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

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.
J Stud Alcohol 1992 Sep
PMID:Cirrhosis mortality and occupation. 140 39

The antioxidant status of alcoholic patients was assessed by direct measurement of the plasma antioxidants alpha-tocopherol and beta-carotene and of selenium as a marker of glutathione peroxidase. Overall, the alcoholic group showed significant decreases in the mean plasma values of beta-carotene, zinc and selenium when compared to the control subjects. When the patients were subdivided according to their liver histology, beta-carotene showed a progressive decrease in plasma concentration with increasing liver damage, whereas alpha-tocopherol levels were only depleted in the patients with cirrhosis. There were significant decreases in the plasma concentrations of both alpha-tocopherol and selenium in all patients with alcoholic skeletal muscle myopathy, whereas patients with normal muscle biopsies showed adequate antioxidant status. Such results support a role for free radical-mediated damage in end organ injury, particularly myopathy, in alcohol misusers.
Alcohol Alcohol 1992 Jul
PMID:The antioxidant status of patients with either alcohol-induced liver damage or myopathy. 141 10

Long-term administration of ethanol into animals within 1-6 months resulted in distinct alterations of blood serum fatty acid composition as well as in elevation of the saturation rate simultaneously with a decrease of fatty acid polyunsaturation. Calculated coefficients, which included ratios between fatty acid with various rates of unsaturation, were highly informative. Alterations of fatty acid composition in blood serum, registered during observations, reflected the state of fatty acid metabolism in tissues. Analysis of fatty acid spectrum in blood serum enabled to evaluate the severity of impairments in liver tissue and pancreas under conditions of alcohol intoxication: increase in the rate of phospholipid catabolism, in content of cholesterol, triglycerides and total lipids was observed both in blood serum and liver tissue. These impairments of lipid metabolism may produce alcohol hepatitis, which is the basis for liver tissue alcohol cirrhosis.
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PMID:[Features of lipid metabolism impairment in chronic alcoholic intoxication]. 144 Dec 98

Alcoholic liver disease is associated with abnormalities in circulating levels of thyroid, adrenal and gonadal steroid hormones. The relative importance of ethanol consumption and severity of liver disease in the aetiology of these changes and their relationship to clinical abnormalities are unclear. We studied 31 subjects with alcohol-induced liver disease divided into three groups according to the severity of histological features: fatty change, hepatitis and cirrhosis. Circulating concentrations of thyroid, adrenal and gonadal steroid hormones, together with their major binding proteins, were measured in all subjects, and changes related to histology and tests of liver function, as well as clinical endocrine status. A reduction in circulating free tri-iodothyronine (fT3) was seen in subjects with alcoholic hepatitis and cirrhosis, in association with normal or reduced levels of thyrotrophin (TSH). The absence of abnormalities in subjects with fatty change despite similar ethanol intake to the other groups, and correlations between fT3 and liver function tests, suggest that changes in fT3 reflect the severity of underlying liver disease. Similarly, marked increases in circulating cortisol in the hepatitis and cirrhosis groups, and correlations between cortisol and liver function, suggest that changes largely reflect hepatic disease. The absence of clinical features of hypothyroidism or Cushing's syndrome in these groups, despite abnormalities of fT3 and cortisol, suggest an altered tissue sensitivity to hormone effects. In contrast, increases in circulating oestradiol and reductions in testosterone were found in all three groups in males. These findings suggest that both direct effects of ethanol and hepatic dysfunction determine changes in gonadal steroids in males.
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PMID:Severity of alcoholic liver disease and markers of thyroid and steroid status. 146 52

The blood and plasma concentrations of thiamin and thiamin phosphate esters were determined concomitantly by high-performance liquid chromatography (HPLC) in 22 patients with alcoholic liver cirrhosis, and also in 10 of them 24 hr after a 100 mg thiamin i.m. injection. Sixteen patients were abstaining from alcohol at the time of the study, 6 were currently misusing alcohol. The control group included 30 healthy volunteers, of whom 10 were given the same thiamin injection as the patients. Blood thiamin diphosphate was the only compound decreased in the abstaining patients compared to controls (70.9 +/- 21.9 nmol/l vs. 84.4 +/- 19.0 nmol/l), but all thiamin compounds in blood and plasma were decreased in the misusing patients. All thiamin compounds (except blood monophosphate) were also significantly lower in the misusing than in the abstaining patients (plasma thiamin: 5.3 +/- 1.3 vs. 11.7 +/- 8.3 nmol/l; plasma monophosphate: 1.0 +/- 1.1 vs. 4.1 +/- 2.9 nmol/l; blood diphosphate: 45.7 +/- 18.3 vs. 70.9 +/- 21.9 nmol/l). Thiamin phosphorylation ratio was decreased in the patients after thiamin administration compared to controls (2.83 +/- 0.74 vs. 3.68 +/- 0.58). Plasma thiamin was higher in the abstaining patients than in the controls (11.7 +/- 8.4 nmol/l vs. 7.3 +/- 2.5 nmol/l), and above the mean + 2 SD of the controls in 31% of the abstaining patients. In conclusion, current ethanol misuse is associated with low thiamin concentrations, and liver cirrhosis is associated with a decreased thiamin diphosphate concentration and thiamin phosphorylation.
Alcohol Alcohol 1992 Sep
PMID:The concentration of thiamin and thiamin phosphate esters in patients with alcoholic liver cirrhosis. 147 55

We report the 10-year survival of 510 patients with a histological diagnosis of alcoholic liver disease. Eight centres in Scotland and North England contributed to this study. Information was available on 92% of the initial cohort. Age was important, with each decade increasing mortality by 55%. A highly significant interaction between sex and histology was observed with a marked survival benefit for males with non-cirrhotic alcoholic liver disease, while in cirrhotic subjects the pattern was reversed. Patients with decompensated liver disease had a relative increase in mortality in excess of 86% while the increase in mortality for alcoholic hepatitis, 'active' cirrhosis and 'inactive' cirrhosis were 52%, 57% and 91% relative to fatty liver. Alcohol intake at the time of diagnosis did not influence outcome. This study emphasises yet again the increased mortality rate of individuals abusing alcohol compared with the general population.
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PMID:A prospective study of alcoholic liver disease and mortality. 148 5

Cirrhosis was induced in Sprague-Dawley rats via ligation of the common bile duct. Changes in gastric blood flow and mucosal architecture were examined. Using an ex vivo gastric chamber preparation, the susceptibility of the cirrhotic gastric mucosa to injury by 20% ethanol was also examined. The gastric mucosa of cirrhotic animals was abnormal, even before ethanol administration. The macroscopically visible damage in these animals ranged from superficial hyperemia to epithelial sloughing. These gastric lesions were similar in appearance to the gastropathy described in cirrhotic patients, including "cherry-red spots" and areas of generalized erythema. Cirrhotic rats had a lower resting gastric transmucosal potential difference than control rats, and their gastric mucosa was also significantly more susceptible to damage by topical ethanol application. Ethanol administration caused a significant increase in gastric blood flow in control rats, whereas it significantly decreased gastric blood flow in cirrhotic rats. This lack of a reactive hyperemic response in cirrhotic rats may be responsible for the increased susceptibility of the gastric mucosa to ethanol-induced damage.
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PMID:Characterization of spontaneous and ethanol-induced gastric damage in cirrhotic rats. 149 5

Male Sprague-Dawley rats with CCl4-induced cirrhosis (confirmed by increased collagen content and light microscopy) were fed either ethanol (Group A, n = 9) or isocaloric carbohydrate diet (Group B, n = 8) for 4 weeks. Histologic and hemodynamic measurements were obtained in the awake state before (time 1) and after the 4 weeks of diet (time 2). Portal-systemic shunts were evaluated using radiolabelled microspheres. Liver weight was increased in Group A (16.5 +/- 0.5 vs. 14.2 +/- 0.5 g, mean +/- SE, p less than 0.005) as was the ratio of liver weight over total body weight (3.41 +/- 0.05 vs. 2.86 +/- 0.09%, p less than 0.0001, +19.2%). Hepatocytes surface area was increased in the ethanol group (357 +/- 9 vs. 294 +/- 7 microns 2, p less than 0.0001). In Group B, only 9 +/- 2% of hepatocytes had steatosis as opposed to 69 +/- 3% of centronodular and 34 +/- 3% of perinodular hepatocytes in Group A (p less than 0.001). Portal pressure remained stable in both groups (time 1 (A) 16.9 +/- 0.8, (B) 15.8 +/- 1.1 mmHg, n.s.; time 2 (A) 15.9 +/- 0.7, (B) 15.8 +/- 0.6 mmHg, n.s.). Portal-systemic shunts did not change with time or diet (time 1 (A) 10.6 +/- 3.7%, (B) 4.1 +/- 2.1%, n.s.; time 2 (A) 13.4 +/- 5.9%, (B) 10.8 +/- 4.3%, n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of alcohol-induced hepatomegaly on portal hypertension in cirrhotic rats. 150 55

Previous research relating television advertising and alcohol consumption indicates no meaningful relationships. This study focused on observed drinking behaviour in comedy, soap opera, drama, and police/detective programmes produced for British, American and Canadian television. Results indicated British television fiction had three times the amount of alcohol consumption seen in either American or Canadian programming. In spite of this more frequent portrayal of alcohol consumption, examination of World Drinking Trends and other alcohol-related statistics (i.e. cirrhosis and alcohol-related auto accidents) indicated no greater level of alcohol misuse in the U.K. than in Canada or the United States. In fact, available statistics indicate significantly lower rates of liver cirrhosis in Britain as opposed to Canada and the United States. Hypotheses regarding the absence of relation between fictional and actual alcohol consumption were discussed.
Alcohol Alcohol 1992 Mar
PMID:Alcohol consumption in television programming in three English-speaking cultures. 152 12

Changes in the legal restrictions for alcohol consumption in 1969 liberated purchasing and marketing of low-alcohol beer. Subsequently, within the space of 5 years, the per capita consumption of absolute alcohol increased from 4.2 to 6.5 liters. To evaluate the possible effects of this change upon liver cirrhosis mortality as well as prevalence of liver cirrhosis in autopsy series, we surveyed mortality statistics and data from 8,533 medicolegal autopsies in 1968 through 1988. Liver cirrhosis mortality statistics revealed a highly significant (p less than 0.001) increase from 6.4 to 13.7 per 100,000 during the period, and similarly, the prevalence of liver cirrhosis in the autopsy series showed a highly significant (p less than 0.001) increase from 3.0% to 6.1%. More specifically, this increase was attributable to a highly significantly (Chi-square 15.4, p less than 0.001) increased proportion of alcoholic liver cirrhosis occurring at a younger age and almost exclusively in males. The stepwise mode of increase as well as the changes in sex and age distribution of cirrhosis since 1969 could be interpreted as an effect of distribution of consumption to a new generation of consumers. The forensic autopsy series seemed to reflect changes in per capita consumption with a shorter time lag than with mortality statistics. Additionally, only 7% of the 448 cirrhotics singled out from this material exhibited liver cirrhosis as a cause of death and were thus also included in the official mortality statistics, suggesting the greater accuracy of our forensic autopsy series.
Alcohol Clin Exp Res 1992 Aug
PMID:Delayed increases in liver cirrhosis mortality and frequency of alcoholic liver cirrhosis following an increment and redistribution of alcohol consumption in Finland: evidence from mortality statistics and autopsy survey covering 8533 cases in 1968-1988. 153 Jan 26


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