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)

Excessive ethanol consumption has been related with the development of liver cirrhosis, as well as with rapid intestinal transit time and diarrhea. Moreover, heavy drinking is associated with an increased incidence of cancer of the oropharynx, larynx, esophagus, and colorectum. Acetaldehyde of microbial origin has recently been suggested as a possible pathogenic factor behind this alcohol-associated gastrointestinal morbidity. The present in vitro study was aimed to investigate alcohol dehydrogenase activity and acetaldehyde formation capacity of some major aerobic bacteria representing the normal colonic flora in man. Cytosolic alcohol dehydrogenase activity and cytosolic protein concentration were determined spectrophotometrically. Alcohol dehydrogenase activity was then calculated as nmoles of reduced substrate produced by milligrams of protein per minute. The ability of different bacteria to produce acetaldehyde was determined by incubating the intact bacterial suspension in closed vials containing ethanol (final concentration 22 mM) for 1 hr at 37 degrees C. The acetaldehyde formed during the incubation was analyzed by headspace gas chromatography. Marked differences in the alcohol dehydrogenase activity and acetaldehyde forming capacity were found among the strains tested. The alcohol dehydrogenase activity varied from 606 +/- 91 nmol/min/mg protein (Escherichia coli IH 50546) to 1 +/- 0.2 nmol/min/mg protein (E. coli IH 50817), and acetaldehyde formation varied from 1,717 +/- 2 nmol acetaldehyde/10(9) colony-forming units (Klebsiella oxytoca IH 35403) to 5 +/- 2 nmol acetaldehyde/10(9) colony-forming units (Pseudomonas aeruginosa ATCC 27853). There was a statistically significant correlation (r = 0.77; p < 0.001) between alcohol dehydrogenase activity and acetaldehyde production from ethanol, strongly suggesting the catalytic role of bacterial alcohol dehydrogenase in this reaction.
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PMID:In vitro alcohol dehydrogenase-mediated acetaldehyde production by aerobic bacteria representing the normal colonic flora in man. 889 13

We investigated whether the reduction of plasma tyrosine in alcoholic liver disease would affect the branched-chain amino acid/tyrosine molar ratio (BTR) measured using an enzymatic assay method in alcoholic cirrhosis. BTR values were higher in patients with compensated and decompensated alcoholic cirrhosis (5.68 +/- 2.29 and 3.28 +/- 0.75) due to reduction of the tyrosine level relative to those in patients with nonalcoholic cirrhosis (3.64 +/- 1.22 and 2.53 +/- 0.99). A decrease in tyrosine level and an increase in BTR value were observed after single ethanol administration to healthy subjects. As significant elevation of serum immunoreactive insulin levels followed elevation of serum glucose levels after alcohol loading, it was thought that insulin accelerated intrahepatic metabolism of aromatic amino acids, resulting in reduction of the tyrosine level. The same mechanism may be applied to tyrosine reduction in patients with alcoholic cirrhosis during heavy drinking.
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PMID:Influence of alcohol on branched-chain amino acid/tyrosine molar ratio in patients with cirrhosis. 962 91

Economists have examined the impact of alcohol prices on various outcomes related to alcohol consumption, including nonfatal and fatal motor vehicle accidents, other accidents, liver cirrhosis, and other alcohol-related mortality, crime, and education attainment. Price, in the context of this research, includes not only the monetary price of alcoholic beverages, but also a wide variety of other "costs" of drinking and heavy drinking, including the time spent obtaining alcoholic beverages and the legal costs associated with drinking and related behavior. This research clearly demonstrates that increases in the monetary prices of alcoholic beverages, which could be achieved by increasing taxes on alcohol, can significantly reduce many of the problems associated with alcohol use and abuse. In addition, control policies that raise other "costs" of drinking, including reduced availability of alcoholic beverages, higher legal drinking ages, and others, are also effective in reducing the consequences of alcohol use and abuse.
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PMID:The effects of price on the consequences of alcohol use and abuse. 975 52

Alcohol taken in moderation may prevent atherosclerosis, whereas heavy drinking has the opposite effect, in part by promoting oxidation of low density lipoproteins (LDL), a pathogenetic factor in atherogenesis. We assess here: 1 ) whether similar alterations can be reproduced in baboons fed 50% of energy as ethanol (the average intake of alcoholics) for 7- 8 years, and 2 ) whether such alterations are affected by supplementation with polyenylphosphatidylcholine (PPC), a mixture of polyunsaturated phosphatidylcholines, shown to prevent alcoholic fatty liver, fibrosis, and cirrhosis. Ten animals were given the ethanol-containing diet and ten were pair-fed isocaloric control diets. In half of the pairs, the diets were supplemented with 2.8 g of polyenylphosphatidylcholine/1000 kcal. Alcohol feeding increased LDL-lipoperoxides and made LDL-proteins more negatively charged, changes that were attenuated or prevented by PPC. The oxidizability of LDL was determined in vitro by the formation of conjugated dienes after oxidation with copper. Alcohol shortened the lag time (which measures LDL antioxidant capacity); this effect was normalized by PPC supplementation. By contrast, PPC produced no changes in the controls. Thus polyenylphosphatidylcholine, by markedly attenuating the ethanol-induced increase in LDL oxidation, opposes one of the effects whereby alcohol promotes atherosclerosis.
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PMID:Oxidation of LDL in baboons is increased by alcohol and attenuated by polyenylphosphatidylcholine. 1035 29

Alcohol-related liver disease (ALD) is a common indication for orthotopic liver transplantation (OLT) in adults. Although return to 'heavy drinking' post-OLT is believed to be uncommon, the prevalence and severity of alcohol-related liver injury in such patients is not well characterized. We retrospectively reviewed the records of 68 adult patients who underwent OLT for ALD to determine the incidence of return to heavy drinking and to assess their clinical outcome. Follow-up ranged from 8-99 months (mean 42) post-OLT; 54 patients were followed for > or = 12 months. Ten patients (15%) had evidence of coexisting viral hepatitis (hepatitis C in 9 and hepatitis B in 1) before OLT. Six of 68 patients (8%) returned to heavy drinking post-OLT, and three of those died of alcoholic hepatitis at nine months, 2.5 and 3.5 years after OLT. In two of these three patients, premortem liver biopsy showed histologic features of alcoholic hepatitis in addition to bridging fibrosis or cirrhosis. None of the three patients who died of ALD had coexisting viral hepatitis. Of the 57 patients surviving for > or = 3 months post-OLT, 4 of 8 patients (50%) with steatosis and Mallory bodies in their native livers returned to heavy drinking compared to only 2/49 (4%) without these histologic findings (P<0.05). In conclusion, the incidence of heavy drinking post-OLT was uncommon, however, it was associated with fatal alcoholic hepatitis in 50% of patients. Rapidly progressive alcohol-related liver injury was seen even in the absence of coexisting viral hepatitis. The presence of steatosis and Mallory bodies in the native liver, which suggests recent or ongoing alcohol-related liver injury, predicted a return to heavy drinking post-OLT.
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PMID:Rapidly progressive liver injury and fatal alcoholic hepatitis occurring after liver transplantation in alcoholic patients. 1040 63

To establish their ability to predict malnutrition, irregular feeding, alcoholic intake, derangement of social and familial links and organic complications (liver cirrhosis) were assessed in 181 hospitalized male alcoholic. BMI was under 18.5 kg/m(2) in 8.9%, between 18.5-20 kg/m(2) in 8.9%, 20-25 kg/m(2) in 42%, 25-30 kg/m(2) in 32.2% and over 30 kg/m(2) in 8.2% of patients. Malnutrition was related to the intensity of ethanol intake, development of social or familial problems, irregularity of feeding habits and cirrhosis with ascites. Irregularity of feeding habits was also related to heavy drinking and to social or familial derangement. By logistic regression analysis, the only variables which independently predict malnutrition were irregular feeding habits and liver cirrhosis with ascites. In a second step, irregular feeding was dependent on social or familial troubles and daily intake of ethanol. So, malnutrition related to alcoholism seems multifactorial in its pathogenesis.
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PMID:Nutritional assessment in alcoholic patients. Its relationship with alcoholic intake, feeding habits, organic complications and social problems. 1081 89

The traditional approach to alcoholism is treatment of underlying psychological and behavioral problems. Earlier and more direct avenues to prevent or counteract alcohol's effects include a focus on early detection of alcoholism, using, in part, biochemical markers of heavy drinking such as carbohydrate-deficient transferrin (CDT) and screening, among heavy users of alcohol, for signs of medical complications. Only a few heavy drinkers eventually develop liver cirrhosis. Because no practical genetic markers exist indicating who will develop fibrosis and cirrhosis, heavy drinkers who have signs of liver injury should undergo liver biopsy to determine whether they have perivenular fibrosis, a recognized precursor lesion to cirrhosis. Those who do should start intense treatment efforts, such as correction of nutritional deficits, curbing alcohol consumption, and participation in ongoing controlled trials. Some "supernutrients" have been effective in baboons, including S-adenosylmethionine for the treatment of alcohol-induced liver injury and polyenylphosphatidylcholine for the prevention of fibrosis. Both drugs are now being tested in humans. Prednisolone improves survival in patients with alcoholic hepatitis who have either spontaneous hepatic encephalopathy or a high "discriminant function."
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PMID:Alcoholic Liver Disease. 1109 76

The alcohol-withdrawal syndrome is a well-known clinical situation, so does its treatment. However, new researches have shown that the risk of severe withdrawal manifestations increases proportionally with the number of previous detoxifications, according to a sensitisation stress model. As a consequence, special attention should be paid to patients with a clinical history of multiple alcohol detoxifications, even if they never previously had delirium tremens and/or comitiality. Even in the absence of characteristic neurologic lesions, long-lasting heavy drinking is associated with brain dysfunction, concerning mostly the frontal cortex. This is clinically associated to neuropsychological deficits, specifically disorders of working memory and the so-called "executive functions". These deficits have a dramatic importance, because they impair drastically the outcome of alcoholic patients after detoxification. In Belgium like in other countries, an increasing prevalence of hepatitis C is present in alcoholic patients. This is due probably to the increase of a former illegal drugs consumption in those patients. This association between alcoholism and hepatitis C is of major importance, because alcohol consumption increases the viral load and the risk of cirrhosis and hepatocarcinoma. Furthermore, alcohol reduces the response to interferon therapy.
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PMID:[Clinical and therapeutic aspects in the treatment of alcohol addiction]. 1242 55

Gastroduodenal ulcers and gastroduodenal erosions are particularly frequent in cirrhotic patients, but their precise cause is unclear. The aim of this study was to identify pathogenic factors associated with ulcers and erosions in patients with cirrhosis. We studied 64 consecutive patients with cirrhosis referred for gastroscopy. The severity of portal hypertensive gastropathy was graded with an endoscopic score. H. pylori status was determined by histological examination of gastric biopsy samples or by the [13C] urea breath test. The daily alcohol intake within the preceding week was recorded. The Child-Pugh score was determined. Fifteen patients had gastroduodenal ulcer and 20 had gastroduodenal erosions. Cirrhosis was related to alcohol in 44 patients and hepatitis B or C virus in 14 patients. The portal hypertensive gastropathy was graded as severe in 12 patients and mild in 25 patients. H. pylori infection, found in 37 patients, was not related to the gastroduodenal lesions. Univariate and multivariate analysis showed the links between gastroduodenal erosions and hypertensive gastropathy and recent heavy drinking. Gastroduodenal ulcer was independently associated only with the severity of the gastropathy. In conclusion, in these patients with cirrhosis, the presence of gastroduodenal ulcer was significantly related to hypertensive gastropathy but not to H. pylori infection. Recent alcohol intake favored the occurrence of gastroduodenal erosions.
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PMID:Gastroduodenal ulcer and erosions are related to portal hypertensive gastropathy and recent alcohol intake in cirrhotic patients. 1282 73

About 5,000 people die each year from chronic liver disease in England and Wales alone. In many patients, the liver injury is due to chronic excessive alcohol consumption and manifests as alcoholic hepatitis (an acute inflammation of the liver), cirrhosis, or alcoholic hepatitis superimposed on a background of cirrhosis. Mild alcoholic hepatitis may be asymptomatic and reversible, but where the hepatitis is more severe, up to 65% of those affected die from it. The incidence of alcoholic hepatitis in the UK seems set to increase with the rise in heavy drinking, particularly among women. Here we review how patients with alcoholic hepatitis should be managed.
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PMID:Management of alcoholic hepatitis. 1287 88


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