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)

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

In patients treated with sclerotherapy, most rebleeding episodes are observed before variceal obliteration. This prospective randomized study aimed to assess if propranolol together with sclerotherapy could reduce the rebleeding rate before variceal obliteration. Seventy-five patients (59 male, 16 female; mean age, 54 +/- 15 years) with cirrhosis (from alcohol abuse in 91%) admitted with upper gastrointestinal bleeding, which was endoscopically proven to originate from ruptured esophageal varices, were included. After initial control of bleeding, the patients were randomized into the following two groups: group 1 treated with sclerotherapy alone (36 patients) and group 2 treated with sclerotherapy plus propranolol (39 patients). They were followed up to variceal obliteration. In group 2, 7 patients rebled as compared with 14 patients treated with sclerotherapy alone (P less than 0.005). When considering only rebleedings from esophageal varices, 4 patients rebled in group 2 vs. 10 in group 1 (P less than 0.10). The total number of rebleeding episodes was lower in group 2 than in group 1 whether considering all causes (8 vs. 17; P less than 0.07) or variceal rebleedings alone (4 vs. 13; P less than 0.01). Mean total blood requirement per patient was lower in group 2 than in group 1 (1.4 +/- 3.4 vs. 2.79 +/- 6.4 units of blood, respectively; P less than 0.01). Mortality was similar in both groups of patients (14% vs. 13% in groups 1 and 2, respectively, NS). It is concluded that patients treated with sclerotherapy should be given propranolol before variceal obliteration.
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PMID:Propranolol reduces the rebleeding rate during endoscopic sclerotherapy before variceal obliteration. 156 86

We retrospectively reviewed 159 episodes of bacteraemic pneumococcal infection in 157 adult patients at the Helsinki University Central Hospital during two periods between 1976 and 1979 and 1986 and 1989. We looked especially at changes in underlying diseases and prognostic factors. The overall case fatality rate was 21% and there was a small diminishing trend in that rate from 28% (16/58) in the late 1970s to 17% (17/101) in the late 1980s. The patients who died in the late 1980s were younger than those who died in the earlier period. The most common underlying factors were alcohol abuse, cardiovascular diseases and chronic obstructive pulmonary diseases. Old age was neither a predisposing factor nor did it predict the outcome. No significant changes in underlying diseases or prognostic factors were noted during the two periods studied except a small decrease in connective tissue diseases as underlying conditions. The factors related to increased fatality included hepatic cirrhosis, a combination of pneumonia and meningitis, complications such as shock, respiratory insufficiency, central nervous system disorders and circulatory acidosis, and laboratory findings such as thrombocytopenia, absence of leucocytosis and increased amounts of serum creatinine, aspartate aminotransferase and alanine aminotransferase on admission to the hospital. Previous splenectomy and malignant diseases were not associated with higher mortality. The thrombocytopenia at the time of positive blood culture and the circulatory acidosis as a complication seemed to be independently the most useful predictive factors for a fatal outcome using multivariate logistical regression analysis after adjustment to classic risk factors.
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PMID:Pneumococcal bacteraemia during a recent decade. 156 6

One hundred and forty-six patients with chronic liver disease have been studied. Some of them (15) showed a clinical picture characterized by cryptogenetic liver cirrhosis associated with hypotriglyceridemia and hypobetalipoproteinemia. These patients had compensated cirrhosis and no history of alcohol abuse; they did not suffer major illness in the past and had no signs of portosystemic encephalopathy. The pathogenetic mechanism of this association and the possible role of genetic factors are discussed. The HLA system has been studied and the A2 antigen found with high frequency, raising the possibility that patients with this syndrome may represent a particular subgroup among these with liver cirrhosis.
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PMID:[Cryptogenetic liver cirrhosis with hypobetalipoproteinemia. Typing of the HLA histocompatibility system]. 157 90

Excessive consumption of ethanol results in reversible redox changes in the liver that are mainly responsible for the accumulation of triglycerides and the fatty liver of the alcoholic patient. In spite of continuing alcohol abuse, only a fraction of all alcoholics will develop alcoholic hepatitis and eventually cirrhosis. Genetic predisposition and environmental factors (in particular the often poor nutrition of the alcoholic) probably play an important role in the evolution of these complications. The generation of reactive oxygen species increases during the metabolism of ethanol, but their pathogenetic role in alcoholic liver disease in man is not clear. Acetaldehyde, a metabolite of ethanol, can react with proteins and form stable adducts. Such neoantigens may elicit an immunologic response which could in part be responsible for the liver cell damage associated with excessive alcohol consumption. Since no satisfactory animal model for alcoholic liver disease exists, the relative importance of the various factors involved in alcoholic liver disease is difficult to assess.
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PMID:[Pathogenesis of alcoholic liver disease]. 158 33

Two types of factors can theoretically modulate alcohol metabolism toward increased acetaldehyde production. These factors are the following: (a) individual, genetically determined isoenzymes with distinct catalytic properties, and (b) modifications of enzyme activity induced by alcohol itself or liver damage. To investigate the respective roles of these factors in white individuals, we studied the alcohol dehydrogenase phenotype, together with liver alcohol dehydrogenase and aldehyde dehydrogenase activities, in 161 patients. Patients with alcoholic cirrhosis (n = 31) were compared with three types of controls: patients with nonalcoholic cirrhosis (n = 25) and excessive (n = 62) and moderate drinkers (n = 43) without liver disease. No association between alcohol dehydrogenase-3 phenotype and alcoholic cirrhosis was found. The prevalence of atypical alcohol dehydrogenase in the four groups was less than 1%. Patients with cirrhosis, regardless of its cause, had significantly lower alcohol dehydrogenase activity than the patients without cirrhosis (p less than 0.05 and p less than 0.01 vs. excessive and moderate drinkers, respectively). Among the noncirrhotic patients, alcohol dehydrogenase activity was significantly lower in the excessive drinkers than in the moderate drinkers (p less than 0.001). Aldehyde dehydrogenase activity was not different between cirrhosis-free excessive and moderate drinkers; in contrast, compared with these two groups, it was significantly lower in the two cirrhosis groups (p less than 0.01). These results suggest that no phenotypic pattern of alcohol dehydrogenase-3 associated with alcoholic cirrhosis in white patients exists, that liver alcohol dehydrogenase activity falls as a consequence of both alcohol abuse and cirrhosis and that liver aldehyde dehydrogenase activity is unaffected by alcohol abuse and only falls after the onset of cirrhosis.
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PMID:Polymorphism of alcohol dehydrogenase, alcohol and aldehyde dehydrogenase activities: implication in alcoholic cirrhosis in white patients. The French Group for Research on Alcohol and Liver. 832 17

A questionnaire-based survey involving 11,801 hemophiliacs from 54 hemophilia centers in the USA and Europe documented the occurrence of hepatocellular carcinoma (HCC) in 10 patients. The crude rate of HCC was 3.2/100,000 patients/year, at least 30 times higher than the background incidence of this tumor in the countries of origin of the patients. All patients were Caucasians with hemophilia A, 39 to 74 years of age, and had liver cirrhosis. All had one or more risk factor for cirrhosis and HCC: 5 were positive for serum hepatitis B surface antigen, 4 had the antibody to hepatitis C virus, and 4 had histories of alcohol abuse. Serum alpha-fetoprotein, measured in 6 patients, was significantly elevated in 4 (range: 807-1399 ng/ml), and only moderately elevated in 2 (25 and 171 ng/ml). The onset of HCC was asymptomatic in 5 patients, whereas it was accompanied by jaundice, abdominal pain, or ascites in the remaining patients. Thus, HCC seems to be a more important secondary disease for hemophiliacs than formerly recognized. Since HCC is often asymptomatic, screening hemophiliacs with chronic liver disease with periodic ultrasound scans might increase the changes of detecting HCC at a stage amenable to surgical treatment.
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PMID:Hepatocellular carcinoma in hemophilia. 165 Jan 34

This study, aimed at elucidating the epidemiological features of primary liver carcinoma developing in non-cirrhotic livers, was based on 25,103 autopsies performed between 1975 and 1984 in Trieste, Italy. These autopsies correspond to approximately 70% of all deaths that occurred in this area. Various factors allegedly related to carcinomas were analysed in reference to our previous study on cirrhotic livers and in comparison with 5,603 autopsies in Kurume, Japan. There were 28 cases of hepatocellular carcinoma (HCC), 16 of cholangiocellular carcinoma (CCC) not associated with cirrhosis in Trieste, and 48 HCC and 19 CCC in Kurume. On the basis of our findings, it was concluded that cirrhosis, regardless of its cause, is the main pathogenetic factor in HCC; it is responsible for a much higher frequency (14.2:1) than in non-cirrhotic livers, as well as for early occurrence of tumours (an average of 6 years earlier in cirrhotic liver) in Trieste. Patients in Trieste were older than those in Japan, and the frequency of HCC among all autopsies was much greater in the latter. By contrast, the influence of cirrhosis on cholangiocellular carcinoma (CCC) was negligible, as such association appeared purely coincidental or absent. The incidence of CCC among autopsies was greater in Japan. Our data on CCC were not sufficient to demonstrate any clear aetiopathogenetic association between this tumour and alcohol abuse and hepatitis B virus (HBV) infection, except for a possible aetiological role of gallstones. The frequency of CCC relative to HCC was greater in Trieste than in Japan; the incidence of HCC was much less in Trieste, whereas CCC was more frequent in Japan.
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PMID:Primary liver cancer in non-cirrhotic liver. Epidemiological study based on autopsies performed in Trieste, Italy and Kurume, Japan. 165 97

Hepatitis C virus (HCV) is a recently characterised non-A, non-B hepatitis (NANBH) agent, which appears to be important in both parenteral and sporadic NANBH. HCV infection has been associated with the development of chronic liver disease, cirrhosis and hepatoma. Groups of patients in the western Cape with chronic liver disease and hepatoma were screened for antibodies to HCV and the results were confirmed by standard neutralisation tests. Three of 19 patients with cirrhosis secondary to alcohol abuse or classic auto-immune chronic active hepatitis were considered to have antibodies to HCV at initial screening. All of these were false-positive results. Five of 20 patients with presumptive chronic NANBH were considered possibly to have antibodies to HCV. Only 1 patient with post-transfusional NANBH was confirmed to have specific HCV antibodies. Two of 30 patients with hepatoma had specific anti-HCV antibodies in contrast to 11 others with serum HBsAg positivity. One hundred blood transfusion donors and 25 antenatal patients were tested concurrently and shown to be negative for anti-HCV. Specific antibodies to HCV were present in very few patients with cirrhosis, presumptive NANBH and hepatoma tested in this local survey. False-positive reactions appeared to occur at a higher rate than true-positive results.
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PMID:Hepatitis C virus antibodies in patients with liver disease. The western Cape experience. 165 34

The aim of the present study was to evaluate whether hepatitis C virus plays any role in the development of hepatocellular carcinoma in cirrhotic patients. The role of age, sex, alcohol abuse, and infection by other hepatitic viruses, such as hepatitis B and Delta viruses, was also assessed. We found that mean age and male/female ratio were significantly higher in patients with HCC plus liver cirrhosis than in those with liver cirrhosis alone. Also, the prevalence of HCV infection was found to be higher in HCC patients compared to cirrhotics. Further, by means of multiple logistic regression, we evaluated the independent role of each variable in the development of HCC. Age, male sex, and to a lesser degree, HCV infection, as assessed by anti-HCV positivity, were the only risk factors which significantly correlated with the development of HCC. Moreover, when age and sex were excluded from the statistical model, HCV infection, but not HBV, HDV, and alcohol abuse, appeared to be associated with HCC. In conclusion, based on these data, age and male sex are the most important factors for the development of hepatocellular carcinoma in cirrhotic patients. Hepatitis C virus, at least in the Mediterranean area, may play a role as an additive risk factor of HCC in patients suffering from liver cirrhosis.
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PMID:Hepatitis C virus infection is an additive risk factor for development of hepatocellular carcinoma in patients with cirrhosis. 165 21


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