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)

Acute alcoholic hepatitis is the first alcoholic lesion of the liver in the process of progression to cirrhosis. It is due to the toxic action of alcohol on hepatocytes, in particular in the centrolobular region. It may affect a liver which is the site of fatty infiltration, fibrosis or cirrhosis, i.e. during all the stages of alcoholic liver disease. Its severity depends upon the degree of alcoholic intoxication. It may be fatal by malignant hepatic failure in a quarter of cases or, at the extreme, be totally asymptomatic. The aims of treatment are: 1) in the immediate, to prevent death; 2) subsequently, to prevent progression to cirrhosis. The majority of the wide range of treatments suggested have been evaluated in controlled trials. It is thus easy to show that corticosteroids are effective in severe acute alcoholic hepatitis, i.e. with encephalopathy and coagulation disturbances, but no in ordinary forms. Although logical, nutritional supplements, whether enteral or parenteral, have no influence on the course of acute alcoholic hepatitis. The same applies to anabolic steroids, the association insulin-glucagon, antifibrosis agents or "hepatoprotectors". The elimination of alcoholic intoxication remains the most important point, accepted by all hepatologists.
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PMID:[Treatment of acute alcoholic alcoholism]. 768 Jan 91

Despite recent advances in our knowledge of the mechanisms of alcohol-induced liver damage, abstinence from alcohol and supportive measures remain the mainstays of management for the majority of patients. Progress has been made in our understanding of ethanol metabolism, the role of acetaldehyde, and both genetic and environmental factors responsible for the variation in individual susceptibility to alcoholic liver disease. Evidence for the involvement of the immune system and the effects of alcohol on hepatic fibrosis are also reviewed. Recent therapeutic trials of corticosteroids in acute alcoholic hepatitis have confirmed their benefit in patients who have a high risk of mortality. For patients with end-stage cirrhosis, orthotopic liver transplantation is now an accepted therapy in selected patients who have a good prognosis for future abstinence.
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PMID:Liver damage: mechanisms and management. 814 89

Nutritional inadequacies are frequent in patients with liver damage, specially in those with advanced chronic liver disease, and this fact, as in other pathological circumstances, may influence their clinical evolution and outcome. Therefore, nutritional therapy may play an important role in the management of these patients. The present paper will deal with some aspects of the nutritional management in patients with liver disease. Special emphasis will be paid to the role of artificial nutritional support in the treatment of acute alcoholic hepatitis, the current status of artificial nutrition in advanced cirrhosis, and some nutritional implications in the management of hepatic encephalopathy.
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PMID:Nutritional therapy in liver disease. 819 52

Having briefly analyzed the metabolism of ethanol in man, the author describes hepatocellular damage induced by alcohol abuse and histological, clinical and biohumoral features of acute alcoholic hepatitis, chronic hepatitis and cirrhosis. Seventy-five clinical cases of acute alcoholic hepatitis, chronic hepatitis and cirrhosis are also illustrated, studied and observed during five years.
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PMID:[Acute hepatitis, chronic hepatitis, cirrhosis: the intermediate and final stages in liver damage induced by chronic alcohol abuse]. 847 14

Diagnosis of liver cirrhosis relies on hepatic biopsy. So far, attempts have failed to achieve a serologic test that differentiates cirrhosis from other hepatic conditions. The aim of this work was to assess the diagnostic value of the ratio of serum angiotensin converting enzyme activity (SACE) and the levels of protein C4 of serum complement (SACE/C4) in differentiating cirrhotic from noncirrhotic alcoholic liver diseases. In this study, 68 active alcoholic patients (17 with fatty liver or minimal changes, 11 with acute alcoholic hepatitis and 40 with cirrhosis) were included. Twenty healthy subjects were studied as a control group. Liver biopsy was performed in all patients. SACE levels were significantly higher in the group with cirrhosis when compared with the group of patients without cirrhosis and the control. On the other hand, serum C4 level decreased as liver damage progressed. SACE values above 25 IU/l had a sensitivity of 92.5 percent (95 percent confidence interval, 87.5 to 97.5) and a specificity of 79 percent (95% percent confidence interval, 70.5 to 87.5), in detecting those patients with liver cirrhosis. The sensitivity further increased to 95 percent (95 percent confidence interval, 90.5 to 99.5) and the specificity to 100 percent when the SACE/C4 ratio was used and a cutoff point of 145 was chosen. To conclude, in alcoholics SACE is specifically elevated in patients with cirrhosis, and the SACE/C4 ratio is a excellent biochemical index for the diagnosis of cirrhosis in alcoholic patients.
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PMID:Serum angiotensin converting enzyme and C4 protein of complement as a combined diagnostic index in alcoholic liver disease. 893 30

Though the hepatotoxicity of ethanol has been established, only 8% to 20% of chronic alcoholics develop cirrhosis. The aim of this study was to assess whether being overweight is a risk factor for alcoholic liver disease. One thousand six hundred four alcoholic patients were studied. According to the liver biopsies, 194 patients had a normal liver; 402 had steatosis without fibrosis; 281 presented with fibrosis, with or without steatosis; 119 presented with acute alcoholic hepatitis (AAH) without cirrhosis; 232 indicated cirrhosis without AAH; and 179 presented with cirrhosis with AAH. One hundred ninety-seven patients had clinically obvious cirrhosis. In the study, five variables were studied as risk factors: age, sex, daily consumption of alcohol during the previous 5 years, the total duration of alcohol abuse, and tendency to be overweight (body mass index [BMI] > or = 25 in women and > or = 27 in men). The BMI was calculated according to the minimum weight over the 10 previous years. In the first stepwise logistic regression analysis, age, being overweight for at least 10 years, being of the female sex, and the total duration of alcohol abuse were independently correlated with the presence of cirrhosis. In the second analysis, female sex being overweight were the two independent risk factors of AAH. In the third analysis, being overweight for at least 10 years was the only independent risk factor of steatosis. These results show that the presence of excess weight for at least 10 years is a risk factor for cirrhosis, AAH, and steatosis. Our results suggest that there is a possible potential for the metabolic effects of ethanol ingestion caused by excess weight in patients with alcoholic liver disease.
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PMID:Excess weight risk factor for alcoholic liver disease. 898 74

The applicability of liver transplantation for ALD remains limited because of ethical arguments and also because of the perception of poor outcome after transplantation. Patients with alcoholic cirrhosis are known to do as well as patients with nonalcoholic liver disease after receiving liver allografts; however, the outcome in patients with severe acute alcoholic hepatitis in this setting is unclear. We studied 9 liver transplant recipients in whom severe acute alcoholic hepatitis was retrospectively diagnosed; 8 had underlying cirrhosis, and 1 had advanced fibrosis. All had Maddrey's discriminant function > 32, and most had hepatic encephalopathy and hepatorenal syndrome. History regarding abstinence was unreliable in some patients. Episodes of acute cellular rejection responded quickly to therapy, and despite recidivism in some patients, long-term survival was comparable to that of patients receiving transplants with alcoholic cirrhosis alone and those with a milder degree of alcoholic hepatitis and cirrhosis. This study suggests that severe acute alcoholic hepatitis may not be an appropriate contraindication for liver transplantation.
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PMID:Survival and quality of life after liver transplantation for acute alcoholic hepatitis. 934 46

Body retinoids are stored in the lipid droplets of hepatic stellate (Ito) cells. In chronic liver disease, the stellate cells differentiate into myofibroblast-like cells, a process whereby they lose their retinoid-containing lipid droplets. We studied the relation between liver retinoid content, the number of lipid droplets per stellate cell, and the number of stellate cells per mm2 in human alcoholic liver disease. Semithin sections of liver biopsies from normal subjects and patients with early (steatosis, inflammation, and mild fibrosis) and late (cirrhosis and cirrhosis with acute alcoholic hepatitis) alcoholic liver disease were morphometrically evaluated. Liver retinoid content was determined by HPLC. In normal patients, liver retinoid content was 901 +/- 213 IU/g of liver (mean +/- SEM). There was a decrease in liver retinoid content in early alcoholic liver disease (409 +/- 50 IU/g) and a further reduction in cirrhosis (153 +/- 50 IU/g). In patients with acute alcoholic hepatitis, retinoid content was strikingly low (5.2 +/- 1.8 IU/g). There was a progressive decrease in the number of stellate cells per mm2 associated with progressive liver damage. We found a fair correlation between the number of stellate cells per mm2 and liver retinoid content in all patient groups (overall correlation: 0.71). In normal subjects, the mean number of lipid droplets per stellate cell was 7.4 +/- 0.7. In patients with early alcoholic liver disease and in patients with alcoholic cirrhosis, this value was increased to 13.6 +/- 0.8 and 10.4 +/- 2.0, respectively. In patients with acute alcoholic hepatitis, only a few lipid droplets were present (4.2 +/- 0.5). There was a good correlation between liver retinoid content and mean number of lipid droplets in normal patients (r = 0.58). In alcoholic cirrhosis, however, correlation was poor (r = 0.34). In early alcoholic liver disease, the correlation was absent (r = 0.004). In conclusion, the major finding of our study is that the correlation between the mean number of lipid droplets per stellate cell and liver retinoid content varies according to the hepatic pathology considered. Marked lipid droplet accumulation occurs in stellate cells in early alcoholic liver disease and, to a lesser extent, in alcoholic cirrhosis, but there is no correlation between the mean number of lipid droplets per stellate cell and liver retinoid content. Therefore, not retinoids but probably lipids are responsible for the accumulation of lipid droplets. We also find that there is a fair correlation between the number of stellate cells per mm2 and liver retinoid content in all patient groups. Finally, we confirm the decrease in hepatic retinoid content that occurs in alcoholic liver disease in humans, even at the early stages of the disease.
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PMID:Hepatic stellate cells and liver retinoid content in alcoholic liver disease in humans. 958 58

Patency and direction of flow in portal veins and their branches are generally assessed by duplex Doppler ultrasonography (DDUS), whereas few data are available on hepatic arterial hemodynamics. In this study, resistive (RI) and pulsatility indexes (PI) were calculated at DDUS in 21 controls, 22 chronic alcoholic patients without evidence of liver damage, 19 patients with acute alcoholic hepatitis (AAH), 30 patients with chronic viral hepatitis (CVH), 23 patients with alcoholic cirrhosis, and 22 patients with viral-related cirrhosis. Diagnosis was based on clinical and histological findings. Mean +/- SD RI was similar in controls and CVH patients (0.64 +/- 0. 02 and 0.66 +/- 0.04, respectively), significantly decreased in alcoholic patients without liver damage and AAH patients (0.61 +/- 0. 07 and 0.60 +/- 0.07) (P < .05), and significantly increased in patients with alcoholic (0.72 +/- 0.04) and viral-related cirrhosis (0.74 +/- 0.04) (P < .05). It was <0.60 in 9 of the 19 AAH patients (47%) and 11 of the 22 alcoholic patients without liver damage (50%), and >0.70 in 39 of the 45 cirrhotic patients (87%) and 12 of the 71 noncirrhotic patients pooled together (17%). A significant correlation was observed between RI and PI (r = .83; P < .05). The coefficients of variation for intraobserver variability were 6.3% +/- 5.1% for RI and 10.1% +/- 6.2% for PI, and the corresponding figures for interobserver variability were 5.2% +/- 3.5% and 9.3% +/- 4.6%. These findings support the existence of ethanol-related hepatic arterial vasodilation in AAH and alcoholic patients without liver damage. Progression of liver damage from AAH to cirrhosis profoundly impairs the hepatic responsiveness as a consequence of fibrosis with vascular distortion.
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PMID:Hepatic artery resistance in alcoholic liver disease. 979 99

To address the hypothesis that elevated blood alcohol increases systemic oxidant stress, we measured urinary excretion of isoprostanes (iPs), free radical-catalyzed products of arachidonic acid. Ten healthy volunteers received acute doses of alcohol (Everclear-R) or placebo under randomized, controlled, double-blind conditions. Urinary iPF2a-III increased in a time- and dosage-dependent manner after dosing with alcohol, with the peak urinary iPF2a-III excretion correlating with the rise in blood alcohol. To determine whether oxidant stress was associated with alcohol-induced liver disease (ALD), we then studied the excretion of iP in individuals with a documented history of alcohol-induced hepatitis or alcohol-induced chronic liver disease (AC). Both urinary iPF2a-III and urinary iPF2a-VI were markedly increased in patients with acute alcoholic hepatitis. In general, urinary iPF2a-III was significantly elevated in cirrhotic patients, relative to controls, but excretion was more pronounced when cirrhosis was induced by alcohol than by hepatitis C. Excretion of iPF2a-VI, as well as 4-hydroxynonenal and the iPF2a-III metabolite, 2,3-dinor-5, 6-dihydro-iPF2a-III, was also increased in AC. Vitamin C, but not aspirin, reduced urinary iPs in AC. Thus, vasoactive iPs, which serve as indices of oxidant stress, are elevated in the urine in both acute and chronic ALD. Increased generation of iPs by alcohol in healthy volunteers is consistent with the hypothesis that oxidant stress precedes and contributes to the evolution of ALD.
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PMID:Alcohol-induced generation of lipid peroxidation products in humans. 1049 16


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