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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients attending a clinic for diseases of the liver were tested for blood-ethanol by a gas chromatographic technique sensitive to about 5 mg/dl (1 mmol/1). Of 172 patients (51 men, 121 women) 36% gave a history of heavy drinking (greater than 80 g ethanol/day; equivalent to 8 fl oz of whisky or 1 litre of wine) and 13% had ethanol in the bloodstream at values of 8-400 mg/dl. 42 patients (24%) had the liver-biopsy changes of alcoholic liver disease, and 17 of these had ethanol in the blood at one time or another. Nearly half (22/49) of all patients admitting heavy drinking also had detectable blood-ethanol. In all cases but 1 where blood-ethanol was found, a drinking history was admitted on first attendance, and alcoholic liver disease was nearly always found on subsequent biopsy. Blood-ethanol and admission of drinking were most constantly found in association with alcoholic steatosis and hepatitis. Both features were less commonly present in cases of alcoholic cirrhosis. Only 1 patient of 22 with "cryptogenic" cirrhosis on biopsy was found to have both ethanol in the blood and an alcoholic history, although 5 had an alcoholic history alone. The value of serial blood-ethanol estimations in the treatment of alcoholics and the detection of relapses is demonstrated. The findings confirm the relatively low frequency of alcoholism as a contributor to cirrhosis in the United Kingdom. Alcohol does not seem a major cause of cryptogenic cirrhosis. Casual blood-ethanol estimation is a useful and objective adjunct to techniques of investigating diseases of the liver.
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PMID:Casual blood-ethanol estimations in patients with chronic liver disease. 5 Nov 46

Recently developed tests that measure levels of alpha-amino-n-butyric acid (AANB) and serum glutamic dehydrogenase (GDH) may improve screening for early detection of heavy drinking and liver injury, respectively. With these tests, a "three-level" approach to the problem is now possible: (1) detection of heavy drinking on the basis of a biochemical marker (such as AANB); (2) detection of liver injury (necrosis and inflammation) on the basis of serum liver tests (such as GDH); and (3) detection of alcoholics in whom cirrhosis is prone to develop by the screening of liver biopsy specimens for precirrhotic lesions (such as pericentral sclerosis).
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PMID:Alcoholism and alcoholic liver injury: new diagnostic and prognostic tests. 58 Aug 76

The activity of ethanol metabolising enzymes was assessed in 51 patients with alcoholic and non-alcoholic liver disease using tracer doses of [1-14C]ethanol and measuring 14CO2 excretion in the breath. Alcoholic patients with only fatty infiltration of the liver showed significantly increased activity compared with controls. Comparing alcoholic patients with cirrhosis and a serum albumin greater than 28 g/l, activity in those with a recent history of continued heavy drinking was significantly greater than in patients who had abstained from alcohol. In addition, both groups of alcoholic cirrhosis showed significantly more activity than patients with non-alcoholic cirrhosis. The activities of patients with acute alcoholic or viral hepatitis were normal when their prothrombin times were less than 7 sec prolonged, but were reduced when prolongation exceeded 7 sec. These results demonstrate that in chronic alcoholic liver disease, even with cirrhosis, alcohol can still increase the activity of ethanol oxidising enzymes provided hepatic function remains adequate. However, this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction.
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PMID:[1-14C]Ethanol breath test in alcoholic liver disease. 65 31

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

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.
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PMID:Heavy alcohol consumption and physical health problems: a review of the epidemiological evidence. 79 60

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

1. Male death rates from hypertension and stroke in England and Wales in 1949-53 were highest in those socio-economic and occupational groups with the highest death rates for cirrhosis of the liver (and presumably with highest alcohol intake. 2. In prevalence data from the Busselton population in Western Australia in 1969, there was a significant association between hypertension and a history of heavy drinking. 3. Together with other data, these observations suggest that up to 30% of hypertension in affluent countries may prove to be attributable to the use of alcohol.
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PMID:Alcohol use, hypertension and coronary heart disease. 107 3

Cirrhosis, the ninth leading cause of death in the United States, has been associated with abusive alcohol consumption patterns. Since the workplace serves as a major exposure variable for alcohol consumption over a significant portion of the lifecourse, and since heavy drinking has been shown to differ by type of occupation, this study examines the relationship between type of occupation and cirrhosis mortality. The California Occupational Mortality Study data set (1979 to 1981) provided the information on primary occupation and liver cirrhosis mortality. Crude and sex-specific mortality rates were calculated based on information from a 20% sample of the 1980 California census (included in the data set). Ninety-five percent confidence intervals were calculated around all rates to determine if any were significantly different from rates for the entire state. The findings uphold the view that an association exists between occupation and cirrhosis mortality. The highest mortality rates were found among persons with blue-collar type jobs (e.g., construction laborers and machinists) or jobs where alcohol was easily available (e.g., bartenders and waitresses). Future research needs to specify the factors associated with occupation that may promote the chronic heavy drinking that leads to cirrhosis.
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PMID:Cirrhosis mortality and occupation. 140 39

Eastern Austrian regional mortality patterns of oral cancer (oral cavity, pharynx and larynx) and oesophageal, lung and urinary bladder cancer were compared to smoker rates and to liver cirrhosis mortality by type of residence: Vienna (1.7 x 10(6) inhabitants), middle towns (50,000-100,000 and 10,000-50,000 inhabitants), small towns (2000-10,000 inhabitants) and rural areas categorized by agrarian quota less than or equal to 10%, 10%-20% and greater than 20%. The study area (Vienna, Lower Austria and Burgenland) covers 23,600 km2 with 3.23 x 10(6) inhabitants. In men, liver cirrhosis correlated negatively with smoker rates (r = 0.74, P = 0.1). Deaths from oral cancer and oesophageal cancer correlated significantly with deaths from liver cirrhosis (r = 0.81, P = 0.03; r = 0.78, P = 0.04, respectively) but not with smoker rates; lung cancer and bladder cancer correlated significantly with smoker rates (r = 0.91, P = 0.01; r0.83, P = 0.04, respectively), but not with liver cirrhosis. In women, similar urban-rural gradients for all parameters resulted in a positive correlation between liver cirrhosis and smoker rates (r = 0.59, P = 0.22) and a significant correlation of lung cancer with liver cirrhosis (r = 0.75, P = 0.05). Oral cancer correlated significantly with liver cirrhosis (r = 0.83, P = 0.02), but not with smoker rates; lung cancer correlated more significantly with smoker rates (r = 0.92, P = 0.01) than with liver cirrhosis; bladder cancer correlated positively with smoker rates (r = 0.70, P = 0.12). Geographical distribution of oral and oesophageal cancer in Eastern Austria seems thus to be highly subject to the prevalence of heavy drinking. Sociocultural influences upon the occurrence of these cancers seem to be mediated through drinking habits rather than through smoking habits alone.
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PMID:Tobacco-related cancer in relation to prevalence of drinking and smoking in eastern Austria. 151 83

A review of the many attempts to establish an association between occupations and alcoholism reveals that most do not deal with data about clinically defined alcoholism but instead use data about cirrhosis mortality, self-reported alcohol problems, and frequent and heavy drinking. The present study establishes an association between occupations and diagnoses of Alcohol Dependence Disorder and Alcohol Abuse Disorder, using data from a large population-based household interview study. Statistical adjustment using logistic methods reveals that apparent associations between occupations and alcohol-related disorders previously reported in the literature are due to characteristics of those employed in various occupations. The prevalence of alcohol dependence and abuse in two high risk industries, construction and transportation, is confirmed. More than one in four construction laborers and one in five skilled construction trades workers received a DIS/DSM-III diagnosis related to alcohol abuse. In the transportation industry one in six heavy truck drivers and material movers received an alcohol diagnosis. Analyses of the data from individuals currently employed and not employed in their occupation reveals reduction in risk for those who leave some occupations and increased risk for those who leave other occupations. Evidence is presented that employment in some occupations may be protective for Alcohol Dependence. The findings support the view that occupation may be associated with Alcohol Dependence and Alcohol Abuse independent of demographic variations. Previously proposed explanatory models for associations between occupations and alcohol problems are called into question because they do not take into account the demographic characteristics and employment status of workers.
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PMID:Alcoholism and occupations: a review and analysis of 104 occupations. 153 Jan 36


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