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)

The incidence of primary liver cell carcinoma was investigated in a prospective study over 6 yr and 5 mo in 403 clinically unselected patients derived from a homogeneous population by means of serial determination of alpha 1-fetoprotein (AFP) by radioimmunoassay. The diagnosis of liver cirrhosis was proved in 90% by laparoscopy and/or histology and/or autopsy. The incidence of primary liver cell carcinoma in liver cirrhosis in the clinically studied patients was 4.47%, significantly lower than in the autopsy material (11.03%; p less than or equal to 0.025). In the follow-up study, all patients with increasing AFP concentrations exhibited a primary liver cell carcinoma. A transitory rise of AFP (higher than 50 ng/ml) was observed in 15.1% of patients with liver cirrhosis without primary liver cell cancer. In contrast to the results of animal experiments, this transitory rise of AFP was not followed by malignant transformation of the cirrhotic tissue. Posthepatitic liver cirrhosis was observed in 21.57%, postalcoholic liver cirrhosis in 42.93%, and cryptogenic liver cirrhosis in 27.30%. Liver cirrhosis of other etiology occurred in 8.19%. The incidences of primary liver cell cancer in these 4 groups were 4.94, 4.62, 5.45, and 0%, respectively. These differences are not statistically significant, although in absolute figures postalcoholic liver cirrhosis is the main cause of primary liver cell carcinoma in this sample from West Germany. HBs antigen-positive liver cirrhosis was more often associated with primary liver cell cancer than HBs antigen-negative liver cirrhosis (6.58 versus 3.96%); this difference also is not statistically significant. Observations of larger groups of patients may show a higher risk of developing primary liver cell carcinoma in those with a combination of alcohol abuse and HBs antigenemia and/or acute hepatitis in the history. Patients without these 2 risk factors had an incidence of primary liver cell carcinoma of 2.61%; those with 1 risk factor, 5.77%; and those with both risk factors, 10.71%.
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PMID:Etiology of human liver cancer: controlled prospective study in liver cirrhosis. 8 98

Possible mechanisms whereby alcohol abuse and alcohol-related diseases may promote the development of cancer are analyzed. The mechanisms discussed include: (a) contact-related local effects on the upper gastrointestinal tract; (b) the presence of low levels of carcinogens in alcoholic beverages; (c) induction of microsomal enzymes involved in carcinogen metabolism; (d) various types of cellular injury produced by ethanol and its metabolites and their relationship to cancer, particularly in the liver; (e) the nutritional disturbances frequently associated with alcohol abuse. The relationship between alcohol-induced cirrhosis and hepatocellular carcinoma is also discussed, and case histories of patients seen at the Bronx Veterans Administration Medical Center with hepatocellular carcinoma in the absence of cirrhosis are reviewed. Data are presented demonstrating the induction, by chronic ethanol consumption, of microsomal enzymes which convert procarcinogens to carcinogens. These data were derived from experiments in which the ability of microsomes isolated from liver, intestine, and lung tissues of ethanol-fed and control rats to activate several test carcinogens was examined in the Ames Salmonella-mutagenicity test. The hypothesis is presented that ethanol-mediated induction of enzyme systems which activate procarcinogens to carcinogens in various tissues contributes to the enhanced incidence of cancer in the alcoholic.
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PMID:Alcohol-related diseases and carcinogenesis. 22 Nov 10

Eleven patients with porphyria cutanea tarda were studied. Biochemical confirmation of the clinical diagnosis required only determination of the total urine porphyrin concentration in a sample of urine voided on rising in the morning. The patients were divided for convenience of discussion into four groups differing in age, sex and etiologic factors. Of the six patients in whom a liver biopsy was done one was shown to have micronodular cirrhosis. Except for a modest elevation in the serum glutamic oxaloacetic transaminase values when the patients were first seen, no evidence was found for liver disease apart from the presence of porphyria cutanea tarda. One patient recovered solely by abstaining from alcohol consumption. Five patients underwent phlebotomy; their iron stores had been found to be between 2 and 3 g. Decreasing urine porphyrin values correlated well with decreasing serum ferritin values during the course of phlebotomy. Porphyria cutanea tarda, which is due to a deficiency of uroporphyrinogen decarboxylase, is manifested in association with alcohol abuse, estrogen therapy, exposure to chlorinated hydrocarbons or increased tissue iron stores, or a combination of these factors. Although relatively uncommon, this condition raises important and unresolved issues regarding the hepatotoxicity of alcohol, estrogens, chlorinated hydrocarbons and iron.
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PMID:Porphyria cutanea tarda: clinical and laboratory features. 42 87

A family was studied in which three middle-aged siblings had unexplained cirrhosis and steatosis. Five of nine additional family members had abnormalities of liver function. Liver biopsy in those 5 revealed steatosis in 3, steatosis and fibrosis in 1, and increase in lipofuchsin pigment in another. Detailed investigation revealed no known metabolic defect, adverse environmental exposure, or alcohol abuse. We postulate that this family represents a unique type of idiopathic familial cirrhosis. The role of steatosis in the pathogenesis of cirrhosis in this family remains unsettled. The HLA haplotype A24, B18, DRW 4 X 7 was found in several family members, but the association of the disease with the HLA system remains to be established.
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PMID:Idiopathic familial cirrhosis and steatosis in adults. 49 8

The ocular state of 28 ascertained non-alcoholic females with cirrhosis of the liver was assessed. Only twenty were able to go through the complete colour vision test, and among these, three patients (one without, and two with increased level of serum bilirubin) with acquired colour vision defects were observed. Visual acuity, visual field, intraocular pressure, binocular function, slit lamp microscopy, ophthalmoscopy and tear production were normal in all cases. It is concluded that the frequency of colour vision defects in the present sample is increased, and that alcohol abuse is not a prerequisite for colour vision defects in patients with cirrhosis.
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PMID:Ocular function in cirrhosis of the liver. 57 40

The increase in mortality from alcohol induced cirrhosis of the liver in Sweden, Norway, Finland and Denmark from 1961 to 1974 is compared. Mortality from alcoholic cirrhosis of the liver increased in Finland and Denmark tenfold and fivefold respectively from 1961 to 1974. The increase has been particularly marked since 1968. In Sweden a threefold increase and in Norway a doubling of mortality in males was ascribed to alcohol induced liver cirrhosis. Mortality from non-alcoholic cirrhosis of the liver remained practically unchanged during the period. Increases in mortality from liver cirrhosis due to alcohol abuse run parallel with increases in alcohol consumption; the countries with the highest mortality have the highest consumption. The distribution of consumption of beer, wine and spirit is compared in the four countries: consumption of spirits predominates in Sweden, in Finland spirits and beer, in Denmark beer and wine and in Norway spirits and beer. Doubling of alcohol consumption in a country is followed by a fourfold increase in the number of addicts, and fourfold increase in alcohol induced diseases.
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PMID:Alcoholic cirrhosis of the liver in the Scandinavian countries 1961-1974. 60 97

Evidence exists that alcohol abuse frequently coexists with narcotic addiction and methadone maintenance treatment, and it is the major factor in the development of cirrhosis and liver failure. This study of patients hospitalized for alcohol detoxification compares the quantity of alcohol consumed by alcohol abusers, addicted to narcotics or in a methadone maintenance treatment program, to that consumed by patients not involved with narcotic addiction. Mean daily alcohol consumption was not significantly different in either group using narcotics, including methadone, or in the subgroup of methadone maintenance patients, from the amount consumed by nonnarcotic abusers. Determination of temporal sequence in the use of these substances revealed that in 68% regular alcohol abuse preceded narcotic use. Alcohol abuse reportedly began after entering a methadone maintenance treatment program in 29% of our patients. Alcohol abusers who were in a methadone maintenance treatment program were significantly younger than those who did not use narcotics, including methadone. Time interval according to the patients' estimates, from onset of regular alcohol consumption to heavy drinking, was not significantly different in the two groups.
Am J Drug Alcohol Abuse 1978
PMID:Quantitative and temporal relationships of alcohol use in narcotic addicts and methadone maintenance patients undergoing alcohol detoxification. 74 73

This is a study of alcoholic mortality in which time, cause, and age at death were variables of critical interest. Five cohorts of 100 members each were followed 12, 11, 9, 6, and 4 years. A total of 133 cases were located as deceased. The overall case fatality rate (CFR) was .0371. Higher CFR's were observed in years 1 to 6. Cardiovascular disease, violence (homicide, suicide, accidental), cirrhosis, carcionomas, and acute intoxication were the leading causes of death. Violent deaths were more prevalent in younger admission age groups. The cardiovascular/other ratio increased in older admission age groups.
Am J Drug Alcohol Abuse 1978
PMID:Alcoholic mortality: a 12-year follow-up. 74 74

Alcoholism policy since the repeal of Prohibition has been largely based on the assumption that alcohol problems are the result of the failure of a small minority to "control" their drinking. Thus, in sharp contrast to the approach to other drug policies, the problem of alcohol abuse has been viewed as one of "bad users" rather than "bad substances." This regard of alcoholism has helped exonerate the majority of drinkers and the alcohol industry from responsibility. However, mounting epidemiological evidence demonstrates that a primary factor in rates of diseases such as cirrhosis is the per capita use of alcohol and suggests that alcohol problems can be controlled or reduced only if all involved in the manufacture, sale or consumption of alcohol accept the burdens of restrictions over its availability and use. This acceptance will not be forthcoming, however, unless the prevailing market ethic of individual responsibility and minimal collective obligations to protect and preserve life is replaced with a new public health ethic rooted in social justice. This new ethic would assign the highest priority to life and would stress the obligations of all citizens to share the burdens of reasonable restrictions over all health hazards. In this paper a new alcohol policy is outlined based on just and reasonable limits on the availability, marketing and consumption of this substance.
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PMID:Exploring new ethics for public health: developing a fair alcohol policy. 102 6

Malnutrition is common among alcoholics because alcohol displaces protein-, vitamin-, and mineral-containing foods in the diet, and chronic alcohol consumption results in maldigestion and malabsorption of essential nutrients. In addition, alcohol exerts direct toxic effects on both the liver and gut, resulting in structural alterations in the intestine and the development of fatty liver, alcoholic hepatitis, and cirrhosis. Liver injury is preceded by an adaptive phase characterized by accelerated metabolism of drugs (including ethanol), and hyperlipemia, secondary to hypertrophy and hyperactivity of the smooth endoplasmic reticulum. Side effects include enhanced hepatotoxicity of CCI4 and possibly energy wastage. Alcoholics should not be led to beleive that correction or prevention of nutritional deficiency will prevent liver damage in the face of continued alcohol abuse.
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PMID:Alcohol and malnutrition in the pathogenesis of liver disease.. 117 54


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