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)

Sixteen of 110 hemodialysis (HD) patients fulfilling criteria of non-A, non B hepatitis (NANBH), i.e. alanine aminotransferase (ALT) greater than 50 U/ml in the absence of both serologic markers for acute HBV and HAV infections and clinical evidence of another cause of hepatitis, were tested for the presence of antibodies against hepatitis C virus (anti-HCV) by enzyme immunoassay (Ortho, Diagnostics). All (100%) were anti-HCV-positive. There were 5 patients with a monophasic (M) rise pattern (1 or 2 ALT rises), and 11 cases demonstrated a polyphasic (P) rise elevation pattern (more than 2). The mean ALT value of the M group was 202.3 +/- 209 U/ml and that of the P group was 116.6 +/- 39.1 U/ml. The patients received a mean of 19.1 +/- 16.2 units of packed red cells during the follow-up period (69.9 months). Only 1 patient received no blood transfusion. Six patients had a past HBV infection and 3 became HIV-infected in the course of this study. The high rate of infection of hemodialysis patients with hepatitis C virus in our setting points to the need for improved control measures.
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PMID:Hepatitis C virus in chronic hemodialysis patients with non-A, non-B hepatitis. 131 55

The complete nucleotide sequence of hepatitis C virus (HCV) cloned from the liver tissue of a Taiwanese patient with post-transfusion type C hepatitis was determined. The 5' end of HCV genomic RNA was located 341 nucleotides upstream from the initiation codon for the viral polyprotein open reading frame. The 5' end of the viral antigenomic RNA was shown to have 13 consecutive As. Thus the 3' terminus of the viral genome is a stretch of U which ends about 50 nucleotides downstream from the stop codon of the large open reading frame. The nucleotide sequence homology between this HCV strain and two Japanese isolates was 90.5 and 90.7%, respectively. Homology with the United States strain, however, was only 77.8%. Accordingly, the indigenous Taiwanese HCV strain is of the same subtype as the Japanese isolates. Novel features of the viral genome termini are possibly relevant to HCV genome replication.
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PMID:The Taiwanese hepatitis C virus genome: sequence determination and mapping the 5' termini of viral genomic and antigenomic RNA. 131 49

The presence of antibody to the hepatitis C virus was determined in 254 alcoholic patients with non-B chronic hepatitis and a titre of antinuclear antibodies of 1/40 or lower. Alcoholic hepatitis was present in 12 patients, steatohepatitis in 20, active chronic hepatitis in 22, cirrhosis in 181, and hepatocarcinoma in 19. Twenty patients had previously received blood transfusion alone or during surgery, 49 had undergone previous surgery without transfusion, a clinical episode of hepatitis could be traced in 14, 4 patients were drug addicts, 41 had received blood transfusion after the diagnosis was made, and 128 presented with alcoholism alone. Anti-hepatitis C antibody was found in 20 out of 2,000 blood donors (1%) in our hospital. Anti-hepatitis C antibody was found in 87 patients (34.2%) in our series, a figure unaltered by past medical history. Patients with anti-HC antibody had higher levels of AST, ALT, total proteins, gamma-globulin, and IgG. The incidence of active chronic hepatitis was higher among patients with anti-HC antibody, whereas the incidence of steatohepatitis was higher among patients without anti-HC. Regarding findings on liver biopsy, the incidence of anti-HC was significantly higher (p less than 0.001) among patients with active chronic hepatitis (72.7%) than in any other group; no significant differences were found between patients with cirrhosis (33.3%), hepatocarcinoma (31.5%), steatohepatitis (15%), or alcoholic hepatitis (16.7%). Among HBsAg-negative patients, the incidence of anti-HC was similar between those with (39.7%) and without other serum markers of HB (32.9%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevalence and significance of the C virus antibody in chronic hepatopathy not related to B virus in alcoholics]. 131 33

The presence of antibody to hepatitis C virus was determined in 316 HBsAg-negative patients with non-alcoholic chronic hepatitis who did not receive any blood transfusion once the diagnosis was made. A titre of antinuclear antibodies of 1/40 or lower was found in 18 patients. Persistent chronic hepatitis was present in 21 patients, active chronic hepatitis in 145, hepatic cirrhosis in 128, and hepatocarcinoma in 22 patients. One hundred and three patients had previously received blood transfusion, 76 had undergone previous surgery without transfusion, a clinical episode of hepatitis could be traced in 14, 13 patients were drug addicts (all of them HIV negative), 1 patient had received multiples injections, another had been treated with acupuncture, and 108 patients were free of any of the above. Anti-HCV was present in 76.6% of patients; a significantly higher proportion (87.4%) was found among patients who had received blood transfusion than in patients with previous surgery (72.4%) (p = 0.012), clinical hepatitis (57.1%), or without previous hepatic disease (70.3%) (p = 0.003). The incidence of anti-HCV was lower among cirrhotics (70.3%) than in patients with active chronic hepatitis (84.1%) (p = 0.006); in contrast, previous blood transfusion was significantly higher (p = 0.001) among the latter (40.7%) than in cirrhotics (21.9%). The incidence of anti-HCV was similar among patients with (78.6%) and without (75.8%) type B infection. Our results suggest that infection with virus C may account for a high proportion of non-alcoholic non-B chronic hepatitis.
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PMID:[Prevalence of hepatitis C virus antibody in chronic HBsAg-negative non alcoholic hepatopathy]. 131 34

To examine the role of hepatitis C virus (HCV) infection in spontaneous hepatitis B surface antigen (HBsAg) clearance during the course of chronic hepatitis B virus (HBV) infection, serum specimens from 32 asymptomatic HBsAg carriers and 22 patients with chronic hepatitis type B who underwent spontaneous HBsAg clearance were studied for antibody to HCV (anti-HCV) using commercial EIAs. The results were compared with those of control groups matched for age, sex, hepatitis B e antigen, antibody to hepatitis delta virus, and cirrhosis. Eight (25%) of the asymptomatic carriers and 9 (41%) of the patients with chronic hepatitis were seropositive for anti-HCV in contrast to 1.6% and 9.1% of their respective control groups (P less than .01). Serum alanine aminotransferase level was persistently abnormal after HBsAg clearance in one asymptomatic carrier and in four patients with chronic hepatitis. These patients were seropositive for anti-HCV and at least one of them was negative for HBV-DNA by polymerase chain reaction. The data suggest that HCV superinfection may not only suppress HBV or terminate the HBsAg carrier state but may also assume the role of HBV as the cause of persistent hepatitis or transaminase elevation.
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PMID:Role of hepatitis C virus infection in spontaneous hepatitis B surface antigen clearance during chronic hepatitis B virus infection. 131 69

To assess whether the hepatitis C virus plays an important role in Chinese patients with acute and chronic liver disease, antibodies to HCV (anti-HCV) were measured by enzyme immunoassay in 67 patients with type A and B acute viral hepatitis, 165 patients with non-A, non-B (NANB) hepatitis, 438 patients with chronic hepatitis, 200 patients with postnecrotic liver cirrhosis, 72 patients with alcoholic liver disease, 55 patients with non-alcoholic fatty liver, 24 patients with toxic and drug-induced hepatitis, and 20 patients with other chronic liver diseases. Anti-HCV was not detected in sera from patients with type A and B acute viral hepatitis, toxic and drug-induced hepatitis, primary biliary cirrhosis, Wilson's disease, or lupoid hepatitis. The anti-HCV prevalence was found to be highest in patients with NANB hepatitis (59% in sporadic and 73.2% in transfusion-associated), 16.4% in non-alcoholic fatty liver, 5.6% in alcoholic liver disease, 6.8% in chronic hepatitis, and 16% in postnecrotic liver cirrhosis. In patients with chronic hepatitis, the anti-HCV prevalence was significantly higher in HBsAg-negative (15/34, 44.1%) than in HBsAg-positive cases (15/404, 3.7%; P less than 0.0001). The results indicate that HCV is a major agent of NANB hepatitis and plays an important role in HBsAg-negative chronic liver disease in Taiwan.
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PMID:Prevalence of anti-HCV among Chinese patients with acute and chronic liver disease. 131 64

In a prospective study of posttransfusion hepatitis, 14 patients who were diagnosed with posttransfusion hepatitis C were enrolled randomly for the study of hepatitis C virus (HCV) RNA in saliva. Saliva and serum samples were collected on the same day. Spouses of 11 married patients were also tested for anti-C100 and HCV RNA. Paired serum and saliva samples were tested for HCV RNA by a nested polymerase chain reaction (PCR). Two primer pairs specific for the non-coding region of HCV were used for the PCR and a oligonucleotide sequence between the primers was used as the probe for Southern hybridization. Six patients were positive for HCV RNA by first round PCR amplification and an additional four patients were detected after second round PCR. All patients were negative for HCV RNA in saliva after first round PCR, while seven were positive after second round PCR amplification. All seven patients were positive for HCV RNA in paired serum samples. HCV RNA was detectable in saliva from 1 week to 38 months after the onset of hepatitis. All spouses were negative for anti-C100 and HCV RNA. We conclude that HCV RNA is present in the saliva of approximately half of patients with acute and chronic hepatitis C, and the presence of HCV RNA correlates with HCV viremia. The efficiency of HCV transmission is low among spouses.
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PMID:Hepatitis C virus RNA in saliva of patients with posttransfusion hepatitis and low efficiency of transmission among spouses. 131 67

Oral fluid samples were compared with serum samples as a specimen source for hepatitis A, B, and C virus markers. Oral fluid was obtained with a treated absorbent pad and tested by using existing commercial enzyme immunoassays with only minor modifications. Compared with serum sampling the sensitivity and specificity of oral sampling were 100% (51 of 51 samples) and 98% (46 of 47 samples) for hepatitis A virus immunoglobulin M, 100% (29 of 29 samples) and 100% (29 of 29 samples) for hepatitis B virus surface antigen, and 100% (13 of 13 samples) and 100% (13 of 13 samples) for hepatitis C virus antibody, respectively. The decline of hepatitis A virus immunoglobulin M in oral samples was parallel to, though somewhat more rapid than, that of hepatitis A virus immunoglobulin M in serum samples. It is proposed that oral sampling represents a safer and more convenient procedure for reliable hepatitis virus testing than blood sampling and that it has wide application in patient and outbreak management.
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PMID:Clinical evaluation of oral fluid samples for diagnosis of viral hepatitis. 131 64

Sera from 103 patients were tested for hepatitis C virus RNA by nested polymerase chain reaction assay. Using primers from the highly conserved 5'-untranslated region, we detected hepatitis C virus RNA in 67 (88.2%) of 76 patients positive for antibody to hepatitis C virus by both second-generation and neutralization enzyme immunoassays. Hepatitis C virus RNA was detected in 93% of patients who had been infected for 10 yr or less and in 89% of those who had been infected for longer than 10 yr. Hepatitis C virus RNA was detected in all patients with chronic hepatitis, active cirrhosis or hepatocellular carcinoma and in 50% of those with nonspecific reactive hepatitis or inactive cirrhosis. Hepatitis C virus RNA was not detected in sera from 22 patients negative for antibody to hepatitis C virus or in 5 patients positive for antibody to hepatitis C virus by second-generation but not by neutralization enzyme immunoassay. Using primers from the less conserved nonstructural region 4, we detected hepatitis C virus RNA at a lower frequency, in 66% of patients who were positive for antibody to hepatitis C virus by both second-generation and neutralization enzyme immunoassays. The detection rate was higher in patients with frequent parenteral exposure. Our study showed that hepatitis C viremia can be detected in most patients with hepatitis C virus infection, including those with long-standing infection or advanced liver disease.
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PMID:Hepatitis C viremia in patients with hepatitis C virus infection. 131 37

We reanalyzed the results of a pilot study of recombinant alpha-interferon therapy for chronic non-A, non-B hepatitis in light of the recent discovery of the hepatitis C virus and the development of diagnostic assays for this agent. Stored serum samples from 10 patients treated between 1984 and 1986 were tested for antibody to hepatitis C virus and hepatitis C virus RNA before, during and after therapy. In addition, the current clinical, serum biochemical and virological statuses of these patients were evaluated to determine the long-term effects of interferon therapy. All patients had evidence of hepatitis C virus infection, with hepatitis C viral RNA, antibody to hepatitis C virus or both markers detectable in serum. Serum hepatitis C virus RNA was found to disappear in seven of eight patients whose aminotransferase levels became normal with interferon therapy but remained present in two patients who did not respond to therapy. Levels of hepatitis C virus RNA decreased and disappeared when serum aminotransferases fell to normal levels but rose with subsequent elevation of aminotransferase levels in two patients who had relapses in disease when interferon was stopped. During a follow-up of 3 to 6 yr, hepatitis C virus RNA remained undetectable in the six patients whose serum aminotransferase levels remained normal after interferon therapy. However, neither initial titers of hepatitis C virus RNA nor disappearance of viral RNA from serum during treatment predicted a sustained response. Thus long-term beneficial responses to alpha-interferon can occur in patients with chronic hepatitis C and are associated with sustained loss of hepatitis C virus RNA from serum.
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PMID:Long-term follow-up of patients with chronic hepatitis C treated with alpha-interferon. 131 38


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