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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serologic and tissue markers of hepatitis B virus (HBV) were studied in 50 patients in whom hepatocellular carcinoma (HCC) was confirmed at autopsy. Serologic and tissue markers included serum hepatitis B surface antigen (HBsAg), tissue HBsAg, tissue hepatitis core antigen (HBcAg), and serum antibody to HBcAg (anti-HBc). Twenty-two patients had HCC arising in alcoholic cirrhosis; 2 of the 22 (9.1%) had one or more of the HBV tissue and serologic markers. This infection rate is similar to the rate of 7.9% observed in 63 control alcoholic cirrhotic patients without HCC. In contrast, 15 of 20 (75.0%) patients with HCC in nonalcoholic chronic active liver disease showed evidence of active HBV infection. One of 8 patients with HCC in normal liver had serum HBV markers. This result indicates that there is an extremely high prevalence of HBV infection among HCC patients with nonalcoholic chronic liver disease in the U.S.A. The prevalence of HBV infection in these patients is as high as that observed in Asia and Africa. Thus, it can be concluded that the lower prevalence rate of active HBV infection in HCC patients in the U.S.A. is the result of statistical dilution of HCC-B-viral disease by the large numbers of the alcoholic cirrhotic patients with HCC, and that if chronic active hepatitis type B were as common in the United States as it is in Africa and Asia, the frequency of occurrence of HCC might also be as high.
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PMID:Hepatocellular carcinoma in the U.S.A., etiologic considerations. Localization of hepatitis B antigens. 21 88

Sera of 173 patients with various forms of liver disease along with serum precipitates produced by polyethylene glycol were screened for the presence of a microsomal antigen referred to as ubiquitous tissue antigen (UTA) and its antibody by double diffusion precipitation in agarose gel. UTA was detected in 7 or 26 patients with chronic active hepatitis, 1 of 5 with alcoholic hepatitis, 2 of 14 with alcoholic cirrhosis and 18 of 98 with hepatoma. Antibodies to UTA were found only in 2 patients with chronic active hepatitis, 1 with alcoholic cirrhosis and 1 with hepatoma. No UTA or its antibody were noted in sera of 5 patients with alcoholic fatty liver, 10 patients with hepatitis B, and 15 asymptomatic carriers of HBsAg. Positivity for the UTA or its antibody was restricted to severe, chronic cases irrespective of diagnosis, indicating that persistent tissue destruction might be necessary for antigen release or antibody formation.
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PMID:Detection of a microsomal antigen and its antibody in human liver diseases. 22 26

Recent evidence indicates that viral hepatitis is sometimes associated with the production of extrahepatic tissue injury. Hepatitis B virus (HBV) infection is most commonly incriminated but non-type B hepatitis may also be involved. Three types of syndromes have been recognized. First, a serum sickness-like prodrome consisting of skin eruptions, urticaria and polyarthralgias or arthritis may occur from one to six weeks prior to the onset of hepatitis in 15 to 20 per cent of patients and usually disappears by the time the patient becomes jaundiced. There is extensive evidence that circulating immune complexes are responsible for these symptoms. Second, about 30 to 40 per cent of patients with typical polyarteritis nodosa have persistent hepatitis B surface antigenemia (HBs Ag). Circulating immune complexes composed of HBs Ag, antibody, and complement have been demonstrated together with deposits of immune complexes at sites of vascular injury. Third, an immune complex type of glomerulonephritis may occur following hepatitis B virus infection, usually in association with chronic active hepatitis. Thus there is impressive evidence that hepatitis viruses, especially HBV, may produce a variety of extrahepatic manifestations in which the mechanism of pathogenesis involves an immunologic process rather than direct viral invasion and cytopathogenicity.
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PMID:Extrahepatic manifestations of viral hepatitis. 24 19

Immunological abnormalities are demonstrable in patients with various types of liver damage. These may be (a) non-specific and unrelated to pathogenesis, e.g. auto-antibodies such as anti-nuclear factor; (b) specifically directed against liver antigens but not pathogenetic, e.g. cell mediated immune (CMI) reactions to liver antigen as seen in experimental carbon tetrachloride poisoning; (c) of such a nature as to modify the pathology produced by hepatotoxic agents, e.g. hepatitis B virus or alcohol; (d) primarily responsible for hepatic pathology, e.g. in idiopathic chronic active hepatitis. The latter two possibilities remain unproven although there is growing evidence that immune responses do play some role in the pathogenesis of acute and chronic hepatitis B and possibly also in the pathogenesis of alcoholic liver disease. It seems much less likely that primary abnormalities of the immune systems are responsible for any type of liver disease. In summary, therefore, the available evidence suggests that immune reactions could develop as a consequence of liver damage and only in certain circumstances do these reactions play a role in the development and continuation of hepatic pathology.
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PMID:Immunological abnormalities associated with liver disease: cause or effect? 27 38

The cytotoxic effect of peripheral lymphocytes on chicken red blood cells (ChRBC) coated with purified hepatitis B surface antigen (HBsAg) has been studied as an in vitro parameter of cell-mediated immunity in acute and chronic infection with hepatitis B virus. Using this technique, the mean cytotoxic index of lymphocytes from patients with acute hepatitis B (29.13 +/- 20.88) was significantly higher than that obtained with lymphocytes from control subjects (6.53 +/- 3.75). Only 33.3% of the patients with HBsAg-positive chronic active hepatitis exhibited lymphocyte cytotoxicity to HBsAg-coated target cells and the mean cytotoxic index (11.66 +/- 6.60) was in these cases significantly lower than that found in acute hepatitis B. Healthy chronic carriers of HBsAg failed to show lymphocyte cytotoxicity to target cells. The effector cells detected in acute hepatitis B by this in vitro assay have been demonstrated to be T-lymphocytes, as T-cell depleted subpopulations lacked cytotoxic activity. Target cell lysis could be blocked by addition of HBsAg-coated unlabelled ChRBC as well as of purified HBsAg in the culture tubes. It is suggested that damage to the liver cells in acute hepatitis B is related to the presence of cytotoxic T-lymphocytes reacting with HBsAg on the surface of infected hepatocytes. An inadequate lymphocyte response to the antigen may be responsible for the persistence of the infection in the liver with varied clinical manifestations and associated hepatic lesions.
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PMID:T-lymphocyte cytotoxicity to HBsAg-coated target cells in hepatitis b virus infection. 30 24

A Farr technique has been used to assay antibodies to double-stranded DNA in the serum of patients with acute and chronic liver disease and carriers of HBsAg from the United Kingdom and Iraq. These antibodies were found in all groups from both countries. The highest levels were found in chronic active hepatitis and cirrhosis. In the Iraqi patients there was a strongly positive correlation between DNA-binding antibody levels and the presence of hepatitis B markers but not with disease activity. In the patients from the United Kingdom there was little correlation with disease activity and none with autoantibodies. Ninety-five per cent of asymptomatic carriers of HBsAG had elevated DNA-binding antibodies. It is suggested that hepatitis B-specific DNA might be one trigger to DNA antibody formation, though in liver disease a variety of factors are clearly operative.
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PMID:DNA-binding antibodies and hepatitis B markers in acute and chronic liver disease. 30 8

A 23 year old woman with chronic active hepatitis documented by liver biopsy demonstrated persistent hepatitis B surface antigen, hepatitis B virus specific DNA polymerase hepatitis B core antigen (HBcAg), for approximately one year. The number of circulating T lymphocytes that rosetted with sheep erythrocytes was decreased, and a rosette-inhibitory factor was present in her peripheral blood. Interferon treatment (1 X 10(6) U/day intramuscularly for 82 days) resulted in a decrease of HBsAg and disappearance of HBcAg, (HBeAg) and specific DNA polymerase. In addition, the number of T lymphocytes increased to normal, and the rosette-inhibitory factor disappeared from the circulation. These findings suggest that the effect of interferon in chronic active hepatitis is mediated in part through its action on the immune system.
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PMID:Fibroblast interferon treatment of a patient with chronic active hepatitis. Increased number of circulating T lymphocytes and elimination of rosette-inhibitory factor. 31 5

HBsAg and anti-HBc, the antibody to core antigen of hepatitis B virion, were titrated by solid phase radioimmunoassay in 40 sera of HBsAg carriers with acute and chronic hepatitis and in 20 healthy subjects carrying anti-HBc alone or associated with anti-HBs. No correlation was found between HBsAg and anti-HBc titers in the single category of patients. In contrast, geometric mean titer of anti-HBc (ranging from 2(14) to 2(15)) of patients with chronic active hepatitis was significantly higher ( p = < 0.01) than that of patients with acute or chronic persistent hepatitis and healthy HBsAg carriers (ranging from 2(9) to 2(14)). Anti-HBc titer of 20 subjects without detectable HBsAg was less than 2(7). These data suggest that in subjects with persistent B virus infection, anti-HBc response is correlated with synthesis of viral genome rather than of surface antigens, so that a much higher titer of anti-HBc was detected only in patients with a more active liver disease.
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PMID:[Antinuclear antibody (anti-HBc) and liver pathology in acute and chronic virus B hepatitis]. 31 42

Circulating immune complexes were measured by a radioimmunoassay specific for HB complexes in different clinical situations related to hepatitis B virus infection. The leukocyte migration inhibition test (LMIT) was performed simultaneously. Comparison with the clinical situation suggests that immune complexes are not responsible for the lesions, but that these lesions might be produced by the immunity demonstrated by the LMIT. A deficiency of this immunity is responsible for the persistence of infection. However, in chronic active hepatitis, LMIT is as deficient as in carriers and in this form of hepatitis the frequency and quantity of complexes are the highest: it is thus possible that in this case the lesions are nevertheless produced by the complexes.
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PMID:[Comparison between the presence of specific circulating immune complexes and the leukocyte migration inhibition test in different clinical forms of hepatitis B]. 33 69

In a study of persistent abnormalities of liver-function tests in hemophilic patients deficient in factor VIII or IX and treated with factor VIII or IX concentrates, we examined 14 liver biopsies from 13 anti-HBs-positive patients. None had any symptoms of liver disease. All had chronically abnormal levels of alanine aminotransferase. Histologic studies showed chronic persistent hepatitis in eight patients, chronic active hepatitis in four and fatty infiltration with portal fibrosis in one. Indirect immunofluorescence of antiserums containing anti-HBs or anti-HBc (or both) revealed nuclear and cytoplasmic fluorescence in the hepatocytes of eight of 12 patients. Specificity testing of these antiserums confirmed that hepatitis B viral markers are present in the hepatocytes of these anti-HBs-positive patients. These histologic derangements are probably related to frequent treatment with blood products obtained from multiple donors and to the persistance of hepatitis B virus in hepatocytes despite the presence of circulating anti-HBs.
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PMID:Asymptomatic structural liver disease in hemophilia. 34 86


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