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 prevalence and bacteriology of bacteriuria was studied in 140 patients with cirrhosis of the liver, referred to the University of Pittsburgh Medical Center for evaluation for liver transplantation (72 males and 68 females; mean age 46 years). Urine samples were obtained for cultures within 24 h after admission. Significant bacteriuria (SB) (> 10(5) bacteria/ml) was present in 25 patients (18%), the most common being E. coli (36%) and coagulase-negative staphylococcus (20%). SB was more common in females than in males (32 vs. 4%, p < 0.001), and was seen in every category of cirrhosis. The occurrence of bacteriuria did not correlate with the severity of the underlying liver disease or with the age of the patient. Based upon these results, it can be concluded that: (1) bacteriuria is common in patients with advanced liver disease and occurs in approximately 20% of the cases; (2) it is more common in females than in males; and (3) its prevalence in patients with primary biliary cirrhosis is similar to that in other types of chronic advanced liver disease.
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PMID:Bacteriuria in patients with cirrhosis. 148 71

The serum levels of the 7S domain of type IV collagen were measured with a radio-immunoassay in 42 patients with primary biliary cirrhosis (asymptomatic: n = 28; symptomatic: n = 14), 10 patients with chronic active hepatitis, 10 patients with liver cirrhosis and 10 healthy female controls. Serum levels of the 7S domain of type IV collagen were: 4.28 ng/mL (3.88-4.72 ng/mL; mean and range of mean +/- s.d.) in healthy controls; 5.97 ng/mL (5.07-7.02 ng/mL) in patients with chronic active hepatitis; 8.23 ng/mL (6.40-10.58 ng/mL) in patients with liver cirrhosis; and 6.79 ng/mL (4.76-9.67 ng/mL) in patients with primary biliary cirrhosis. Patients with liver cirrhosis and primary biliary cirrhosis had higher levels of serum 7S domain of type IV collagen than healthy controls (P < 0.001, respectively). Serum levels of the 7S domain of type IV collagen in patients with asymptomatic primary biliary cirrhosis, 5.83 ng/mL (4.55-7.48 ng/mL) were significantly lower than those in symptomatic primary biliary cirrhosis, 9.18 ng/mL (6.53-12.91 ng/mL; P < 0.001). Serum levels of the 7S domain of type IV collagen increased significantly along with advancement of the histological stages of primary biliary cirrhosis. Serum levels of the 7S domain of type IV collagen in the paired sera of eight patients with asymptomatic primary biliary cirrhosis (mean interval 30 months, range 12-48 months) showed significant rises during the intervals (P < 0.05), while serum levels of albumin and total bilirubin did not change significantly during these intervals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical significance of the serum levels of the 7S domain of type IV collagen in patients with primary biliary cirrhosis. 148 89

A 34-year-old multigravid woman with symptomatic primary biliary cirrhosis (PBC) of the liver had a successful pregnancy. A healthy baby was born prematurely at 36 weeks of gestation. Six months prior to the conception of this pregnancy, stage III PBC had been diagnosed. Portal hypertension and liver cirrhosis had not developed. It is uncommon for pregnancy to occur in the presence of PBC. In the case presented, the outcome of pregnancy was good and the liver function had not been significantly affected by the pregnancy.
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PMID:Pregnancy in primary biliary cirrhosis. 149 49

Two cases of acute hepatic failure are reported in which the diagnosis of Wilson's disease was considered because of low serum ceruloplasmin, low serum copper levels and high 24 h urinary copper. Case 1 had Kayser-Fleischer rings, haemolysis and a high 24 h urinary copper, and so Wilson's disease was confidently diagnosed. Case 2 had high urinary copper excretion, but [64Cu] study indicated a 24:2 h ratio of 0.7 and made the diagnosis of Wilson's disease uncertain. Both patients underwent orthotopic hepatic transplantation, and multiple biopsies were taken from the resected specimen in order to estimate hepatic copper levels. In both cases, hepatic copper levels revealed considerable variation: 0.8-5.2 mumol/g dry wt (case 1) vs 0.02-12.65 mumol/g dry wt (case 2). In case 1, only two of 14 levels were within the diagnostic range for Wilson's disease (greater than 4 mumol/g dry wt), whereas hepatic copper levels in case 2 were in the Wilsonian disease range in three of 16 specimens. These results were in contrast to uniformly high hepatic copper levels in one patient with established cirrhosis secondary to Wilson's disease and two cases of primary biliary cirrhosis. This report indicates that hepatic copper levels vary greatly in acute liver failure, and that estimates from a single biopsy specimen may be misleading as to the cause of the underlying liver disease.
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PMID:Striking variability of hepatic copper levels in fulminant hepatic failure. 151 66

This study was undertaken to determine whether S-adenosyl-L-methionine (SAMe) changes the lipid composition and fluidity of erythrocyte membranes in chronic liver disease. SAMe was administered intravenously at a daily dose of 600 mg for 2 weeks to 10 patients; 6 patients with cirrhosis and four with primary biliary cirrhosis. The elevated free cholesterol to phospholipid molar (C/PL) ratio of the erythrocyte membranes of the patients (0.857 +/- 0.018) significantly decreased after the administration of SAMe (1 week, 0.823 +/- 0.021; 2 weeks, 0.823 +/- 0.013). In all of the four patients whose erythrocyte membrane fluidity was measured, fluidity improved with the administration of SAMe and correlated with the C/PL ratio of the membranes. These results suggest that SAMe decreases the C/PL ratio of erythrocyte membranes and thus improves membrane fluidity in chronic liver disease.
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PMID:Changes in lipid composition of erythrocyte membranes with administration of S-adenosyl-L-methionine in chronic liver disease. 152 32

Transplantation of the liver has progressed in recent years and has become universally accepted for numerous indications of end-stage liver diseases, predominantly cirrhosis induced by viral hepatitis (HBV/HCV), acute hepatic failure and primary biliary cirrhosis. Interdisciplinary research is devoted to prevention of recurrent disease: Risk groups have been defined, in which HBV recurrence can be prevented by immunoprophylaxis. The risk of tumor recurrence can be calculated, adjuvant chemotherapy might improve prognosis of patients with small incidental tumors.
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PMID:[The status of liver transplantation 1992]. 152 92

Forty consecutive patients with esophagogastric varices underwent a modified distal splenorenal shunt with expanded polytetrafluoroethylene (PTFE) interposition and were followed up for 12 to 66 months (mean 44.7). The operations were urgent in 9, elective in 14, and prophylactic in 17 patients. There were 24 males and 16 females. Age ranged from 32 to 76 years with an average of 53.8. The causes of portal hypertension were liver cirrhosis in 32, chronic hepatitis in 4, idiopathic portal hypertension in 3, and primary biliary cirrhosis in 1. Twenty-six patients were in Child's class A, 6 in class B, and 8 in class C. The operative death rate within 1 month was 2.5% and the overall in-hospital mortality rate was 5%. The shunt patency rate was 97.2% at early and 100% at late examinations. Only one patient (2.5%) had upper gastrointestinal bleeding. Hepatic encephalopathy was seen in 8 (20.5%) of 39 surviving patients. Six patients died of liver failure and another six died from various causes during the follow-up period. Twenty-six patients (65%) are alive at present. The 1-, 3-, and 5-year cumulative survival rates were 87.4%, 73.3% and 48.8%, respectively. The current modified shunt can be carried out more safely and easily and yield a similar result to that with the original Warren shunt. In order to avoid hepatic encephalopathy and liver failure, however, it is not wise to persist in this procedure.
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PMID:Long-term results after modified distal splenorenal shunt with expanded PTFE interposition. 154 95

Three patients with symptomatic, noncirrhotic primary biliary cirrhosis who had no evidence of esophageal varices on esophagogastroduodenoscopy and who were treated with ursodeoxycholic acid, 15 mg.kg-1.day-1, for a period of 1-2 years are reported. Initially, all three patients showed improvement in symptoms of fatigue and pruritus, and there was marked improvement or normalization in serum levels of bilirubin, alkaline phosphatase, and alanine aminotransferase. However, after 1-2 years, all three patients progressed histologically to cirrhosis on follow-up liver biopsy, and all had esophageal variceal bleeding documented by esophagogastroduodenoscopy. These three patients represent examples of ursodeoxycholic acid treatment failure despite improvements in symptoms and biochemical liver test results.
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PMID:Progression of primary biliary cirrhosis with ursodeoxycholic acid therapy. 829 25

Studies in vitro and in vivo show that hydrophobic bile acids tend to accumulate in the liver tissue in chronic liver disease, thus damaging hepatocyte membranes. Ursodeoxycholic acid (UDCA) is a hydrophilic bile acid which counteracts hepatotoxicity of more hydrophobic bile acids by partially replacing the pool of bile acids in the liver and/or by inhibiting the intestinal absorption of toxic bile acids. UDCA seems safe and effective in the early stages of primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and possibly in other severe cholestatic syndromes of infancy. Moreover, there is increasing evidence that UDCA improves the common indices of liver function in chronic non-cholestatic hepatic disorders including active cirrhosis, though maintaining the residual functional liver mass. This article reviews the cytoprotective effect of UDCA in chronic cholestatic and non-cholestatic liver disease based on the results of major clinical trials on this topic.
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PMID:Cytoprotection with ursodeoxycholic acid: effect in chronic non-cholestatic and chronic cholestatic liver disease. 157 77

Evaluation of chronic liver disease begins with a carefully taken history, thorough physical examination, and standard laboratory tests. Often, however, other studies are required, such as a viral hepatitis panel, serologic tests for autoimmune markers, tests for antimitochondrial antibodies, measurement of serum iron and ceruloplasmin levels, liver biopsy, and imaging studies of the extra-hepatic bile ducts. Medical treatment of chronic active hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis remains unsatisfactory. Early treatment of hemochromatosis and Wilson's disease can prevent cirrhosis and liver failure. Liver transplantation is now a viable procedure for patients with end-stage chronic liver disease.
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PMID:Chronic liver disease. The scope of causes and treatments. 158 71


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