An antigen/antibody system associated with one form of parenterally transmitted non-A, non-B (NANB) hepatitis has been identified by solid-phase radioimmunoassay (RIA). The antigen is found in 3% of normal subjects and in increased frequency in patients with haemophilia, renal homograft recipients,
Liver Membrane Antibodies Detected by Immunoradiometric Assay in Acute and Chronic Virus-Induced and Autoimmune Liver Disease
β Scribed by K. H. Wiedmann; T. C. Bartholemew; D. J. C. Brown; Howard C. Thomas
- Publisher
- John Wiley and Sons
- Year
- 1984
- Tongue
- English
- Weight
- 622 KB
- Volume
- 4
- Category
- Article
- ISSN
- 0270-9139
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β¦ Synopsis
In this study, we describe a radioimmunoassay to detect liver membrane binding antibodies. The assay was designed to exclude binding of aggregated IgG or immune complexes to Fc y receptors of hepatocytes. When this assay was applied to sera from 142 patients, antibodies were found in highest titer in patients with autoimmune chronic active hepatitis, rarely in patients with hepatitis B virus-induced chronic active liver disease, and in 32% of patients with primary biliary cirrhosis. IgM antibodies were found in 100% of patients with acute Type A but not B or non-A, non-B hepatitis. IgA class antibodies were found in the sera of 57% of patients with alcohol-induced hepatitis. All patient groups showing significant titers of liver membrane antibodies display the lesion of piecemeal necrosis except those with alcohol-induced hepatitis. Further studies are needed to determine whether this antibody is the cause of the lesion.
Chronic active hepatitis, occurring in female patients, associated with antinuclear factor and smooth muscle antibodies, is a disease in which inflammatory necrosis of periportal hepatocytes is thought to be due to autoimmunization to a liver membrane antigen (l), occurring because of defective regulation of the immune system (2). Lesions of similar nature have also been described in hepatitis B virus and drug-induced chronic hepatitis and, more recently, in primary biliary cirrhosis (3) and acute Type A hepatitis (4).
Antibodies to liver-specific lipoprotein (LSP) have been described in most types of acute and chronic liver diseases (5,6). LSP is prepared by mechanical disruption of liver cells (7, 8), and it is likely that the antibodies which bind to it, bind not only to native surface membrane displayed determinants, but also to cryptic determinants and those occurring because of denaturation of the native protein. It seems possible that some of these antibody responses are the result of, rather than the cause of, liver cell necrosis.
To overcome some of these problems, Hopf and col-
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