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 use of L-Dopa in hepatic coma has been the subject of numerous reports since 1970. The following represents our experience with a rather heterogenous group of patients treated at the Massachusetts General Hospital over the past 4 years. Thirty-five patients with severe liver disease, a mean age of 53 +/- 3.5 years, including nutritional cirrhosis with acute coma and acute hepatitis were treated. Four patients were judged grade III, 31 patients grade IV. All patients had previously been treated with protein restriction, orally administered non-absorbable antibiotics, fluid and electrolytes, and in some cases, steroids. L-Dopa was given orally in 21 patients, and as a retention enema in 14. Thirteen of the 35 patients did not respond to therapy. Seventeen responded, but did not survive, and 5 patients responded and survived. There was no difference between any of the groups as far as dosage of L-Dopa and clinical features. The one striking finding as the differences between groups was the time of initiation of L-Dopa therapy. In Group I, the survivors, therapy was started within 1.4 +/- 0.8 days after the onset of coma. In Group II, there was an initiation of therapy at 6.7 +/- 1.6 days, and in the non-responders 9.5 +/- 1.6 days. These differences are highly significant. The results suggest that coma may pass from a reversible to an irreversible stage, and that L-Dopa therapy initiated early in the course of hepatic coma, may be of some benefit.
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PMID:L-dopa in hepatic coma. 126 95

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

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

Circulating immune complexes (CIC) were precipitated and assayed in the blood of 19 adult patients with liver diseases and 39 healthy adult Nigerians. The presence of hepatitis-Bs antigen (HBs-Ag) was also investigated in both the sera and CIC of both study groups. CIC levels were not significantly different in the three different liver diseases studied (acute hepatitis, chronic hepatitis and liver cirrhosis). Higher mean CIC levels which were not correlated with the presence of HBs-Ag, were found in the blood of patients, as compared to blood donors. While HBs- Ag was detected in 42.1% of patient's sera, only 12.8% of blood donor sera had detectable antigen. However, 42.1% of CIC from patients had the antigen, while 53.8% of CIC from blood donors also contained the antigen. It is suggested that the high frequency of HBs-Ag in the precipitated CIC of healthy subjects could account for the occurrence of some post-transfusion hepatitis-B infections.
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PMID:Immune complex levels and HBs-antigenaemia in healthy Nigerians and patients with liver diseases. 130 79

Serum and urinary neopterin levels were measured by radioimmunoassay in 120 healthy controls, 16 asymptomatic HBsAg carriers, 12 patients with acute hepatitis, 13 with chronic inactive hepatitis, 35 with chronic active hepatitis, 46 with liver cirrhosis, 18 with hepatocellular carcinoma, and 6 with alcoholic liver disease. Serum and urinary neopterin levels were significantly higher in almost all patients than in normal subjects. Neopterin levels were highest in acute hepatitis and correlated with the results of liver function tests, but did not show this correlation in chronic liver disease. In chronic liver disease, the levels of serum neopterin in non-A non-B viral patients was significantly increased, compared with those in B viral and alcoholic patients. The rate of abnormal urinary neopterin levels in chronic liver disease was higher than the rate of abnormal serum neopterin levels, but no difference was observed between the rates of abnormal serum and urinary levels in acute hepatitis and asymptomatic HBsAg carriers. These results indicate that serum and urinary neopterin levels may be useful markers for cell-mediated immunity in liver disease, and that the immune system response in chronic liver disease may be different for different pathogens.
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PMID:Clinical significance of serum and urinary neopterin levels in patients with various liver diseases. 131 6

The HCV, a single stranded RNA virus belonging to the family of flavivirus, has been identified as the probable cause of the majority of cases of transfusion-associated NANB hepatitis and community-acquired NANB hepatitis in Japan. The hepatitis virus is present in a least 2% of the blood donor population and is extremely common in high risk groups, such as hemophiliacs and hemodialysis patients. The contribution of HCV infection to sporadic, acute and chronic hepatitis, liver cirrhosis and primary liver cancer has been established. Furthermore anti-HCV in 20% of alcoholic patients with liver injury suggest that HCV may be etiologically associated with liver disease previously attributed to other causes. Therapy of acute and chronic liver disease associated with HCV infection is likely to be undertaken with recombinant IFN alpha in the future to prevent the progression of the disease from acute hepatitis to chronic hepatitis, and from chronic hepatitis to liver cirrhosis or primary liver cancer. However the prevention of HCV infection will be the goal, in addition to screening of donor blood and exclusion to a large degree of positive units likely to decrease the incidence of post-transfusion hepatitis.
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PMID:Hepatitis C: basic and clinical studies. 131 82


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