Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors reviewed the cases of 19 Alaskan Natives (15 men, four women) with primary hepatocellular carcinoma (HCC) diagnosed during 1980-1985. Of these 19 patients, 16 were seropositive for hepatitis B surface antigen (HBsAg). Alpha-fetoprotein (AFP) was elevated in 15 patients (all were HBsAg positive). The patients ranged in age from 8 to 80 years old. Of the 19 patients, 16 were Eskimo, 13 of whom were Yupik. The annual age-adjusted (world standard) incidence of HCC for all Alaskan Natives was 9.3/100,000 for men and 2.2/100,000 for women. The tumor was resected in seven patients; six showed no recurrence of cancer 1 to 4 years after surgery. Histologic evaluation in 18 patients revealed trabecular type of HCC in 15 and acinar HCC in two others. In 16 specimens in which nontumorous liver could be studied, only six had evidence of cirrhosis; ten others showed variants of chronic persistent hepatitis.
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PMID:Primary liver cancer in Alaskan natives. 1980-1985. 244 34

Seventy HBsAg-positive patients, including 24 with primary hepatocellular carcinoma, 34 with chronic active hepatitis, 12 with chronic persistent hepatitis and 30 asymptomatic healthy hepatitis B virus carriers were tested for anti-HBc IgM using the Corzyme-M test. Anti-HBc IgM was detected in 50% of the primary hepatocellular carcinoma patients, 26.5% of the chronic active hepatitis patients, 25% of the chronic persistent hepatitis patients, but in none of the healthy hepatitis B virus carriers. There was no correlation between the presence of anti-HBc IgM and HBeAg, hepatitis B virus DNA, ALT or alpha-fetoprotein levels in either the chronic active hepatitis or chronic persistent hepatitis patients. However, a significantly higher positive rate of anti-HBc IgM was noted in the HBeAg-positive or HBV DNA-positive primary hepatocellular carcinoma patients than in those with negative markers of viral replication, but no correlation was noted between the presence of anti-HBc IgM and serum ALT or alpha-fetoprotein levels in these primary hepatocellular carcinoma patients. Also, no differences in positivity for HBeAg, HBV DNA or levels of serum ALT were noted when patients with high titers of anti-HBc IgM were compared to those with low titers. Thus, anti-HBc IgM cannot distinguish between HBsAg-positive patients with chronic active hepatitis, chronic persistent hepatitis or primary hepatocellular carcinoma, does not correlate with serum ALT or alpha-fetoprotein levels and is only associated with markers for viral replication in primary hepatocellular carcinoma patients. Based on this, anti-HBc IgM appears to have a limited usefulness for diagnosis of either chronic hepatitis B or primary hepatocellular carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is anti-HBc IgM a useful clinical test in patients with HBsAg-positive chronic hepatitis or primary hepatocellular carcinoma? 245 29

A 9-year-old boy with hepatitis B-associated glomerulonephritis and nephrotic syndrome underwent antiviral combination therapy including interferon and acyclovir. Pretreatment evaluation showed that active hepatitis B virus replication with HBsAg, HBeAg, HBV-DNA and DNA-polymerase had occurred for a period of at least 4 years. Signs of liver disease were minimal; serum amino transferases were normal and liver histology showed chronic persistent hepatitis with positive HBcAg, HBeAg and HBsAg immunofluorescence. A kidney biopsy revealed membranous glomerulonephritis with deposition of HBcAg, HBeAg, IgG, C3, C1q and, on electron microscopy, virus-like particles. After 8 weeks of therapy, active viral replication ceased, HBe seroconversion occurred and the nephrotic syndrome disappeared. One year after treatment, the boy was asymptomatic. No viral markers could be detected in the kidney, but low-grade membranous glomerulonephritis persisted with deposition of C1q, IgG and C3, but not HBeAg, HBsAg or HBcAg. Liver histology showed a minimal aspecific portal infiltrate with weak membrane-bound HBsAg immunofluorescence; no HBcAg could be detected. For patients with active viral replication and deposition of HBc, HBe immune complexes in the kidney, antiviral therapy can be beneficial, even in the absence of active liver disease.
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PMID:Improvement of hepatitis B-associated glomerulonephritis after antiviral combination therapy. 247 23

To analyze interleukin-2-dependent immunoregulatory function in hepatitis B virus infection and in other forms of viral hepatitis, levels of soluble interleukin-2 receptors (sIL-2R) were measured by an enzyme-linked assay in sera from patients with acute and chronic viral hepatitis of different etiology. Increased sIL-2R levels were detected in the early phase of acute hepatitis type A and type B, but not during acute non-A, non-B hepatitis. Among 46 patients with chronic hepatitis B virus infection, levels of sIL-2R were significantly increased only in cases with chronic active hepatitis, while they were about normal in chronic persistent hepatitis or in healthy carriers of the infection. These differences were independent of virus replication, being maintained when patients were stratified according to HBeAg/anti-HBe status and to serum HBV-DNA. Nine patients with chronic active hepatitis type B and high sIL-2R levels at presentation were followed prospectively for two to eight years, and in HBeAg-positive patients, the behavior of receptor levels closely paralleled disease activity. These results, which may reflect increased shedding of IL-2R by activated T lymphocytes in patients with active destruction of HBV infected hepatocytes, indicate the usefulness and potential prognostic importance of serum sIL-2R determination in patients with chronic viral hepatitis. Patients with chronic non-A, non-B hepatitis had much lower sIL-2R levels, although their liver disease was similar to hepatitis B cases, suggesting that different pathogenetic mechanisms operate in these patients.
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PMID:Serum levels of soluble interleukin-2 receptors in acute and chronic viral hepatitis. 224 65

We detected the presence and distribution of HBcAg in the liver by immunohistochemistry (ABC method) and the presence of HBV-DNA in serum (spot hybridization) and anti-HBe in serum (ELISA) from 59 cases of hepatitis B hospitalized in our hospital, including 47 cases of CAH, 5 cases of CPH, and 7 cases of subacute fulminant hepatitis. 1. HBcAg in the liver was detected in 25 out of 47 cases (53%) of CAH, in 2 out of 5 cases of CPH and in 4 out of 7 cases of subacute fulminant hepatitis. The total percentage was 53% (31/59). 2. There was no positive correlation between HBV replication activity and liver disease activity (P greater than 0.05). Our results did not support the hypothesis that suggests a direct cytopathic effect of HBV. Oppositely, the fact was that the presence, the amount and the patterns of HBcAg in the liver, and the presence of HBV-DNA in serum were predominant in mild CAH compared with those in severe CAH, predominant in CAH without cirrhosis compared with those in CAH with cirrhosis. There was a tendency of inverse correlation between HBV replication activity and liver disease activity. The results above were in line with the concept that HBcAg expressed on the surface of infected hepatocytes may be relevant target for T lymphocyte cytotoxicity. The results have suggested that an immune response to HBV is present, leading to the destruction of most infected cells. 3. There was a positive correlation between HBV-DNA in serum and HBcAg in the liver (P less than 0.005), indicating that HBV-DNA in serum can represent HBV replication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relationship between HBcAg in the liver and mechanisms of chronic type B hepatitis HBVM in serum]. 259 35

Presence of predominantly small lymphocytes in sinusoids and their immigration into the Disse space as well as into intercellular spaces between hepatocytes were recorded by electron microscopy from liver biopsies of 11 in 18 haemodialysis patients. No degenerative alterations were recordable from adjacent hepatocytes. These findings were obtained from patients with acute hepatitis (one case), minimal or chronic persistent hepatitis (two cases), reactive hepatitis (three cases), lobular and portal hepatitis (one case) as well as from the cases of metabolic-toxic alterations and one case of chronic blood congestion. HBV antigens were serologically identified in six cases. A HBcAg-free HBsAg type was immunohistologically diagnosed in one case only. No correlation was found to exist between the morphological results, on the one hand, and cellular immune pattern in peripheral blood, on the other. The above findings differed from most investigations of hepatitis B cases, in that no evidence could be found to cytotoxic action of lymphocytes upon adjacent hepatocytes. More investigations will be required for interpretation of the above findings, primarily immuno-electron microscopic studies.
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PMID:[Ultrastructure of intralobular lymphocyte migration in the liver of hemodialysis patients]. 261 93

To study the role of genetic factors in hepatitis B virus (HBV)-related liver diseases, HLA typing with 47 specificities of HLA-A, B, C and DR loci using Terasaki's 2-stage microlymphocytotoxicity method was performed in 253 normal subjects and 305 patients with various HBV-related liver diseases, including 95 healthy carries of HBV, 30 with chronic persistent hepatitis (CPH), 74 with chronic active hepatitis (CAH), 51 with liver cirrhosis and 55 with hepatocellular carcinoma (HCC). The frequency of HLA-B17 was significantly higher in patients with HCC than in healthy carriers (27.3% vs 4.2%, Pc less than 0.01). A similar situation was noted for HLA-DR3 in a comparison of patients with CAH and healthy carriers (37% vs 10%, Pc less than 0.05). Comparisons among various groups involving other specificities were statistically nonsignificant. It is concluded that genetic predisposition to the development of CAH, as well as HCC is present in HBsAg carriers, and further clarification of underlying mechanisms is needed.
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PMID:HLA-A, B, C and DR antigens in chronic hepatitis B viral infection. 262 Sep 4

Circulating autoantibodies reacting with human hepatocyte plasma membranes (HHPM) were quantitated in acute and chronic liver disease using an enzyme-linked immunosorbent assay (ELISA). Anti-HHPM were found most frequently in patients with chronic active hepatitis (CAH), a disease postulated to result from autoimmune processes directed at organ-specific antigens on the surface of hepatocytes. The high incidence of anti-HHPM in CAH (75%) contrasted significantly with all other groups assayed, including primary biliary cirrhosis (44%), alcoholic liver disease (21%), acute viral hepatitis (17%), and chronic persistent hepatitis (8%). The titers of anti-HHPM in CAH were significantly greater than in other liver disease and control groups. Anti-HHPM quantitated by ELISA correlated with hepatocellular membrane staining by indirect immunofluorescence. Autoantibodies to HHPM were found with an equivalent frequency in three etiological subgroups of CAH: autoimmune CAH, hepatitis B virus (HBV)-related CAH, and CAH associated with excess alcohol consumption. Anti-HHPM of the IgG and IgA isotypes were found in the highest frequency. There was a trend for patients with a histologically more severe disease to have higher titers of anti-HHPM. Immunoblots of SDS-PAGE-separated HHPM showed antibodies to react with a number of polypeptides, some of which appeared human specific. These data suggest that isolated HHPM are a source of relevant hepatocellular membrane antigens. Further studies of the different antigenic specificities of anti-HHPM are required to define which of these may be of pathogenetic importance in chronic active hepatitis.
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PMID:Autoantibodies to isolated human hepatocyte plasma membranes in liver disease. I. Specificity for chronic active hepatitis. 266 Oct 64

Studies on the quantitative expression of the Major Histocompatibility Complex (MCH) in hepatocytes chronically infected by Hepatitis B Virus (HBV) report that an increased expression of these antigens could be related to a good immunological response. In the present work we analyze the expression of the MCH antigens in cryostatic sections of liver biopsies taken from subjects (19 children) with various forms of HBsAg positive chronic hepatitis. A high expression of HLA class I antigens and a high degree of hepatocyte necrosis was evident in Chronic Active Hepatitis (CAH) and Chronic Lobular Hepatitis (CLH). On the contrary, subjects with histological diagnosis of Chronic Persistent Hepatitis (CPH) showed a low expression of such antigens. There was however, the difference that in subjects with high hepatic cytolysis and high expression of HLA class I antigens, serum HBV-DNA was clearly present in almost all the cases with CAH, but not detectable in all cases with CLH. The expression of HLA class II antigens and of Beta2 microglobulin was the same in all 19 cases. All cases with HBV-DNA positivity with high class I antigen expression had active hepatitis which seems to suggest that all attempts at viral clearance on the part of the immune system have been in vain. We hope our paper will be an additional parameter for evaluating the course of hepatitis during Interferon treatment.
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PMID:Different expression of HLA class I antigens in liver of children with chronic hepatitis B, evaluated by immunohistochemical method. 269 19

Circulating immune complexes composed of HBcAg and anti-HBc have been demonstrated recently in patients with hepatitis B virus replication. After dissociation of immune complexes by chaotropic ions, HBcAg was quantified radioimmunologically. In the present study, we describe 10 patients with hepatitis B virus replication, absent or delayed anti-HBc formation and exposed HBcAg in serum. Four of the 10 patients had acute hepatitis, and six patients had chronic persistent hepatitis. In seven of 10 patients, a secondary immune defect was apparent due to acquired immunodeficiency syndrome, leukemia, histiocytosis X, sarcoidosis or end-stage renal disease. Electron microscopy demonstrated that Dane particles from anti-HBc-negative patients were agglutinated after addition of monoclonal anti-HBc antibodies, whereas Dane particles from anti-HBc-positive sera did not show agglutination. Monoclonal HBsAg-specific antibodies aggregated Dane particles independent of the presence of anti-HBc. Circulating HBcAg was always associated with the Dane particle fraction after density gradient separation. Hepatitis B virus core proteins from patients with and without anti-HBc studied by immunoblotting after sodium dodecyl sulfate-gel electrophoresis showed identical patterns. Hepatocytes from anti-HBc-negative patients were positive for HBcAg but negative for immunoglobulin G by immunofluorescence technique. The data indicate that HBcAg may also be expressed on the surface of Dane particles, where it is commonly masked by anti-HBc.
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PMID:HBcAg expressed on the surface of circulating Dane particles in patients with hepatitis B virus infection without evidence of anti-HBc formation. 274 30


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