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)

The relationship between alcoholic liver disease and hepatitis C virus was studied in 80 patients by searching for hepatitis C virus RNA with the polymerase chain reaction and by measuring hepatitis C virus antibodies. By C-100 enzyme-linked immunosorbent assay, hepatitis C virus antibodies were found in 2 of 10 patients with fibrosteatosis, 8 of 20 patients with alcoholic hepatitis, 14 of 19 patients with chronic hepatitis and 19 of 31 patients with cirrhosis. Percentages of patients with antibodies found by C-100 radioimmunoassay and by enzyme-linked immunosorbent assay based on sequence peptide 42 were lower; of the 16 patients with a low titer by C-100 enzyme-linked immunosorbent assay, 10 were negative by radioimmunoassay and 6 were negative by sequence peptide 42. By a second-generation recombinant immunoblot assay, hepatitis C virus antibodies were found in 1 of 10 patients with fibrosteatosis, 2 of 20 patients with alcoholic hepatitis, 15 of 19 patients with chronic hepatitis and 18 of 31 patients with cirrhosis. Hepatitis C virus RNA was found in 1 of 10 patients with fibrosteatosis, 3 of 20 patients with alcoholic hepatitis, 13 of 19 patients with chronic hepatitis and 20 of 31 patients with cirrhosis. Of the 37 patients with hepatitis C virus RNA, 31 had antibodies by C-100 enzyme-linked immunosorbent assay (25 patients at a high titer [cut-off index greater than 6]), and 31 had antibodies by second-generation recombinant immunoblot assay. Patients with cirrhosis and hepatitis C virus RNA had higher ALT activity than such patients without hepatitis C virus RNA (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection of hepatitis C virus antibodies and hepatitis C virus RNA in patients with alcoholic liver disease. 166 25

Hepatitis C virus (HCV) has been proposed to be a cofactor in the pathogenesis of cirrhosis in patients with chronic alcoholism. The demonstration of a different liver histological pattern in anti-HCV positive patients might provide additional evidence. We studied 164 patients with chronic alcoholism, and histologically proven cirrhosis. For all of them, serum samples were collected at the time of a liver biopsy and stored at -80 degrees C. Testing for anti-HCV antibodies was done using the Ortho Diagnostic Systems Anti-HCV ELISA test. Only reproducible results were considered positive. A semi-quantitative assessment of seven histological parameters was made independently on liver biopsy samples. In the study group, 29 patients (18%) had anti-HCV antibodies. When compared with anti-HCV negative patients, both groups had similar ALT and AST seric activities. Anti-HCV positive patients had a greater score of mononuclear cells infiltrate (0.71 +/- 0.57 vs 0.41 +/- 0.52; p less than 0.05) and a lesser score of alcoholic hepatitis (0.19 +/- 0.57 vs 0.74 +/- 0.74; p less than 0.005). The scores for steatosis, perisinusoidal and perinodular fibrosis, and hepatocellular necrosis were similar in the two groups. In anti-HCV positive patients, with a clearly positive recombinant immunobinding assay (RIBA, Chiron-Ortho Diagnostic Systems), a greater score for hepatic necrosis and a lesser one for fibrosis were demonstrated. Among the seven patients with active cirrhosis, six were anti-HCV positive. Therefore, HCV is likely to play a role in the pathogenesis of liver damage in a few patients with alcoholic cirrhosis, especially, those with active cirrhosis.
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PMID:Pathogenesis of liver cirrhosis in alcoholic patients: histological evidence for hepatitis C virus responsibility. 166 14

Common features of chronic alcoholic liver disease are progressive hypoalbuminemia and liver fibrosis. The molecular mechanisms which account for these effects are still controversial. Therefore, in the present study we evaluated albumin and collagen gene expression in livers of alcohol abusers and patients with viral-induced liver disease. Albumin and pro-alpha 1 (I) collagen mRNA levels were determined in 30 patients who underwent diagnostic liver biopsy. Of 14 alcoholics, 7 had alcoholic hepatitis alone, while the other 7 had cirrhosis plus alcoholic hepatitis. Of 16 non-alcoholic patients with chronic viral infection, 6 had chronic active hepatitis and 10 cirrhosis plus chronic active hepatitis. Total RNA was extracted from a portion of each biopsy, hybridized with a human albumin or collagen cDNA clone and compared to 2 normal surgical specimens which served as controls. The Northern hybridization studies revealed that: despite the presence of inflammation and fibrosis, the albumin mRNA levels of alcoholics were similar to normal controls; these alcoholics had significantly higher levels of albumin mRNA than did patients with similar histological stages of disease due to viral infection; and all the categories of patients had markedly increased procollagen mRNA levels when compared to controls. Given these results it is tempting to speculate that alcohol may actually increase albumin mRNA content in man as it does in animals. Furthermore, the increased procollagen mRNA levels in fibrotic livers suggest that an increase in collagen synthesis may be a significant factor in the pathogenesis of hepatic fibrosis.
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PMID:Albumin and procollagen type I gene regulation in alcohol and viral-induced human liver disease. 167 41

The work deals with a group of 212 patients suffering from various forms of precirrhotic alcoholic liver disease and includes a period of 8.5 years (January 1981-June 1989). At least two liver biopsies were performed in all patients. according to the histological diagnosis, the patients were distributed into 6 subgroups: simple hepatic steatosis--24 cases (11.3%), hepatic fibrosis--40 cases (18.8%), hepatic steatofibrosis--69 cases (32.5%), acute alcoholic hepatitis--18 cases (8.5%), chronic active hepatitis--43 cases (20.3%) and chronic persisting hepatitis--18 cases (8.5%). The assessed histological parameters included: fatty transformation, hepatic fibrosis, inflammatory infiltrate within the lobules and in the portal spaces, hepatocellular necrosis, cholestasis, proliferation of the bile ductules and modification of the lobular architectonic. The work is aimed at pointing out the precirrhotic hepatic histological lesions induced by alcohol and fraught with an increased risk of progression towards liver cirrhosis. The histological sequential examination of alcoholic hepatic lesions confirm the possibility of progression and installation of the cirrhotic stage for a number of these lesions. Liver cirrhosis developed in 44 patients (20.7%) within a period of 3-7 years, on an average 5.5 years. The progression toward cirrhosis occurred in 12 patients (5.7%) with steatofibrosis, in 11 (5.2%) with hepatic fibrosis, in 14 (6.6%) with an intralobular inflammatory infiltrate, in 17 (8%) with hepatocellular necrosis, in 3 (1.4%) with cholestasis, in 5 (2.3%) with proliferation of the bile ductules and in 10 patients (4.7%) with a modification of the lobular architectonic. In addition, cirrhosis was detected in 8 patients (3.8%) with alcoholic hepatitis and in 13 patients (6.1%) with chronic active hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The criteria of histological activity and the prognosis in precirrhotic alcoholic hepatopathies]. 167 Jan 14

Severe alcoholic hepatitis is still a therapeutic challenge. It has been recently advocated that a 3-wk infusion with insulin and glucagon reduces its short-term mortality rate. A multicenter, randomized, single-blind, sequential trial was designed to compare this treatment with placebo. The triangular boundary was defined with alpha = 0.05, beta = 0.10 and estimated survival at 4 wk of 50% with placebo, 75% with treatment. Patients with biopsy-proven severe alcoholic hepatitis (presence of one or more of three criteria: encephalopathy, prothrombin activity less than or equal to 50%, bilirubinemia greater than or equal to 100 mumol/L) were randomized into two groups; one treatment group received an infusion (12 hr/day) of an association of insulin (30 IU) and glucagon (3 mg), and a control group received an infusion of glucose. Treatments were administered during a 3-wk period, and the mortality rate was noted at 4 wk. The decision to discontinue the trial was reached on the basis of results from the first 44 patients. Overall results were assessed in the 72 patients included at the time of this decision (treatment group: n = 37; control group: n = 35). Fifty-three patients had cirrhosis. No significant differences were noted between the two groups at inclusion on the basis of clinical, laboratory and histological criteria. The mortality rate was not significantly different in the two groups; 10 patients (27%) in the treatment group and 5 patients (14%) in the control group died. Causes of death were similar in the two groups and consisted primarily of gastrointestinal hemorrhage, hepatic failure and infectious events.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of severe alcoholic hepatitis by infusion of insulin and glucagon: a multicenter sequential trial. 172 3

The epidemiology of alcohol abuse and liver disease among alcoholics, with special emphasis on Poland, was reviewed and liver morphological changes attributable to the action of alcohol discussed. Furthermore, possible mechanisms leading to steatosis, alcoholic hepatitis and cirrhosis were discussed in detail followed by brief review of clinical and biochemical abnormalities accompanying alcoholic liver disease and therapy of this disorder.
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PMID:[Liver damage in alcoholics]. 181 85

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.
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PMID:Approaches to treatment of fibrogenesis in alcoholic liver disease. 184 64

The prevalence and potential value of the detection of signs of portal hypertension by duplex Doppler ultrasound (DDU) of the ligamentum teres and portal vein in patients with known or suspected chronic liver disease and/or portal hypertension was studied in 136 consecutive patients undergoing clinical assessment including that of liver histopathology. Portal hypertension was considered to be present when any of the following DDU signs, previously demonstrated to be specific for portal hypertension, were present: an enlarged and/or patent para-umbilical vein, portal vein obstruction or hepatofugal flow in the portal vein. Of 123 patients with parenchymal liver disease, eighty-three had cirrhosis and, of these, portal hypertension was detected on DDU criteria in 86% of alcoholic cirrhotics and 67% of non-alcoholic cirrhotics. Of the 42 patients with non-cirrhotic liver disease, 1 of 7 patients with metastatic liver disease and 3 of 5 patients with alcoholic hepatitis had DDU signs of portal hypertension. Thus, in patients with parenchymal liver disease, DDU had a sensitivity of 73%, specificity of 90% and predictive values of 94 and 62% for positive and negative studies respectively for the detection of cirrhosis. In all 14 patients with portal hypertension secondary to vascular occlusive diseases, DDU examination of the ligamentum teres, portal vein and hepatic vein gave an accurate guide to the site of the occluding lesion. The high positive predictive value of DDU and its ability to aid in localizing the site of increased resistance to flow through the liver suggest that DDU of the ligamentum teres and portal vein is a potentially useful non-invasive adjunct in the assessment of patients with suspected or known liver disease or portal hypertension.
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PMID:Duplex Doppler ultrasound of the ligamentum teres and portal vein: a clinically useful adjunct in the evaluation of patients with known or suspected chronic liver disease or portal hypertension. 188 80

The authors examined the aminoterminal type III procollagen peptide level of serums and killer-cell activity peripheric blood lymphocytes with 75 patients suffering from ethanol originated liver diseases as well as control samples from 40 healthy volunteers. Determination of type III procollagen peptide (Fab) took place by the RIA method. The cytotoxic activity of killer-cells was tested against human red blood cells. Both in fatty liver and chronic alcoholic hepatitis the level of type III procollagen peptide increased, while in liver cirrhosis the same level reached a value three times of the normal. At the same time in cirrhosis hepatitis an increased killer-cell activity could be observed. Type III procollagen peptide values were also analysed in view of the cytotoxic capacity of killer-cells. At first ill, then healthy control individuals were divided into three groups according killer-cell activity values. Results have shown that in the group with a high level killer-cell activity average type III procollagen peptide values were significantly greater as compared to those of the medium or low level activity groups. These results might indicate a relation between a conditional antibody-dependent cellular cytotoxicity reaction and increasing collagen synthesis.
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PMID:[Serum aminoterminal type III procollagen peptide level and killer cell activity in patients with alcoholic liver diseases]. 195 78

The value of first step isotopic angiography (FSIA) with 99-TC in the study of altered liver kidney and spleen circulation in patients with liver cirrhosis and alcoholic hepatitis is analyzed. This technique is used to evaluate the effect of a 250 mcg IV bolus of somatostatin on the activity/time curve at the three circulatory levels. The ratio of basal hepatic artery/portal flow in cirrhotics was 59 + 11/41 + 11% and 39 + 6/61 + 4 in alcoholic hepatitis, significantly different from normal controls (p less than 0.001). In cirrhotics the degree of alteration in FSIA correlated with the severity of liver disease. Somatostatin significantly improved the ratio of basel hepatic artery/portal flow and diminished the pressure at the root of suprahepatic veins (18.5 +/- - v.s. 16 +/- mmHg, p greater than 0.001). Neither the slopes nor the time of maximum isotopic activity of renal and splenic activity/time curves were modified. We concluded highlighting the clinical value of FSIA as a non invasive test in the study of chronic liver diseases.
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PMID:[Isotopic radioangiography in hepatic cirrhosis. Changes induced by somatostatin]. 197 54


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