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)

Although it is well established that the majority of alcoholics are neurologically compromised, little is known about the etiological factors underlying the central nervous system (CNS) disturbances. Without doubt, ethanol is a neurotoxin; however, the complex array of factors presaging drinking onset and factors concomitant to a lifestyle of alcohol abuse probably also influence the risk for neurologic injury. This chapter reviews the emerging evidence linking liver disease to the neurologic pathology manifested by chronic alcoholics. The observation that the pattern and severity of cognitive deficits is similar between alcoholics and nonalcoholics with cirrhosis, combined with the demonstration that biochemical indices of liver injury correlate with cognitive test performance in alcoholics, illustrates the important role of liver disease as a codeterminant of the CNS disturbance. In addition, the findings from developing research indicating that liver transplantation can reverse the deficits on neuropsychological tests further underscore the importance of advanced liver disease as a determinant of the CNS pathology, and the results suggest the need for aggressive treatment of alcoholic liver disease for restoring the alcoholic's functional cognitive abilities, which, in turn, may improve the prognosis for psychosocial adjustment.
Recent Dev Alcohol 1991
PMID:Hepatic encephalopathy coexistent with alcoholism. 175 84

The fact that only a small percentage of excessive drinkers develop cirrhosis may be due to a genetic susceptibility to the disease. In order to identify possible genetic risk factors for cirrhosis, we studied mixed-race (Negroid-Caucasian) inhabitants of the French West Indies and compared: (1) the frequency of 51 HLA-A, -B, -C and -DR antigens in 41 subjects with alcoholic cirrhosis and in two control groups consisting of 41 excessive drinkers free of liver disease and 51 healthy non-drinkers; and (2) the frequency of Gm and Km haplotypes in the same groups. Analysis of the Gm system also determined the patients' ethnic origins. The frequency of the HLA-A2 antigen was significantly higher in the cirrhotic patients than in the control group of excessive drinkers (chi 2 = 4.47; P less than 0.05), while that of the HLA-B15 antigen was significantly lower (chi 2 = 5.14; P less than 0.05). The frequency of the Cw4 antigen was significantly higher in the cirrhotics than in the non-drinkers (chi 2 = 5.59; P less than 0.05). However, these differences did not persist when the number of comparisons was taken into account. The frequency of Gm and Km haplotypes was not significantly different in the three groups. In conclusion, complementary studies are required to determine the value of the Gm-Km system as a marker of susceptibility to alcoholic cirrhosis. Our results do not identify an association between HLA antigens and cirrhosis specific to a negroid ethnic group and support the notion that such an association is weak.
Alcohol Alcohol 1991
PMID:HLA Gm systems and susceptibility to alcoholic cirrhosis: a study of mixed-race subjects. 176 53

The effects of alcoholism and liver disease on memory functioning in alcoholics were studied by comparing four groups: normal healthy controls, alcoholics without liver disease, alcoholics with biopsy-confirmed cirrhosis, and nonalcoholics with postnecrotic cirrhosis. Memory capacity was evaluated employing the Benton Visual Retention Test (BVRT), the Rey-Osterreith Complex Figure Test, Digit Span, and the Brown Peterson four-word short-term memory test. A 2 x 2 ANOVA revealed significant main effects for both alcohol and cirrhosis on Digits Forward and the total score on the Brown Peterson test. Additionally, there were significant main effects for cirrhosis on the BVRT. The Brown Peterson test was analyzed using a repeated measures 2 x 2 ANOVA. Significant effects for cirrhosis were observed at all three interpolation periods. The effects for alcohol approached significance at the 30-sec (most difficult) interpolation period. Analysis of error patterns on the Brown Peterson test indicated that overall omission errors were most commonly made among all groups. Significant effects were found for alcohol on omissions and intrusion, while the cirrhosis factor yielded significant effects for phonemic, perseverative, and omission errors. This study demonstrates the importance of liver disease underlying the etiology of memory impairments in alcoholics. The results confirm our earlier findings that neuropsychologic deficits seen in alcoholics may be the result of the combination of alcohol abuse and liver disease.
Alcohol Clin Exp Res 1991 Dec
PMID:The role of cirrhosis in memory functioning of alcoholics. 178 89

Cognitive functioning in alcoholic cirrhotics before and 1 year following orthotopic liver transplantation was compared with age- and sex-matched normal subjects. The alcoholic group improved significantly following transplantation on tests measuring psychomotor, visuopractic and abstracting abilities whereas the performance of normal controls remained virtually unchanged. In contrast, memory capacity in alcoholics with cirrhosis did not statistically improve following successful transplantation. Further investigation, using more sophisticated measures of memory function, are required to determine whether memory deficits are either associated with alcohol neurotoxicity or an irreversible component of hepatic encephalopathy. These findings suggest that a reversible hepatic encephalopathy underlies many of the neuropsychologic deficits observed in cirrhotic alcoholics and can be ameliorated following successful liver transplantation.
Alcohol Clin Exp Res 1991 Dec
PMID:Improvement in cognitive functioning of alcoholics following orthotopic liver transplantation. 178 92

It is known that chronic alcoholism causes morphological changes of the myocardium before the development of a specific dilated cardiomyopathy. We studied a group of chronic alcoholics, with normal arterial pressure and without clinical evidence of liver cirrhosis, to evaluate left ventricular function, both before and after withdrawal of ethanol. A M-B mode echo recording of the left ventricle and left ventricular inflow Doppler velocimetry with carotid pulse tracing was performed in each patient within 24 hours of the last alcohol consumption and after a period of abstinence at least 3 weeks. We analysed parameters of left ventricular systolic and diastolic functions, in comparison with a group of normal subjects well matched for age, body surface area and heart rate. The results showed that, in the group of alcoholics, a cardiac hypertrophy exists with increased left ventricular mass and normal parameters of left systolic ventricular function, but with altered ratio PEP/LVET. This last result is the consequence of an abnormal left diastolic ventricular function, as demonstrated from the analysis of the Doppler indexes of left ventricular filling (lower ratio E/A). Left ventricular inflow Doppler velocimetry showed different results in alcoholics and control subjects in the early diastolic flow velocity peak (61 +/- 12 vs 84 +/- 8) and in the peak flow velocity in the atrial contraction phase (62 +/- 10 vs 40 +/- 5.6). We have not observed any change of the echocardiographic parameters after the short period of alcohol withdrawal. We advance the hypothesis that there is an altered diastolic function depending, not only on the hypertrophy of the myocardium, but also on the myocardial interstitial involvement caused by ethanol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Noninvasive evaluation of left ventricular function in alcoholics before and after suspension of ethanol abuse]. 183 30

Using the 1986 National Mortality Followback Survey, alcohol consumption patterns were compared for decedents with and without mention of cirrhosis of the liver as a cause of death. Approximately 55% of cirrhosis decedents had 3 drinks or more daily (80% of decedents with alcoholic cirrhosis, and 40% of decedents with unspecified or other specified cirrhosis). In contrast, only 10% of decedents without cirrhosis had at least 3 drinks daily. Forty percent of decedents with alcoholic cirrhosis had 7 drinks or more daily, compared with 17% for unspecified cirrhosis, and 21% for other specified cirrhosis. The comparable figure was 3% for decedents without cirrhosis. An average of 3 drinks per day was associated with increased cirrhosis proportional mortality, and cirrhosis proportional mortality increased with higher numbers of daily drinks.
Alcohol Alcohol Suppl 1991
PMID:Drinking patterns and liver cirrhosis mortality. 184 57

Alcoholic hepatitis is associated with progressive hepatic fibrosis and the development of cirrhosis. The increased fibrosis is principally the result of increased collagen synthesis which exceeds lesser increases in collagen degradation. No proven therapy exists for progressive hepatic fibrosis in alcoholic liver disease. Sobriety increases long-term survival, but there is no evidence that it affects the process of fibrogenesis once initiated. Corticosteroids increase hospital survival in severe alcoholic hepatitis, while long-term propylthiouracil therapy increased survival in moderately severe alcoholic hepatitis. However, neither therapy was found to decrease hepatic fibrosis. By contrast, long-term therapy with colchicine improved survival and decreased hepatic fibrosis in a few patients with cirrhosis. Potential new therapies which have been shown to decrease fibrosis in animals or by cells in vitro include prostaglandin E2, gamma interferon, and inhibitors of proline hydroxylation.
Alcohol Alcohol Suppl 1991
PMID:Approaches to treatment of fibrogenesis in alcoholic liver disease. 184 64

Recent quantitative neuropathological analyses of the effects of alcohol on the central nervous system have revealed some interesting findings. CT scan studies have suggested shrinkage of the brain in alcoholics and this has been confirmed pathologically. Brain shrinkage relates to a loss of the white matter rather than the grey. However the cortical grey matter is not spared. There is a selective loss of neurones from the frontal region and in this and other cortical regions (motor and cingulate) there is shrinkage of the neuronal soma. This is reflected in a retraction of neuronal dendritic arbor which could account for a loss of white matter but does not explain the reversible brain shrinkage that sometimes follows prolonged abstinence. These studies were extended to specific population groups including moderate drinkers, female alcoholics and alcoholics with cirrhosis of the liver and the Wernicke-Korsakoff syndrome.
Alcohol Alcohol Suppl 1991
PMID:If you drink your brain will shrink. Neuropathological considerations. 184 66

A 63-year-old male patient with compensated cirrhosis underwent transcatheter arterial embolization (TAE) and percutaneous ethanol injection therapy (PEIT) for a minute hepatocellular carcinoma (HCC). Although the HCC was successfully treated, esophageal varices worsened and refractory ascites developed 3 months after the TAE and PEIT. Liver atrophy progressed rapidly compared to the natural course of liver cirrhosis.
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PMID:Liver atrophy after transcatheter arterial embolization and percutaneous ethanol injection therapy for a minute hepatocellular carcinoma. 184 52

Cirrhosis mortality and morbidity rates have declined in many jurisdictions, including the U.S., in recent years. Previous research in Canada and Europe suggests that these declines are linked to changes in per capita consumption of alcohol and changes in the availability and/or utilization of services to reduce abusive drinking (e.g., treatment, Alcoholics Anonymous). In this study, changes in cirrhosis death rates in the 50 U.S. states and the District of Columbia between 1974 and 1983 were regressed onto changes in per capita consumption (1974-83). AA membership (1974-83) and alcoholism treatment (1979-82). No significant relationship between treatment and cirrhosis changes was observed; however, the measure of change in treatment may not reflect the full extent of changes that occurred in the 1974-83 period. As predicted, decreases in per capita consumption and increases in AA membership were significantly associated with decreases in cirrhosis rates.
J Stud Alcohol 1991 Jul
PMID:Reductions in cirrhosis deaths in the United States: associations with per capita consumption and AA membership. 187 10


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