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

We report on the occasional presence of iron granules in plasma cells in two male patients respectively 64 and 71 years old, both with excessive drinking habits. One patient also had liver cirrhosis. In both patients the bone-marrow biopsy showed a macrocytic anemia without megaloblasts. We refer the morphologic data because the cases reported are not many and the presence of iron granules in plasma cells was a curious and rare aspect. The most important feature appearing from the data issued is the gap concerning both the source and mechanism that cause this phenomenon. Some investigations have suggested that the plasma cell iron is located in mitochondria, others have noted that iron granules were located between the Golgi region and the rough endoplasmic reticulum. Moreover, the morphologic data are not related to the number of plasma cells in the bone-marrow and there is no causal relation between alcoholic abuse and plasma cell iron. The first problem is common, the second is rare.
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PMID:With regards to the presence of iron granules in plasma cells. 181 5

Cirrhosis mortality death rates in Ontario for ages 20 and over declined from a high of 9.3 per 100,000 in 1911 to a low of 5.6 per 100,000 in 1919 (p less than 0.001) and after a 17-year period of relative stability, rose steadily to a high of 19.7 per 100,000 in 1975 (p less than 0.0001) and then declined to 13.3 per 100,000 in 1986 (p less than 0.001). Rates were consistently higher for men than for women and the male to female ratio of the rates increased from a low of 1.3 in 1933 to a high of 2.5 in 1986. The rate of increase in the rates for both men and women, and the rate of decline after the mid 1970s was most noted in the younger ages. Differences in trend could not be related to changes in disease classification, method of recording deaths, changes in diagnostic habits such as introduction of needle liver biopsy or to method of standardizing the rates. There was a positive and significant correlation between per capita alcohol consumption and rates of cirrhosis in Ontario from 1932 to 1975. However, while cirrhosis rates declined markedly from 1976 to 1986, alcohol consumption remained stable from 1976 to 1980 and declined only slightly from 1981 to 1986. A possible explanation for lack of correlation between alcohol consumption and the cirrhosis rates from 1976 to 1986 could be that the balance of force favoured recovery i.e. those people who already had cirrhosis who decreased (or stopped) their consumption of alcohol, did not die. Correlations with lagged alcohol consumption could not explain all the changes in the cirrhosis rates. Although cirrhosis rates consistently increased with increasing age from 35 to 85, our results showed that succeeding generations were developing cirrhosis at successively younger ages after the age of 35. Possible explanations for this cohort effect are increased survival from infectious diseases in infancy and childhood, increase in hepatitis B infection, excessive drinking habits being established at younger ages or a change in the pathogenesis of the disease.
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PMID:Changing trends of cirrhosis mortality in Ontario, Canada, 1911-1986. 206 20

There is a significant association between the pro capita alcohol consumption and cirrhosis mortality rate. Cirrhosis usually develops after years of excessive drinking, although in many alcoholic men it never develops, even after decades of drinking. The admission of large amounts of alcohol beverages is very difficult for many patients. This is a serious problem. In order to make easier the diagnosis in those patients, the authors have studied a composed, arbitrary score for alcoholism risk. The diagnosis with only laboratory findings was worse than that with an additional alcoholism risk score, in 48 cirrhotic patients with doubtful history of alcoholic etiology. The alcoholic risk score was based on presence/absence of: 1) car driving or working accidents; 2) familiar or love problems; 3) alcoholic relatives; 4) other alcohol-correlate disease; 5) job type.
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PMID:[A method for identification of liver cirrhosis of alcoholic etiology]. 264 53

The relation between alcohol consumption and several causes of death, including breast cancer, was examined in a population of 581, 321 women enrolled in a prospective study in 1959 and followed for 12 years. Women who drank occasionally had about the same breast cancer mortality rate as nondrinkers; those who drank one to four drinks per day had SMRs 7-26% higher; five drinks per day, 1.89; and six or more drinks per day, 1.65. The two highest-consumption groups' risks were significantly higher than those of nondrinkers after multivariate adjustment for several breast cancer risk factors. Distinctive dose-response relationships were observed for two known alcohol-related conditions: cirrhosis of the liver and cancer of the aero-digestive tract, suggesting that results for other causes are not seriously biased by misclassification of drinking habits. Death rates from all causes combined were elevated for drinkers of three or more drinks per day. Whether or not the association of elevated breast cancer death rates ultimately turns out to be causal, there is ample reason to continue to warn the public against excessive drinking.
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PMID:Alcohol and breast cancer: a cohort study. 324 67

Per capita consumption of alcohol rose steadily in the U.K. from 1970 to 1979, but fell by 11% between 1979 and 1982. This fall in consumption was followed by a 19% fall in first admissions for alcohol dependence, a 16% fall in drunkenness convictions, a 7% fall in drinking and driving convictions and a 4% fall in cirrhosis mortality. Between 1970 and 1982 there were highly significant (P less than 0.01) correlations between per capita consumption and convictions for drunkenness and drinking and driving, first admissions to hospital for alcohol dependence, and mortality from cirrhosis, pancreatitis and cancer of the oesophagus. These findings add weight to the argument that per capita consumption is the crucial variable determining the magnitude of the burden imposed on the community by the harmful effects of excessive drinking.
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PMID:The beneficial consequences of the United Kingdom's declining per capita consumption of alcohol in 1979-82. 653 63

There is considerable evidence in favour of genetic factors influencing excessive drinking behaviour and development of alcohol dependence (alcoholism), although readily identified markers of these genes have not been established. In addition, environmental factors undoubtedly play an important role. Although the probability of developing a significant liver disease (alcohol-induced hepatitis with or without cirrhosis) is related to the amount of alcohol ingested, there is a great variation in susceptibility which presumably stems from either genetic or additional environmental influences. The probable linkage of development of severe alcohol-induced liver disease with alleles of the HLA-B locus would suggest the influence of a gene(s) on chromosome 6. Such a gene may determine the rate or type of metabolism of alcohol or, since the immune response genes are present on chromosome 6, may indicate genetically controlled variation in the level of the immune and inflammatory response to alcohol-induced changes in liver membrane antigenicity. Further studies are needed to confirm these associations and to determine the type of factor involved.
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PMID:Genetic factors in determining susceptibility to alcohol dependence and development of alcohol-induced liver disease. 678 10

The cross-sectional, observational studies from four groups which have reported a difference between males and females in susceptibility to ethanol-induced liver disease are reviewed. Crucial factors of representativeness of sampled groups, certainty of cirrhosis diagnosis, and quantitation of ethanol intake are examined. Attention is given to the direction of differences between males and females in the variables suggestive of differential susceptibility: age at presentation, years of excessive drinking, age at which excessive drinking began, percent of alcoholics of each sex diagnosed as having cirrhosis, age at death due to cirrhosis, daily ethanol intake, and the male to female ratio among cirrhotics as compared to alcoholics. Based on the consistency of findings among the studies reviewed, as demonstrated by replication of results obtained under different conditions of time, place, methodology, and subsamples of alcoholics studied, a conclusion of enhanced susceptibility to ethanol-induced liver disease among women is reached. Finally, factors which may lend biological plausibility to the above susceptibility differential are considered.
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PMID:Sex-related differences in ethanol-induced liver disease: artifactual or real? 704 71

Mortality rates were drawn from the California Occupational Mortality Study (COMS) to analyze liver cirrhosis deaths within occupations and industries from 1979 to 1981. Age-adjusted Standardized Mortality Rates (SMRs) were made available by the State of California for separate analyses of women, men, blacks and whites. Rankings of occupations with narrow confidence intervals were strikingly similar for blacks and whites. Within occupations, the highest female SMRs were for waitresses, telephone operators, cosmetologists, dress makers, hospital orderlies, textile workers, and laborers. The lowest female SMRs were for skilled crafts workers and teachers. High male occupations included water transportation workers, bartenders, loggers, laborers, roofers, construction workers, farm workers, iron workers, and painters. Low male occupations included teachers, physicians and dentists, managers, factory supervisors, business sales workers, heavy equipment operators, and other professionals. High female industries included eating and drinking places, laundry/dry cleaning, nursing and personal care facilities, aerospace, beauty shops, and entertainment. Low female industries included wholesale trades and education. High male industries included water transportation, military, guard services, eating and drinking places, iron and steel mills, and railroads. Low male industries included research/engineering labs, education, and computer manufacturing. This study was descriptive. It remains unknown whether certain jobs cause excessive drinking and cirrhosis, or whether people who are prone to develop cirrhosis select certain jobs.
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PMID:Liver cirrhosis deaths within occupations and industries in the California occupational mortality study. 832 68

Most hepatocellular carcinomas (HCC) in Japan are found in chronic liver diseases with persistent infection of hepatitis B or C virus. Thus, the high risk group for HCC is evident and most small HCC, less than 2 cm in diameter, are detected by a regular follow-up of every three months using ultrasonography (US) in patients with liver cirrhosis or chronic hepatitis over 40 years of age. Approximately half of localized lesions less than 2 cm in diameter found by US are not HCC. Thus, liver biopsy using fine needles is important to make a definite diagnosis in such small lesions. The most important factor in mass survey for HCC is to select people with risk factors for HCC from the whole population. We selected people for a mass survey using US who have risk factors such as 1) abnormal liver function tests, 2) past history of liver diseases, 3) HBV or HCV carrier, 4) past history of blood transfusion, and 5) excessive drinking. About one percent of the people surveyed showed HCC. The detection rate is excellent. In future, serum tumor markers for HCC such as AFP and PIVKA-II will be useful for diagnosis of small HCC because recent studies indicate that such small HCC also produce such tumor markers in about half of the cases.
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PMID:[Early detection of hepatocellular carcinoma--high risk group and mass survey]. 838 56

Much progress has been made in the understanding of the pathogenesis of alcoholic liver disease, resulting in improvement of prevention and therapy, with promising prospects for even more effective treatments. The most successful approaches that one can expect to evolve are those that deal with the fundamental cellular disturbances resulting from excessive alcohol consumption. Two pathologic concepts are emerging as particularly useful therapeutically. Whereas it continues to be important to replenish nutritional deficiencies, when present, it is crucial to recognize that because of the alcohol-induced disease process, some of the nutritional requirements change. This is exemplified by methionine, which normally is one of the essential amino acids for humans, but needs to be activated to S-adenosylmethionine (SAMe), a process impaired by the disease. Thus, SAMe rather than methionine is the compound that must be supplemented in the presence of significant liver disease. Indeed, SAMe was found to attenuate mitochondrial lesions in baboons, replenish glutathione, and significantly reduce mortality in patients with Child A or B cirrhosis. Similarly, polyenylphosphatidylcholine (PPC) corrects the ethanol-induced hepatic phospholipid depletion as well as the decreased phosphatidylethanolamine methyltransferase activity and opposes oxidative stress. It also deactivates hepatic stellate cells, whereas its dilinoleoyl species (DLPC) increases collagenase activity, resulting in prevention of ethanol-induced septal fibrosis and cirrhosis in the baboon. Clinical trials with PPC are ongoing in patients with alcoholic liver disease. Furthermore, enzymes useful for detoxification, such as CYP2E1, when excessively induced, become harmful and should be downregulated. PPC is one of the substances with anti-CYP2E1 properties that is now emerging. Another important aspect is the association of alcoholic liver disease with hepatitis C: a quarter of all patients with alcoholic liver disease also have markers of HCV infection, with an even higher incidence in some urban areas but, at present, no specific therapy is available since interferon is contraindicated in that population. However, in addition to antiviral medications, agents that oppose oxidative stress and fibrosis should also be tested for hepatitis C treatment since these two processes contribute much to the pathology and mortality associated with the virus. In addition to antioxidants (such as PPC, silymarin, alpha-tocopherol and selenium), anti-inflammatory medications (corticosteroids, colchicine, anticytokines) are also being tested as antifibrotics. Transplantation is now accepted treatment in alcoholics who have brought their alcoholism under control and who benefit from adequate social support but organ availability is still the major limiting factor and should be expanded more aggressively. Finally, abstinence from excessive drinking is always indicated; it is difficult to achieve but agents that oppose alcohol craving are becoming available and they should be used more extensively.
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PMID:Alcoholic liver disease: new insights in pathogenesis lead to new treatments. 1072 99


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