Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the relationship between hepatitis C virus (HCV) infection and hepatocellular carcinoma (HCC), frozen serum samples from 213 patients with histologically proven liver cirrhosis alone (96 alcoholics, 59 HBsAg positive, 29 non-A, non-B hepatitis, 29 cryptogenic) and 40 patients with liver cirrhosis and HCC (12 alcoholics, 7 HBsAg positive, 7 non-A, non-B hepatitis, 14 cryptogenic) were analyzed for antibodies to hepatitis C virus (anti-HCV) with the ortho-HCV-ELISA. The results were as follows. 50 of 253 (20%) patients were anti-HCV positive. The prevalence of anti-HCV was significantly higher in patients with HCC than in patients without HCC (14 of 40 [35%] vs 36 of 213 [17%]; p less than 0.001). In anti-HCV-positive patients HCC were significantly more frequent than in anti-HCV-negative patients (14 of 50 [28%] vs 26 of 203 [13%]; p less than 0.001). The significantly higher occurrence of HCC in anti-HCV-positive patients was not related to other known risk factors such as alcoholism or chronic hepatitis B virus (HBV) infection. Patients with HCV infection as the only risk factor also had a significantly higher occurrence of HCC (12 of 38 [32%] vs 26 of 203 [13%]; p less than 0.001). Our data suggest that chronic HCV infection plays an important role in the pathogenesis of HCC, in particular in patients with cirrhosis unrelated to alcohol or HBV infection.
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PMID:[Hepatitis-C virus and hepatoma]. 131 Nov 25

Our study was designed to evaluate the clinical significance of the ELISA-anti-HCV test. 90 patients with histologically proven chronic non-A, non-B hepatitis (NANBH) and a control group consisting of 36 patients with primary biliary cirrhosis (PBC) were analyzed for antibodies to hepatitis C virus (anti-HCV). Frozen serum samples were tested with the ortho-HCV-ELISA. 67 of 90 (74%) patients with chronic NANBH showed antibodies to the hepatitis C virus. The prevalence of anti-HCV in patients with parenterally transmitted and sporadic chronic NANBH was 70% (23 of 33) and 77% (44 of 57) and in patients with chronic active and chronic persistent NANBH 73% (27 of 37) and 76% (40 of 53) respectively. No significant difference in the prevalence of anti-HCV in the 4 subgroups of patients with chronic NANBH was found. 2 of 36 patients (6%) with PBC were anti-HCV positive without evidence of previous HCV infection. Our results bear out the experience of other authors, that HCV is the commonest pathogen of chronic NANBH. The low prevalence of anti-HCV in patients with PBC suggests good specificity. There have been reports in the literature of "false positive results", particularly in autoimmune hepatitis, and it has been shown that borderline positive test results are often unspecific and therefore to be interpreted with care.
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PMID:[Anti-HCV test in patients with chronic non-A, non-B hepatitis]. 131 Nov 26

The prevalence of hepatitis C virus (HCV) infection in 182 prospectively followed adult patients (110 males, 72 females) with acute non-A, non-B hepatitis and its correlation with progression to chronic hepatitis were studied. These patients were followed for a mean of 24.7 +/- 13.1 (range, 6-57) months. By using a specific enzyme immunoassay for the detection of antibodies against C100-3 polypeptide of HCV, 96 (52.7%) were found antibody positive. HCV was implicated in 64/89 (71.9%) of the cases with classical parenteral exposure but only in 18/64 (28.1%) of the community-acquired cases. Progression to chronic hepatitis was observed more frequently in antibody-positive than in antibody-negative cases (60/96 or 62.5% vs. 27/86 or 31.4%, P = 0.00002). Progression was also observed more often in males than in females (66/112 or 58.9% vs. 21/70 or 30.0% P = 0.0001), both in the antibody positive (48/68 or 70.6% vs. 12/28 or 42.9%, P = 0.01) and in the antibody negative (18/44 or 40.9% vs. 9/42 or 21.4%, P = 0.043) cases. These data indicate that (a) acute hepatitis due to HCV is characterized by a high rate of chronicity, especially in males, and (b) a non-A, non-B, non-C agent or a different strain of HCV may be responsible for the majority of the community-acquired cases of non-A, non-B hepatitis in Greece.
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PMID:Role of hepatitis C virus in acute non-A, non-B hepatitis in Greece: a 5-year prospective study. 131 Dec 75

Localization of hepatitis C virus (HCV) RNA was investigated by non-radioactive in situ hybridization in human liver specimens of chronic non-A, non-B (NANB) hepatitis patients who were seropositive for antibodies to HCV (anti-HCV). For in situ hybridization, T-T dimerized synthetic oligodeoxynucleotide probes were used and DNAs hybridized in situ were detected immunohistochemically using specific antibodies against T-T dimer. The data demonstrates that HCV-RNA was localized in the cytoplasm of hepatocytes in human liver biopsies obtained from the patients with chronic NANB hepatitis seropositive for anti-HCV.
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PMID:Detection of hepatitis C virus (HCV) RNA in paraffin embedded tissue sections of human liver of non-A, non-B hepatitis patients by in situ hybridization. 131 61

A multicenter prospective study was carried out to evaluate whether a vapor-heated factor VIII concentrate transmitted blood-borne viral infections over a surveillance period of 15 months. Thirty-five patients with hemophilia and von Willebrand disease who had never received any blood components were treated. Twenty-eight were analyzed and found not to have non-A, non-B hepatitis. Sera from 20 of these 28 patients were also tested for the antibody to the hepatitis C virus. None had sero-converted during the follow-up period. None of the patients analyzed developed markers of the hepatitis B virus (n = 17) or the human immunodeficiency virus (n = 31). This vapor-heated factor VIII concentrate carries a low risk of transmitting hepatitis and human immunodeficiency virus infection.
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PMID:Low risk of viral infection after administration of vapor-heated factor VIII concentrate. International Investigator Group. 131 76

Hepatitis C (HC) has been recently diagnosed by determination of specific antibodies that represent the former so-called non-A, non-B hepatitis. We studied the prevalence of plasma HCV antibodies among 61 unselected patients on hemodialysis (HD) and 43 on continuous ambulatory peritoneal dialysis (CAPD). Plasma C-antibodies were determined through the ELISA test system. Transfusion policy was the same in both groups. The prevalence of hepatitis C virus antibodies was significantly higher in hemodialysis patients than among those on CAPD. Time on dialysis, previous blood transfusions, and renal transplantation seem to increase the prevalence of C hepatitis antibodies among hemodialysis patients. The effect of these parameters on CAPD was smaller. Understanding the reasons for these differences may help prevent this disease among dialysis patients.
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PMID:Prevalence of hepatitis C antibodies (HCV) in a dialysis population at one center. 154 76

A 57 year old man with auto-immune chronic active hepatitis, regularly treated with immunosuppressive therapy, had hepatocellular carcinoma (HCC) 10 years after diagnosis of the hepatitis. Assays of the hepatitis C virus antibodies against capsid and non-structural proteins revealed seronegativity in serial serum samples of this patient stored in the previous 10 years during follow up. The seronegative hepatitis C antibodies excluded hepatitis C virus as the cause of the HCC. The occurrence of HCC in this case suggests the necessity of surveillance for early detection of liver cancer in patients with auto-immune chronic active hepatitis undergoing long-term immunosuppressive therapy.
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PMID:Development of hepatocellular carcinoma in a man with auto-immune chronic active hepatitis. 131 68

Antibody to recombinant hepatitis C virus (HCV) protein C100 (anti-C100) was measured for a period of 6 months by enzyme immunoassay in nine prospectively followed non A-nonB (NANBH) cases which occurred after cardiac surgery at a hospital in Rio de Janeiro (Brazil). At least seven cases were infected with HCV; four of these developed chronic hepatitis as shown in liver biopsy at the 6th month after transfusion. The first elevation of alanine aminotransferase (ALT) occurred between 15 and 45 days after transfusion and ALT values remained elevated for 45 days in resolving hepatitis, whereas in chronic cases fluctuation levels were observed until the end of the study. Anti-C100 appeared after 15 to 30 days, decreased after some weeks, and rose finally to high concentrations except in one resolving case where it disappeared. We conclude that both in acute and chronic hepatitis C an early antibody response occurs which may, however, be undetectable in some cases. After several months all chronic and some resolving cases develop a second stronger response.
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PMID:Early appearance and biphasic kinetics of IgG antibody against hepatitis C virus protein C100-3. 131 60

A nonisotopic in situ hybridization (NISH) assay was used to detect hepatitis C virus (HCV) RNA. A synthetic oligonucleotide complementary to bases 252-301 of the highly conserved 5' noncoding region of the HCV genome was end-labeled by terminal deoxynucleotidyltransferase using digoxigenin-conjugated dUTP. The hybridized oligomer was revealed by an immunohistochemical reaction after incubation with an alkaline phosphatase-conjugated anti-digoxigenin antibody and subsequent amplification with a complex of alkaline phosphatase and anti-alkaline phosphatase antibodies. The intracellular distribution of HCV RNA was monitored in the livers of two chimpanzees experimentally infected with the H strain of HCV and compared with the serum alanine aminotransferase activity, serum HCV RNA, and liver histopathology. Most cells were stained in the cytoplasm as early as 2 days after inoculation, 1 and 2 days, respectively, before the appearance of viral RNA in the serum. The time course of HCV RNA replication was correlated with increases in serum alanine aminotransferase. However, neither one paralleled the appearance of liver cell necrosis nor showed any correlation with the inflammatory response. The NISH signal was not found in liver biopsy specimens taken from these two animals before inoculation with HCV, from chimpanzees with acute hepatitis type A, B, or delta, or from two animals never experimentally infected with any hepatitis agent; moreover, it disappeared when the positive specimens were predigested with RNase and it was not observed after hybridization of positive controls with a labeled oligomer unrelated to HCV RNA. Thus, detection of liver HCV RNA by NISH is a sensitive and specific method for studying HCV replication at the cellular level. Intracellular replication of HCV did not appear to be associated with histopathologic changes in the liver, although the correlation with increases of liver enzyme activity in the serum suggested possible damage to the liver cell membrane.
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PMID:Detection of intrahepatic replication of hepatitis C virus RNA by in situ hybridization and comparison with histopathology. 131 16

The relationship between hepatitis C virus RNA and hepatitis C virus-associated antibodies (antibody against the putative capsid protein and C-100 antibody) was determined by nested polymerase chain reaction and enzyme-linked immunosorbent assay in serial serum samples obtained from eight chimpanzees experimentally infected with hepatitis C virus. Three different patterns emerged from the polymerase chain reaction data: the first (group 1) was acute resolving hepatitis with transient appearance of HCV RNA (two cases). The second (group 2) had chronic hepatitis with persistent hepatitis C virus RNA positivity (four cases) and the third (group 3) had chronic hepatitis with intermittent appearance of hepatitis C virus RNA (two cases). In four of eight animals, hepatitis C virus RNA was first detectable in serum 1 wk after inoculation. Although serum HCV RNA was detected in all infected chimpanzees, two were positive only for antibody against the putative capsid protein, whereas two were positive only for antibody to C-100 antigen. In four of eight cases, antibody against the putative capsid protein appeared earlier than did antibody to C-100 antigen, was detected just before or coincident with rising glutamate pyruvate transaminase values and remained positive for a long time even after recovery. Six of eight animals (75%) were still hepatitis C virus RNA positive 1 yr after inoculation, suggesting that the risk of development of the chronic carrier state is high in hepatitis C virus infection. Furthermore, there did not appear to be a good correlation between antibody titer in serum and hepatitis C virus infectivity titer.
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PMID:Three different patterns of hepatitis C virus infection in chimpanzees. 131 87


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