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)

It is well known that primary hepatocellular carcinoma could be derived from chronic hepatitis and liver cirrhosis in epidemiologic studies. However, it is still not clear what kinds of hepatocyte are premalignant cells. Recently we have focused on liver cell dysplasia as a possible premalignant cell, and showed localization of alpha-fetoprotein in the cytoplasma of these cells. Although the dysplastic cells were often seen in the liver of chronic active hepatitis, hepatitis B virus associated DNA polymerase activity was also significantly high in the sera from the patients with chronic active hepatitis. In this paper, we discuss the possible role of hepatitis B virus through hepatocarcinogenesis in human.
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PMID:Early lesions and development of primary hepatocellular carcinoma in man--association with hepatitis B viral infection. 7 Mar 87

Circulating complete and defective hepatitis B virus forms, as represented by full, DNA polymerase-positive and empty, DNA polymerase-negative Dane particles, respectively, were investigated in sera from patients with chronic hepatitis B virus infection and related to the presence of e antigen and antibody and to the histological findings on liver biopsy. Complete hepatitis B virus particles were detected in the serum of all patients postive for e antigen, their percentage ranging from 15 to 61% of the total Dane particle population. Although most of these cases had chronic persistent or chronic active hepatitis, complete viral particles were also found in serum of 3 healthy carriers of hepatitis B surface antigen who had e antigen. These results indicate that e antigen is a marker of active virus replication and support its association with infectivity. It is also associated with liver damage because production of complete virus is a feature of chronic hepatitis. In the presence of anti-e, detection of Dane particles in serum appeared to be related to the histological findings. Most of the healthy carriers had no Dane particles in serum, whereas 80% of the cases with chronic liver disease had circulating Dane particles. However, in contrast to the cases with e antigen, 98 to 100% of Dane particles in these cases appeared to be defective in nucleic acid material on electron microscopy after positive staining. All of the patients with chronic active hepatitis in this group had progressed to cirrhosis and it is possible that production of complete virus particles is reduced in the later stages of the illness.
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PMID:Full and empty Dane particles in chronic hepatitis B virus infection: relation to hepatitis B e antigen and presence of liver damage. 70 Mar 29

Sera from patients with acute hepatitis, cirrhosis or chronic hepatitis, as well as sera from healthy carriers and controls were examined for HBS antigen, DNA polymerase activity and for antibodies to HBS, HBC and DNA polymerase. The data presented suggest that in acute hepatitis the DNA polymerase test enabled us to diagnose at least 20% more cases of hepatitis B than with the RIA but that the DNA polymerase test is of little value for the screening of blood donors since all the healthy carriers gave negative results. As concerns the antibodies to DNA polymerase they appeared in at least 50% of the patients with acute hepatitis, they were transient and only detectable at the early beginning of the disease. These antibodies were also found to be different from the anti-HBS and anti-HBC antibodies.
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PMID:Transient antibodies to DNA polymerase in acute hepatitis B and related diseases. 96 84

In acute cases of hepatitis, DNA polymerase activity was found 2 to 3 times more frequently than positive radioimmunoassay. For each case the DNA polymerase reactivity was shown to be associated with hepatitis B antigens. Inhibitors to this DNA polymerase, with properties of IgM and IgG antibody, were found in 13 of 34 cases of acute hepatitis but only in 1 case out of 22 of cirrhosis. During the course of the acute disease these antibodies were detected 3 times more frequently than those to HBs antigen; the two types of antibodies were almost always found separately in different patients, those to DNA polymerase were apparently transient and developed earlier since they were found as early as 3 days after the clinical onset and no later than the 6th week following the onset.
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PMID:Comparison of DNA polymerase and radioimmune assays for the detection of hepatitis B antigens and antibodies. 120 57

Three patients with submassive hepatic necrosis developed acute liver failure during the severe reactivation of chronic hepatitis B. The activity of hepatitis B virus (HBV) DNA polymerase increased in all three patients immediately before the onset of hepatic failure. Liver biopsy specimens obtained before and after the episode of submassive hepatic necrosis showed progression to advanced liver cirrhosis. The nucleotide sequences of the precore and core regions of HBV-DNA were investigated in two of the three patients and in another two patients with piecemeal and bridging necrosis. The nucleotide and amino acid sequences of the HBV-DNA core region changed after reactivation in the the two patients with submassive hepatic necrosis, while the sequences in the other two patients with piecemeal necrosis remained unchanged before and after reactivation. These results suggest that the antigenicity of the HBV-DNA core region may have been changed before and after severe reactivation. Due to mutation at the core region, a different type of epitope would be expressed on the hepatocytes after submassive hepatic necrosis, which would not be a target for the cytotoxic T cell. This was evident by the continuation of the normal serum GPT for 5 and 9 years, respectively.
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PMID:Mutation of the core region of HBV-DNA and submassive hepatic necrosis in patients with anti-HBe-positive chronic hepatitis B. 139 28

The aim of the study was to test the clinical value of HBV DNA polymerase (DNAp) determination in patients with various forms of HBV infection, namely: acute hepatitis, chronic hepatitis, cirrhosis and healthy HBV carriers. The determination of DNAp was found to be particularly useful in patients with chronic HBV infection with active virus replication (HBeAg+) independent of histopathological changes.
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PMID:[Hepatitis B virus DNA polymerase activity in various clinical forms of HBV infection]. 140 93

We analyzed the binding of 125I-labelled IFN-alpha to peripheral blood mononuclear cells in 19 healthy controls, 25 asymptomatic HBV carriers (AsC), and 69 patients with HBs antigen positive chronic liver disease (CLD). Histological examination showed that of the 69 patients with CLD, 14 had chronic persistent hepatitis (CPH), 46 had chronic active hepatitis (CAH), 9 had liver cirrhosis (LC). The mean number of IFN-alpha/beta receptor sites per cell totaled 1270 +/- 340 in the healthy controls, 1440 +/- 290 in AsC, and 1600 +/- 480 in CLD (with 1770 +/- 480 in CPH, 1580 +/- 490 in CAH, and 1420 +/- 410 in LC). HBV carriers had more IFN-alpha/beta receptor sites than the healthy controls (AsC: P less than 0.1, CLD: P less than 0.01). In CLD, patients with LC tended to have fewer IFN-alpha/beta receptor sites than those with CPH or CAH. The number of IFN-alpha/beta receptor sites in CLD was correlated with the HBe antigen titer (P less than 0.01), and activity of HBV-DNA polymerase (P less than 0.05). These results were suggested that IFN-alpha/beta receptor sites was higher at the HBV carrier state, and correlated with viral replication.
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PMID:[Interferon-alpha/beta receptors in patients with chronic HBV infection]. 214 66

We have studied antibodies (anti-pol antibody) against the polymerase gene product of hepatitis B virus by solid-phase enzyme immunoassay using synthetic peptides coded for by this gene. Sera from six patients with acute hepatitis B, 112 chronic hepatitis B virus carriers and six healthy individuals with naturally acquired immunity to hepatitis B virus were tested for anti-pol antibody. In acute hepatitis B virus infection, anti-pol antibody was detected in three of six patients. In chronic hepatitis B virus infection, anti-pol antibody was detected in 17 of 29 (59%), in 23 of 33 (70%) of cirrhotic patients and in 18 of 24 (75%) patients with cirrhosis complicated by hepatocellular carcinoma, compared with 4 of 19 (21%) asymptomatic carriers and 2 of 7 (29%) patients with chronic persistent hepatitis. Titers of anti-pol antibody were higher in cirrhotic patients with and without hepatocellular carcinoma than in patients with chronic active hepatitis. The presence of anti-pol antibody, however, had no relationship with hepatitis B virus-associated DNA polymerase activities and other viral replicative markers. As for sera from six healthy individuals with naturally acquired immunity to hepatitis B virus, two (33%) were positive for anti-pol antibody. These results indicate that the immune response toward the polymerase gene product is induced during acute and chronic hepatitis B virus infection. In chronic hepatitis B virus infection, anti-pol antibody may serve as a new marker indicative of a long period of hepatitis B virus-induced hepatitis.
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PMID:Detection of antibodies against the polymerase gene product in hepatitis B virus infection. 239 Oct 62

The future of patients with chronic hepatitis (HC) due to B virus depends above all on the tendency of the interaction between viral activity and immune response. Viral activity (replication) (RV) can be expressed in these patients by two variants: a) "complete" or "early", associated with the presence in serum of HBsAg, HBeAg, and significant DNA polymerase activity, and b) "incomplete" or "late", in which anti-HBe is found in serum and there are scant or no histopathologic changes ("healthy carriers" in some cases). In prolonged infections viral replication declines gradually, although viral capsid protein continues to be synthesized and DNA-HBV is integrated into the genome. Viral replication per se does not condition the histologic damage (DH) expressive of liver cirrhosis with HBV (HCB). Other publications take a different view of this problem. The increase in viral replication often is proportional to a rise in serum GPT (an expression of histologic damage), but viral replication is not always associated with a progressive disease course. The immune defense leads to cytolysis and subsequent elimination of the HB virus. Some patients with high HBsAg levels have little active forms of liver cirrhosis; the DNA-HBV integrated would be capable of producing HBsAg but not HBcAg. It is precisely this that induces the response of cytotoxic T lymphocytes at the level of the hepatocyte surface. The presence in serum of anti-HBe IgM would be related to the expression of HBcAg on the hepatocyte membrane and/or the liberation of HBcAg particles by lysed hepatocytes. The relationship between the degree of histologic damage and serum aminotransferase levels is better established.
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PMID:[Viral replication, histologic damage and enzymatic activity in chronic hepatopathies caused by B virus]. 266 54

Twenty-one adult patients with chronic hepatitis B and active viral replication as indicated by the presence of hepatitis Be antigen (HBeAg), increased DNA polymerase (DNAp) and positive hepatitis B virus DNA (HBV-DNA) for more than 6 months, were entered into a prospective trial of recombinant human interferon therapy. Ten patients had chronic persistent or chronic lobular hepatitis, 8 chronic active hepatitis and 3 postnecrotic cirrhosis. All cases were treated with 5 x 10(6) units of recombinant interferon alfa-2B given subcutaneously every other day for 12 weeks. During treatment, 18 patients (86%) showed a significant reduction of DNAp levels, which reached normal values in 10 patients (48%). Viral replication was controlled over a 10-month follow-up period in 7 out of 21 patients (33%). Of these 7, five patients became HBeAg negative and HBeAb positive. HBsAg disappeared in one patient. The only serious adverse effect was thrombocytopenia in one patient in whom rapid recovery occurred when interferon was withdrawn. Treatment was also terminated in a second patient because of local reactions at the injection sites occurring after 10 weeks of therapy. Our data indicate that relatively small doses of recombinant alfa-2B interferon given during a 12-week period induce a significant reduction in viral replication and might approximately triple the spontaneous seroconversion rate observed in patients with chronic hepatitis B.
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PMID:Prospective trial of recombinant leucocyte interferon in chronic hepatitis B: a 10-month follow-up study. 268 91


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