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)

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.
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PMID:Quantitative and temporal relationships of alcohol use in narcotic addicts and methadone maintenance patients undergoing alcohol detoxification. 74 73

Alcoholic hepatitis is the precursor of cirrhosis. Susceptibility is independent of amount and duration of ethanol intake or of diet. Centrilobular hyalin, the key morphologic abnormality, sensitizes lymphocytes to secrete factors which may account (in part) for necrosis, liver cell destruction, increased collagen synthesis and development of cirrhosis. Diagnosis may be facilitated by detection of alcoholic hyalin antigen (AHAg) and antibody (AHAb) in serum of patients with alcoholic hepatitis. Treatment requires abstinence. Steroids have not reduced mortality rates. Measures to improve immunologic reactivity may be helpful. Persons unable to abstain should be enrolled in a surveillance group.
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PMID:Alcoholic hepatitis. 77 53

A review of morbidity and mortality studies bearing on the hazards to physical health of chronic heavy alchol use indicates that such use carries a risk of premature death greatly exceeding normal expectancy. While the life style typical of many heavy drinker contributes to this risk, the effects of alcohol per se account for a substantial part of the excess mortality. The lowest level of consumption at which there is a significant increase in the death rate has yet to be determined. It is certainly below 120 g/day- the lower limit of consumption of most clinical alcoholics-and quite possibly below 35-60g: levels which appear to carry an increased likelihood of cirrhosis and certain cancers. On the other hand, the mortality experience of drinkers commonly identified as 'moderate' in the literature does not seem to differ notably from that of life-long abstainers. The relationship between heavy drinking and elevated mortality is exhibited in populations at large by the generally close covariation of cirrhosis death rates and per capita alcohol sales. There are also indications of co-variation between the latter and the excess of male over female general mortality in the middle age range.
Drug Alcohol Depend 1975 Sep
PMID:Heavy alcohol consumption and physical health problems: a review of the epidemiological evidence. 79 60

To elucidate the effects of chronic alcohol ingestion in monkeys a synthetic, adequately balanced, fluid diet providing 40% of total calories from ethanol was gavaged through a stomach tube daily over a period of three months. Clinical, biochemical, radioisotope, and histopathological studies were performed at the beginning and end of the experiment. It was observed that chronic alcohol feeding at this dose level caused maked accumulation of triglycerides, cholesterol, and phospholipids in the serum and the liver. In the heart triglycerides and cholesterol ester were increased. Incorporation studies showed increased synthesis of triglycerides in the heart muscle and liver. Histologically the heart showed fatty change of the myocardium and evidence of focal myocytolysis, atrophy of muscle bundles, and early fibrosis. The liver showed generalized fatty change but no cirrhosis.
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PMID:Myocardial lesions induced by prolonged alcohol feeding in rhesus monkeys. 80 51

The rate of ethanol metabolism (EMR) was determined in alcoholic patients with or without hepatic necrosis, steatosis, and/or cirrhosis. Fifty six cases were studied after 9-25 days of abstinence (mean 15 days). A significant increase in EMR (P less than 0.01) was found in alcoholics with hepatic necrosis (265 +/- 20.5 mg/kg/hr) compared with alcoholics with normal liver histology (154 +/- 17) and nonalcoholic controls (159 +/- 15). In alcoholics with liver steatosis but without necrosis a lesser increase in EMR (207 +/- 20, P less than 0.05 was also observed. Patients with slight fibrosis but without other abnormalities in their liver biopsies and cirrhotics with overt liver failure (jaundice, ascites) showed EMR similar to controls.
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PMID:Possible relationship between the rate of ethanol metabolism and the severity of hepatic damage in chronic alcoholics. 85 61

Adult human liver biopsies were cultured from normal, alcoholic hepatitis, chronic active hepatitis, fibrosis plus alcoholic hepatitis (active cirrhosis), inactive cirrhosis, and drug hepatitis. The synthesis of collagen was estimated in cultures from 58 livers by measuring the conversion of [(14)C]proline to the [(14)C]hydroxyproline of collagen; that of glycosaminoglycans in cultures from 57 livers by the incorporation of [(3)H]acetate and (35)SO(4) into glycosaminoglycans (GAG). The synthesis of procollagen was increased only in cultures from alcoholic hepatitis, both in the pulse medium (P < 0.05) and in the chase medium (P < 0.02). The synthesis of insoluble collagen was increased in cultures from chronic (active) hepatitis (P < 0.01), fibrosis plus alcoholic hepatitis (active cirrhosis) (P < 0.001), and inactive cirrhosis (P < 0.05). Essentially all radioactive GAG was soluble in culture media. The predominant GAG were chondroitin-4 or -6-SO(4). The synthesis of GAG was increased only in cultures from fibrosis plus alcoholic hepatitis (active cirrhosis) both in the pulse medium (P < 0.01) and chase medium (P < 0.001). The data indicate that in the absence of immuno-competent cells or their secretory products, tissue cultures from livers showing biopsy evidence of active fibrosis in vivo may demonstrate increased synthesis of collagen and GAG in vitro. Increased (soluble) procollagen synthesis in cultures from alcoholic hepatitis was not associated with histologically demonstrable overt hepatic fibrosis in vivo, nor was it associated with increased GAG synthesis in vitro. No significant difference was demonstrable in collagen or GAG synthesis in paired cultures which contained either 300 mg/dl ethanol or 3.75 mg/dl methylprednisolone compared to their respective controls.
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PMID:The rate of synthesis of glycosaminoglycans and collagen by fibroblasts cultured from adult human liver biopsies. 87 75

Thirty-five Black patients with cirrhosis of the liver were admitted to the professorial unit over a 1-year period and were included in a carefully planned prospective study. Men predominated over women in a ratio of 3:1. Alcohol consumption in the form of African beer was significantly higher in cirrhotic patients than in a control population. The clinical picture was neither predominantly that of alcoholic nor of cryptogenic cirrhosis. Hepatomegaly, porphyria cutanea tarda, ascites, splenomegaly and oesophageal varices were common. There was a complete absence of gynaecomastia, spider naevi and liver palms. Histologically, the majority of patients had macronodular cirrhosis, and only 1 patient had micronodular cirrhosis and minimal fatty change. Hepatitis B surface antigen (HbsAg) was not detected in any patient, despite a positive HbAg rate of 4% in Black African blood donors, determined by means of the same laboratory technique.
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PMID:Cirrhosis of the liver in Rhodesian Blacks. 88 20

Data are presented on the rate of removal of tolbutamide from the blood from studies in heavy drinking, unemployed, male alcoholic subjects. In such subjects tolbutamide was removed faster than it was in normal subjects and faster than in patients with cirrhosis who are not drinking. This rapid removal rate persists for 4 to 9 wk after hospitalization and is reproduced with 400 gm of pure ethanol in 2 or 3 wk but cannot be reproduced with lesser amounts of beverage alcohol taken outside of the experimental study. Similar acceleration of the clearance rates was observed for warfarin and for phenytoin but could not be demonstrated for aminopyrine.
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PMID:Drug metabolism in heavy consumers of ethyl alcohol. 91 32

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

Tests on 100 alcoholic patients revealed increased lipoprotein levels in 24%. Type IV was the most frequently ecountered (80%), followed by type II or V. The average plasma triglyceride level of the alcoholic group was significantly increased in comparison with a control population. The causal mechanism of alcoholic hyperlipoproteinemia remains poorly understood. The combination of a genetic defect of lipid metabolism, nutritional factors and acute alcohol excess may have an essential bearing on the incidence of hyperlipoproteinemia. Acute excessive intake of alcohol was significantly increased in comparison with alcoholic subjects wihtout hyperlipoproteinemia. The critical dose may be a daily ethanol consumption of about 200 gm. There appeared to be no correlation between acute pancreatic injury or active liver disease and serum lipid elevation. On the other hand, the observation was confirmed that alcoholic patients with hepatic cirrhosis usually do not develop hyperlipoproteinemia. Ethanol-induced hyperlipoproteinemia may be a risk factor for the development of atherosclerosis and pancreatitis.
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PMID:[Alcohol-induced hyperlipoproteinemia]. 91 92


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