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)

Liver dysfunction was observed in 33% of patients treated by hemodialysis and kidney transplantation. Fifty-eight percent of these cases of hepatitis occurred in patients with past or present HBs antigenemia, and 77% of HBsAg-positive patients showed evidence of LD. However, during the course of a program conducted from 1969 to 1976 and involving 267 patients, the decrease in the prevalence of HBs antigenemia observed during the last two years did not lead to any reduction in LD incidence. In a small number of patients, potentially hepatotoxic drugs could be incriminated, but in our experience azathioprine never appeared to be involved. In a few patients, LD was due to granulomatous disease of the liver, such as tuberculosis and schistosomiasis. Twenty-one (7%) of the 267 patients at risk developed chronic hepatitis, which contributed to death in nine patients. In 12 cases (three deaths), this form of hepatitis occurred in HBsAg-positive patients, and in nine cases (six deaths), in HBsAg-negative patients. In three of these latter individuals, cytomegalovirus could be incriminated. Routine monthly screening for CMV in kidney recipients confirmed the high incidence of this viral infection in such patients. Studies on murine CMV infection have demonstrated that this infection can be enhanced by histoincompatible graft or by cyclophosphamide in a model that is very close to the kidney recipient. As in mice, CMV infection in kidney recipients apparently results from reactivation of a latent infection. It seems to play a major role in the LD observed and could apparently lead to chronic hepatitis and even to cirrhosis of the liver. Finally, the occurrence of LD in HBsAg-, anti-HBs- and antiCMV-negative patients would suggest the responsibility of other viruses for the pathogenesis of liver disease in patients treated by hemodialysis and kidney transplantation. Besides Epstein-Barr virus, other viruses, such as hepatitis C virus, should be thoroughly scrutinized.
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PMID:Liver disease in patients undergoing hemodialysis and kidney transplantation. 11 44

The relationship between hepatocellular carcinoma (HCC) and hepatitis C virus (HCV) infection was investigated. Antibody to hepatitis C virus was detected in 88.8% and 87.0% of 240 patients with hepatocellular carcinoma and liver cirrhosis, respectively. A history of blood transfusion was shown in only 21.8% (21/96) of the HCV antibody positive HCC patients. Of 196 patients with chronic hepatitis type C and the HCV antibody positive liver cirrhosis, 10 developed HCC during the follow-up period of two years. A high prevalence of HCV antibody was also shown among 83 patients with alcoholic liver cirrhosis and HCC associated with alcoholic liver cirrhosis. HCV-RNA was detected in all patients with alcoholic HCC. These data support a causal association between hepatitis C virus and hepatocellular carcinoma.
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PMID:[Clinical study on relationship between hepatocellular carcinoma and hepatitis C virus infection in patients with chronic liver disease]. 127 47

The authors performed 20 liver transplantations from living related donors between June 1990 and July 1991. The 20 pediatric patients (14 biliary atresia, two Budd-Chiari syndrome, one liver cirrhosis after hepatitis C viral infection (HCV hepatitis), 1 progressive intrahepatic cholestasis, 1 liver cirrhosis, 1 protoporphyria) were transplanted with 11 left lobes, eight left lateral segments, and one right lobe. The choice of donors was restricted to the parents of the recipients. The immunosuppressive treatment consisted of FK 506 and steroids. Seventeen recipients are alive, 15 of whom are well and at home. Two recipients, who underwent emergency transplantation, died of postoperative complications. Another recipient died of accidental asphyxia at 6 months after the transplantation. All 20 donors had uneventful postoperative courses and were able to resume their normal social lives. The arterial ketone body ratio (AKBR) increased to above 1.0 within 2 days after the transplantation in all cases. Relatively mild rejection episodes were encountered in only two cases transplanted with ABO-compatible grafts, and these were treated successfully with steroids and FK 506.
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PMID:An appraisal of pediatric liver transplantation from living relatives. Initial clinical experiences in 20 pediatric liver transplantations from living relatives as donors. 128 74

Putative E2/NS1 sequence of hepatitis C virus was expressed in E. coli as a fusion protein with maltose binding protein. Approximately 80 kDa protein was obtained containing 38 kDa E2/NS1 protein. The antibody to this protein was detectable in the same serum from which the sequence was amplified. It was also detectable in none of 7 acute hepatitis, in 2 of 12 chronic persistent hepatitis, in 3 of 25 chronic active hepatitis, and in 2 of 4 cirrhosis. It was detectable in none of 10 normal subjects. In 3 cases who were positive for the antibody before the interferon treatment, it became undetectable after the treatment. Thus, it seems that the antibody is not a neutralizing antibody and is related to active viral replication.
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PMID:Detection of antibody to hepatitis C E2/NS1 protein in patients with type C hepatitis. 128 Apr 30

In 12 of 54 (22%) patients with histologically verified hepatocellular carcinoma, antibodies to hepatitis C virus were found. In patients with hepatocellular carcinoma the frequency of anti-hepatitis C virus positivity was similar whether cirrhosis (6 of 22 patients (27%)) was present or not (2 of 15 (13%)). Out of 54, 23 patients (43%) were negative both for hepatitis B or C markers. Out of 53, 22 (42%) had positive hepatitis B markers, 8 of 22 were HBsAg positive. Patients with hepatocellular carcinoma and cirrhosis had a higher percentage of hepatitis B virus markers than patients with cirrhosis without hepatocellular carcinoma. Our of 70 patients with cirrhosis but without hepatocellular carcinoma, 24 (34%) had antibodies to hepatitis C virus. Our data of similar frequencies of antibodies to hepatitis C virus in patients with hepatocellular carcinoma or with liver cirrhosis but without hepatocellular carcinoma indicate that at least in Austrian patients, hepatitis C virus infections are not an important factor for development of hepatocellular carcinoma.
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PMID:Prevalence of antibodies to hepatitis C virus in patients with hepatocellular carcinoma in Austria. 128 May 9

We developed an enzyme-linked immunosorbent assay (ELISA) system for antibodies to the hepatitis C virus (HCV), using two new recombinant antigens (c11 and c7) derived from the HCV genome. The performance of this ELISA system (Imucheck HCV Ab) was examined. The CV values for both intra-assay precision and reproducibility of identifying HCV antibody in the panel sera ranged from 3.5% to 6.4%. The blood elements in serum and anticoagulants did not interfere in this ELISA system. The specificity of Imucheck HCV Ab to samples from patients with non-A, non-B (NANB)-type chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma was 93.7%, 93.5%, and 81.4%, respectively. These results are more sensitive than those obtained by the first-generation anti-HCV ELISA system. In the samples from patients with NANB-type acute hepatitis, Imucheck HCV Ab enabled detection of HCV antibodies at an early stage. This system increased the sensitivity for blood donor screening and for monitoring patients with acute hepatitis.
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PMID:Performance of an enzyme-linked immunosorbent assay system for antibodies to hepatitis C virus with two new antigens (c11/c7). 128 Oct 50

The extent of involvement of hepatitis C, as compared to hepatitis A and hepatitis B, virus infection in acute and chronic liver disease in the Asir Region, southwestern Saudi Arabia, was assessed in 898 patients hospitalized during the period from June 1990 to November 1991. Acute icteric hepatitis cases with severe onset were distinguished by their referral to the fever hospital while cases with milder onset and those with chronic hepatitis were followed at two general hospitals. Antibodies to the c-100-3 antigen of hepatitis C virus (anti HCV) were detected in a significant proportion of patients with chronic liver disease (chronic active hepatitis (65%), cirrhosis (44%)). Anti HCV was also detected in patients with acute hepatitis with milder onset at the general hospitals (10.9%) but proportionately much less in patients at the fever referral hospital (< 1%) where hepatitis A (52%) and, to a lesser extent hepatitis B (11%), were mostly diagnosed. These results indicate that HCV is a major identifiable infection in hospitalized patients with chronic liver disease in this region but that anti HCV antibodies (c-100-3) are not detected, at least at onset, in sporadic cases with acute manifestations. Testing for additional viral antigens or RNA and a longer follow-up period would be required before exclusion of a role for HCV in acute disease. Alternatively, other viral and non-viral agents may be sought in this illness.
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PMID:Serodiagnosis of hepatitis C in acute and chronic liver disease in southwestern Saudi Arabia. 128 Dec 39

We constructed a cDNA library against the plasma obtained from the patient with acute exacerbation of non-A, non-B liver cirrhosis, and immunoscreened this library with the sera obtained from the patients with non-A, non-B chronic liver disease. One positive clone lambda 22C containing about 1.2 kb cDNA insert was isolated from 10(6) clones. Nucleotide sequence determination and subsequent homology search revealed its identity to the tolA gene of Escherichia coli. Anti-tolA antibody was detected in 54.5% of the patients with NANB chronic liver disease whose sera were negative for antibody to hepatitis C virus (anti-C100). In contrast, anti-tolA was detected only of 14.6% patients with anti-C100 positive NANB chronic liver disease, 10.5% with hepatitis B surface antigen-positive chronic liver disease, 7.7% with alcoholic liver disease and 4.2% in normal control, and no positive case in acute hepatitis of etiology and in primary biliary cirrhosis. However, antibody to the core protein of hepatitis C virus (anti-JCC) was detected 50% of the patients whose sera were negative for anti-C100 but positive for anti-tolA. Recently, it has been reported that hepatitis C virus is rich in mutations and has some variants. These results indicated the presence of a common epitope between the tolA protein and some agent related to non-A, non-B hepatitis, especially to anti-C100 negative non-A, non-B hepatitis such as variants of hepatitis C virus which have mutations in C100 coded region.
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PMID:Anti-tolA antibody in non-A, non-B chronic liver disease. 128 59

Antibody against hepatitis C virus (anti-HCV) was tested in 658 cases of hepatitis and liver diseases with ELISA, ninety of these cases were positive, with a total infection rate of 13.68% (90/658). The positive rate of anti-HCV was highest in patients with chronic severe hepatitis (33.78%) and CAH accompanied by cirrhosis of liver(31.58%). The infection rate in other types of hepatic diseases in order of frequency was as follows: fulminant hepatitis (18.18%), CAH without cirrhosis (15.13%), subacute severe hepatitis (13.43%), CPH (5.88%), primary hepatocellular carcinoma (3.85%), and acute hepatitis (2.42%). Serological markers of HBV infection were detectable concomitantly in 77 of the 90 cases who were anti-HCV positive, but there was no evidence of mutual inhibition of viral replication. There was neither appreciable difference in the level of hyperbilirubinemia in cases of hepatitis with or without anti-HCV, nor significant diversity in the number of death between cases of severe hepatitis with and without anti-HCV.
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PMID:[Detection of serum antibody against hepatitis C virus in patients with hepatitis and liver diseases]. 128 51

To develop a more dependable method of diagnosing hepatitis C, serum anti-hepatitis C virus (HCV) was examined by using a new assay (anti-HCV second generation). The results were compared with those of either the conventional assay (anti-HCV first generation) or HCV-RNA analysis. With the first generation assay, anti-HCV was detected in 69% of post-transfusion acute hepatitis (AH), 44% of sporadic AH, 50% of needlestick exposed AH, 72% of chronic hepatitis (CH), 77% of liver cirrhosis (LC) and 86% of hepatocellular carcinoma (HCC). These results were remarkably increased by using the second generation assay (92% in post-transfusion AH, 72% in sporadic AH, 100% in needlestick exposed AH, 96% in CH, 96% in LC and 97% in HCC). Furthermore, in the early stages of AH (from 1-5 weeks after onset), anti-HCV was not detected in all 18 patients by the first generation assay, but was found in 10 of them by using the second generation assay. The failure to detect anti-HCV with the first generation assay was mainly due to a lack of the core region coding peptide (C22-3) in this assay. In the AH-resolving group, anti-HCV second generation did not disappear, but the titre tended to be lower than that in the CH-developing group. Thus, the second generation assay for anti-HCV was considered to be a more useful tool for not only the diagnosis of hepatitis C but also for determining prognosis.
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PMID:Clinical evaluation of a newly established anti-HCV assay for the diagnosis of hepatitis C in Japan. 128 84


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