficits including dementia in some alcoholics may potentially result from progressive, submicroscopic loss of synaptic receptors in the absence of morphological lesions. The densities of two types of synaptic receptors were determined in autopsy brain homogenates from several brain regions of not grossly demented alcoholics and non-alcoholic controls. In alcoholics, muscarinic cholinergic receptors were decreased by 40% in frontal cortex, temporal cortex and putamen and by 30% in hippocampus. Benzodiazepine receptors were decreased by 30% in hippocampus and by 25% in frontal cortex but not in temporal cortex or putamen. These changes occurred in histologically normal brains in the absence of Wernicke's encephalopathy, coma, liver cirrhosis and cholinergic or benzodiazepine medications. A computer data base matched for differences in death-autopsy time intervals, age and hypoxia. We conclude that chronic exposure to alcohol results in a loss of synaptic receptors with their synapses. To what extent such receptor losses could result in impairment of cognitive function is currently unknown but will depend on other factors such as the availability of spare receptors and what subtypes of receptors are involved. A rationale may emerge for using in alcoholics the cholinergic treatments currently being developed for the cognitive deficits of Alzheimer's disease.
Alcohol Alcohol Suppl 1991
PMID:Loss of synaptic receptors can precede morphologic changes induced by alcoholism. 166 10

A biologic role of ethyl alcohol is analysed. The function of the liver in alcohol metabolism (90% of the total intake) in three oxidizing systems with the use of alcohol dehydrogenase, microsomal ethanol oxidizing system, and H2O2 catalase is described. Epidemiological data are given, clinical course of the alcohol-produced lesions to the liver starting from fatty degeneration, through the acute and chronic hepatitis, alcohol-produced cirrhosis up to the primary cancer of the liver are also presented in the light of authors experience.
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PMID:[Alcohol and the liver]. 166 43

The study was aimed at analysing the epidemiological structure of patients with liver cirrhosis without HBsAg treated in 1980-1988. There were 231 of such cases in this period of time. The most frequent cause of liver cirrhosis in patients under 60 years of life was chronic alcoholism whereas 40% of the diagnosed liver cirrhosis in older persons was of unclear etiology. Patients complaints, clinical examinations, and results of the laboratory tests were analysed. The course of the disease was more severe in alcohol-produced liver cirrhosis leading to the haemorrhage from esophageal varices in 36%, and coma in 8% of cases. Alcohol-produced liver cirrhosis promoted other complications such as: cancer of the liver, hepato-renal syndrome or encephalopathy. Liver cirrhosis of unclear etiology in the elderly may be a consequence of the prolonged exposition to environmental pollutants. More severe course of alcohol-produced liver cirrhosis may depend on simultaneous action of two harmful factors: alcohol and environmental pollutants.
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PMID:[The course of liver cirrhosis not preceded by viral hepatitis with p articular reference to toxic etiology]. 166 47

Immune system derangement in cirrhotic patients with evidence of malnutrition is a well-recognized characteristic of chronic alcohol abuse. However, in vitro studies on cellular immune function performed with lectin mitogens have produced conflicting results. The recent development of more accurate immunological techniques for studying lymphocyte transformation, that use monoclonal antibodies directed against surface structures (CD3 and CD2) involved in antigen recognition, as well in adhesion functions, prompted us to study discrete in vitro T-cell hypo-responsiveness in a series of alcoholic liver disease (ALD) patients with no evidence of malnutrition or hepatic cirrhosis. The results indicated that the CD2 pathway is markedly defective in ALD T lymphocytes, accompanied by reduced interleukin-2 (IL-2) receptor expression upon in vitro activation. This defect cannot be reversed by the addition of recombinant IL-2 (rIL-2) or rIL-1. Faulty intracellular signal transduction by protein kinase C (PKC) and defective intracellular Ca2+ mobilization may be responsible for the CD2 pathway impairment. The addition of small amounts of phorbol 12-myristate, 13-acetate, but not Ca2+ ionophore A23187, is able to overcome the defect, thereby suggesting a direct PKC involvement. The hypothesis of a direct ethanol effect on transmembrane signal transduction systems is suggested by the demonstration of an expansion of circulating virgin (naive) T cells (CD3+/UCHL1-low) that binds tyrosine phosphatase (CD45RA antigen) on their surface.
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PMID:T-lymphocyte activation pathways in alcoholic liver disease. 167 85

(1) Liver cirrhosis was induced in male rats by treatment with carbon tetrachloride and phenobarbitone for 130-142 days. Detailed histological examination showed all livers from rats treated with carbon tetrachloride had annular fibrosis, necrosis, loss of normal hepatic architecture and other features that were consistent with an established micronodular cirrhosis. (2) Plasma biochemical analysis showed a significant reduction in total protein concentration (13%), which was due entirely to a reduction in plasma albumin (29%). There were also large increases in the plasma activities of alkaline phosphatase (110%) and aspartate aminotransferase (159%), when compared to phenobarbitone-treated controls. Plasma cholesterol was also increased (67%), but other plasma analytes were not significantly altered. (3) The soleus (Type I), plantaris (Type II) and gastrocnemius (Types I and II) muscles were dissected and examined for possible differential effects. There were minor reductions in all three muscle weights, but these changes did not reach statistical significance. The protein, RNA and DNA concentrations, total muscle content and content relative to body weight in cirrhotic rats were also not significantly altered in any of the muscles. Cirrhosis did not cause any perturbations in derived parameters, i.e. amount of synthetic apparatus per cell, RNA/DNA ratio, apparent cell size, protein/DNA ratio and the capacity for protein synthesis or RNA/protein ratio. (4) The gastrocnemius was fractionated into soluble, stromal and myofibrillar proteins. The concentrations and contents of all three proteins were unaltered in cirrhotic animals, compared to controls. (5) It is concluded that in this experimental model of cirrhosis there were no effects on those skeletal muscle variables which are strikingly altered by chronic alcohol feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Alcohol 1990
PMID:Liver histology, blood biochemistry and RNA, DNA and subcellular protein composition of various skeletal muscles of rats with experimental cirrhosis: implications for alcoholic muscle disease. 170 23

In vitro models have shown that metabolites of ethanol (acetaldehyde and lactate) stimulate collagen synthesis, thereby, suggesting that they may be important as fibrogenic mediators. The relevance of these findings for fibrogenesis in the human liver in vivo, however, has not as yet been demonstrated. Serum markers for collagen (PIIINP, using radioimmunoassays employing polyclonal antibodies and Fab-fragments (PIIINP-Fab), respectively) and basement membrane (laminin) metabolism were therefore investigated in 25 alcoholic cirrhotics (Pugh-Score: 6.7 +/- 1.9 S.D.) and in 19 comparable nonalcoholic cirrhotics (Pugh-Score: 6.3 +/- 1.5, n.s.) with only slight evidence for inflammation: GOT 28 +/- 22 vs. 24 +/- 21 U/l; GPT 24 +/- 23 vs. 31 +/- 28 U/l; gamma-globulins 24 +/- 8 vs. 22 +/- 5%, respectively (all n.s.). Severity of the disease was assessed by quantitative liver function tests. Levels of PIIINP, PIIINP-Fab and laminin measured by RIA were 21 +/- 19 micrograms/l, 90 +/- 42 micrograms/l and 2.5 +/- 0.8 U/ml in alcoholic cirrhosis and 10 +/- 6 micrograms/l, 61 +/- 10 micrograms/l and 1.9 +/- 0.4 U/ml in nonalcoholic cirrhosis, respectively (all p less than 0.01). Differences on PIIINP and PIIINP-Fab remained significant even after accurate matching for galactose elimination capacity, aminopyrine breath test and hepatic sorbitol clearance. Laminin levels were higher in alcoholic cirrhosis only after matching for the hepatic sorbitol clearance (p less than 0.01). The higher levels of serum markers for collagen and basement membrane metabolism in alcoholic vs. nonalcoholic patients with cirrhosis at equal severity of the disease and with only minimal signs of inflammation may be the clinical reflection of a specific fibrogenic effect of ethanol metabolites.
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PMID:Higher levels of serum aminoterminal type III procollagen peptide, and laminin in alcoholic than in nonalcoholic cirrhosis of equal severity. 173 19

We carried out a hospital based case-control study involving 655 patients with chronic liver disease encompassing chronic hepatitis, asymptomatic liver cirrhosis and symptomatic liver cirrhosis and 655 pair-matched control individuals in order to estimate the dose-response relationship between alcohol consumption and the occurrence of chronic liver disease. Alcohol intake was measured by a questionnaire and expressed as Daily Alcohol Intake (DAI) during the patient life. DAI estimates from patient interviews were in good agreement with those obtained by interviewing a sample of relatives. We found an exponential positive association between DAI and the risk of chronic hepatitis and cirrhosis. However, consuming less than 100g of alcohol every day did not increase the risk of developing chronic liver disease. For asymptomatic cirrhosis the risk was lower than for chronic hepatitis, especially at high DAI, probably because high consumption carried a high probability of liver decompensation. For symptomatic cirrhosis, the risk function showed a similar pattern as for chronic hepatitis. Chronic hepatitis patients were 6-7 years younger than cirrhotics. Our results suggest that the evolution towards cirrhosis once a chronic liver damage has occurred is probably time-dependent, but not or minimally dependent on alcohol intake.
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PMID:A case-control study on alcohol consumption and the risk of chronic liver disease. 175 99

Epidemiological evidence suggests a direct relationship between alcohol consumption and the prevalence of cirrhosis. However, the observation that only 8-30% of alcoholics develop cirrhosis illustrates that individual susceptibility mediates the relationship between alcohol consumption and cirrhosis. This chapter examines the factors that may influence individual risk for alcoholic liver disease. These factors include individual differences in alcohol metabolism and consumption patterns, gender, HLA antigens, family alcoholism history, and immune responsiveness. Important methodological issues in each of these areas are addressed also. From the available evidence, the hypothesis is advanced that there is an underlying vulnerability to liver disease in some individuals, and that alcohol use, although a necessary condition, is not sufficient to trigger disease in all individuals.
Recent Dev Alcohol 1991
PMID:Vulnerability to alcoholic liver disease. 175 83


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