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)

Peripheral blood mononuclear cells (PBMC, n = 26), formalin-fixed paraffin-embedded liver tissues (n = 11) and saliva (n = 15) of primary biliary cirrhosis (PBC) patients were used for the detection of Epstein-Barr virus (EBV) sequences by polymerase chain reaction (PCR) assay. The semiquantitative analysis of EBV-DNA was also carried out in a reconstructive experiment using an EBV-infected cell line. The PBMCs of PBC patients showed increased levels of EBV-DNA (61%) in contrast to chronic active hepatitis patients (19%), liver cirrhosis patients (14%) and healthy individuals (11%). Furthermore, formalin-fixed paraffin-embedded liver tissues, as well as saliva from PBC patients, also demonstrated increased levels of EBV-DNA when compared to healthy individuals and those with other liver diseases. The increased levels of EBV-DNA in the PBMC, liver tissue and saliva of the PBC patients suggest that those patients may have a depressed immune function against EBV infection.
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PMID:Increased expression of Epstein-Barr virus in primary biliary cirrhosis patients. 133 91

Phenotypic expression of sialylated Lewis(x) antigen by means of the monoclonal antiserum SNH3 was studied in 87 livers, which included normal and steatotic livers and livers with chronic persistent and chronic active hepatitis, alcoholic hepatitis, allograft rejection, focal nodular hyperplasia, hepatocellular carcinoma, cholangiocarcinoma, metastatic carcinoma, cirrhosis of various causes (autoimmune, alcoholic, viral, drug induced, Wilson's disease, and primary biliary cirrhosis). The biotin-streptavidin-peroxidase method was used on formaldehyde-fixed, paraffin-embedded sections. Sialylated Lewis(x) antigen was not demonstrated in normal livers. Hepatocellular expression in a diffuse or perinodular honeycomb pattern was seen in cirrhosis, irrespective of cause. Sialylated Lewis(x) antigen was also observed in hepatocytes around metastatic carcinoma in the absence of inflammation, cirrhosis, or regeneration. Some bile ductules, most likely ductular hepatocytes, but not bile ducts, expressed sialylated Lewis(x) antigen. Sialylated Lewis(x) antigen was seen diffusely in fibrolamellar hepatocellular carcinoma, focally in other hepatocellular carcinomas, and either focally or diffusely in cholangiocarcinomas.
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PMID:Expression of sialylated Lewis(x) antigen in chronic and neoplastic liver diseases. 135 99

It has recently been shown that ursodeoxycholic acid administration improves liver function tests in patients with chronic liver diseases. Aim of the present study was to evaluate an ursodeoxycholic acid derivative (bis-hemisuccinate bisodic salt Ursodamor, Farmaceutici Damor, Napoli) in patients with chronic hepatitis. Forty patients (15 M, 25 F) with biopsy proven chronic liver disease participated to the study. Patients were randomly allocated to two treatment groups. Twenty patients (4 PBC, 11 CAH/CPH, 5 cirrhosis) received the ursodeoxycholic acid derivate at the dose of 600 mg/day, while 20 patients (1 PBC, 11 CAH/CPH, 8 cirrhosis) received a placebo. For both groups the treatment period was six months. ALT serum levels were significantly reduced in the treated group (from 84 +/- 14 to 62 +/- 14 p less than 0.0005) while no significant change was observed in the placebo group. In the treated group but not in the placebo group alkaline phosphatases and gamma-GT were also significantly reduced (from 268 +/- 56 to 160 +/- 23 p less than 0.0005 and from 79 +/- 21 to 45 +/- 10 p less than 0.0005). In conclusion, our results suggest that the administration of the ursodeoxycholic acid derivate, bis-hemisuccinate, bisodic salt, improves liver function tests in patients with chronic liver hepatitis. Similarly to ursodeoxycholic acid this new derivate probably interferes with bile acid pool composition by replacing the more detergent and probably more toxic endogenous bile acid.
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PMID:[Effects of therapy with bis-hemisuccinate of ursodeoxycholic acid bisodium salt in patients with chronic hepatitis]. 135 68

To assess the role of the hepatitis C virus in patients with unexplained chronic liver disease, we tested for the presence of anti-hepatitis C antibody (anti-HCV) in the stored serum of patients with cryptogenic cirrhosis and a variety of other chronic liver diseases. The anti-HCV assay was performed by both the enzyme-linked and recombinant immunoblot methods in 16 patients with cryptogenic cirrhosis. Eight of these 16 patients (50%) were seropositive. Six of these eight patients were born outside of the United States, compared with only one of eight seronegative patients (p = 0.021). Of the anti-HCV-positive cryptogenic cirrhotic patients, 50% also had markers of previous hepatitis B infection, compared with only 12.5% of seronegative patients. Evidence of anti-HCV positivity was found in 10%, 19%, 0%, and 0% in patients with alcoholic cirrhosis, autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis, respectively. We conclude that in a suburban American population, hepatitis C accounts for a significant percentage of patients with presumed cryptogenic cirrhosis. Unrecognized risk factors may account for a higher prevalence of HCV in foreign-born patients with cryptogenic cirrhosis. A low prevalence of anti-HCV positivity is found in other forms of chronic liver disease.
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PMID:Prevalence of anti-HCV in cryptogenic cirrhosis in a suburban Detroit community. 137 12

We studied the effect of ursodeoxycholic acid in 19 patients with primary biliary cirrhosis, mainly stages III and IV. The dose of UDCA employed was 10-15 mg/kg body weight per day. After 1 yr, 17 patients were still using UDCA, and the mean values of serum alkaline phosphatase, gamma-glutamyltranspeptidase and alanine-aminotransferase had fallen significantly. Serum bilirubin, initially elevated in 7 of the 13 late-stage (III and IV) patients, showed a further increase in 3 of the 7 patients. In 2 of these 3 patients, UDCA had to be withdrawn (dose reduction had no effect). One patient developed a decompensated cirrhosis in spite of UDCA withdrawal. Pruritus worsened in 4 patients, all of whom were late stage patients. Ten late-stage (III-IV) patients showed improvement in liver biochemistry and clinical findings as did all early-stage PBC patients. Thus, UDCA treatment is not beneficial for all PBC patients. Special care should be taken in the early phase of UDCA therapy in later-stage (III-IV) patients: frequent biochemical checks should be carried out, for instance every 2 weeks in the first 2 months after starting UDCA, especially the estimation of bilirubin.
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PMID:Ursodeoxycholic acid treatment in primary biliary cirrhosis with the emphasis on late stage disease. 140 34

Primary biliary cirrhosis is a progressive noninflammatory destruction of the interlobular bile ducts within the liver, leading to cholestasis and eventual cirrhosis. Ninety percent of affected patients are women. Most patients are initially without symptoms or have mild symptoms such as fatigue or pruritus. A minority of patients have the classical triad of jaundice, pruritus, and xanthelasmas. Almost all patients will have positive anti-mitochondrial antibody test results and an elevation of the serum alkaline phosphatase level. Primary biliary cirrhosis is thought to be an autoimmune disorder with additional liver injury being mediated by the subsequent cholestasis and accumulation of toxic bile acids. New treatment modalities include colchicine, ursodeoxycholic acid, and methotrexate. All patients, including those with only minor symptoms, have increased mortality compared with age-matched controls, thereby emphasizing the need for early diagnosis.
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PMID:Primary biliary cirrhosis: current diagnosis and treatment. 142 Mar 96

Ursodeoxycholic acid (UDCA) allows symptomatic treatment of cholestatic liver diseases such as primary biliary cirrhosis, primary sclerosing cholangitis, intrahepatic biliary atresia, and cholestasis of cystic fibrosis. Patients should be treated at an early stage of the disease in order to prevent progression to cirrhosis. Since UDCA has no toxic effects longterm treatment with this substance is possible without the risk of undesired side effects. In patients with primary biliary cirrhosis and rapid progression of the disease, UDCA may be combined with an immunosuppressive substance (i.e. cyclosporin). In primary sclerosing cholangitis, biliary atresia and cholestasis of cystic fibrosis, UDCA at present seems the only treatment of which a benefit for the patients can be expected. In endstage disease liver transplantation is indicated. The role of UDCA in chronic hepatitis and alcohol induced liver disease needs to be clarified in further studies. Whether the improvement of laboratory tests in such patients indicates amelioration of the course of disease, still is unclear.
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PMID:[Treatment of cholestatic liver diseases; the role of ursodeoxycholic acid]. 144 78

The results of a 3-year, placebo-controlled trial of prednisolone treatment in primary biliary cirrhosis (PBC) are presented. The active (n = 19) and placebo (n = 17) arms were initially well matched for age, menopausal status and disease severity. At 3 years hepatic symptoms were relatively improved in the prednisolone group. Hepatic mortality was 3/19 (prednisolone), 5/17 (placebo) (p = n.s.). For all liver blood tests the trend favoured prednisolone treatment, though the differences were only significant for alkaline phosphatase and protein. All immunoglobulins fell significantly. Quantitative ELISA determination of antimitochondrial antibody showed a significant fall in the prednisolone group compared with placebo (p less than 0.001 at 1 year, p less than 0.05 at 3 years). Deterioration in histology (appearance of cirrhosis) was more common in the placebo group. Overall hepatic function (hepatic mortality, doubling in bilirubin, 6 milligrams fall in albumin, de novo appearance of cirrhosis or symptoms of portal hypertension) was significantly worse in the placebo group (p less than 0.01). After 3 years no significant differences could be detected in bone mineral content (single photon absorptiometry of radius and femur) between the two groups or in comparison with other PBC patients. Thus, after 3 years, prednisolone treatment was associated with a better overall hepatic outcome and little evidence of increased bone loss.
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PMID:A controlled trial of prednisolone treatment in primary biliary cirrhosis. Three-year results. 144

Thanks to the development of a sensitive and specific radioimmunoassay for colchicine, the pharmacokinetics of colchicine is now well-established after single oral doses. Absorption is characterized by a zero-order rate constant while disposition appears biexponential with a rapid distribution phase (t1/2 = 1.8 h) and a long elimination phase (t1/2 = 20 h). All studies confirm the large total body clearance (35 l/h) predominantly by the extrarenal route and the large distribution volume (700 l). Further studies need to be performed to investigate colchicine absorption and to describe the metabolic pathway of the drug. To date, relationships between colchicine plasma levels and pharmacological effects have not been defined. Monitoring of plasma levels in patients with familial Mediterranean fever should improve treatment with colchicine. However, the therapeutic range has not been precisely determined. The use of colchicine in the treatment of liver cirrhosis and primary biliary cirrhosis is a recent development; so, assuming that a large part of total body clearance depends on hepatic function, the influence of hepatic diseases on colchicine disposition needs to be investigated in order to define the most appropriate therapeutic dosing.
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PMID:Pharmacokinetics of colchicine: a review of experimental and clinical data. 144 14

A total of 508 patients had an non-decompression surgery for esophago-gastric varices in our department, from September 1979 to December 1991. These patients consisted of 387 cases of transthoracic esophageal transection with para-esophagogastric devascularization, 40 cases of transabdominal esophageal transection, and 81 cases of Hassab procedure. The original diseases were cirrhosis in 432 patients, IPH in 35, extrahepatic-portal occlusion in 24, primary biliary cirrhosis in 6, Budd-Chiari syndrome in 4, and others in 7. Operative mortality rate was 5.3%. By thoracic approach, esophageal varices completely disappeared. Postoperative cumulative variceal recurrence and bleeding rates at 10 years were 12% and 7%, although recurrence occurred more often than not in cases with hepatocellular carcinoma (HCC). Cumulative survival rates at 5, 10 years were 69%, 46% in liver cirrhosis without HCC. Present study confirmed that our non-decompression surgery is effective in controlling esophagogastric varices in long term of periods.
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PMID:[Results of non-decompression surgery for esophago-gastric varices--postoperative disappearance, recurrence, rebleeding rate of varices, and cumulative survival rate]. 147 Jan 35


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