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Comparison between polyclonal and first and second generation monoclonal radioimmunoassays in the detection of hepatitis B surface antigen in patients with hepatocellular carcinoma
Author(s) -
Kew Michael C.,
Fujita Yumiko,
Takahashi Hiroshi,
Coppins Ann,
Wands Jack R.
Publication year - 1986
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840060414
Subject(s) - polyclonal antibodies , hepatocellular carcinoma , radioimmunoassay , monoclonal antibody , monoclonal , antigen , virology , medicine , antibody , cancer research , immunology
Serum from 221 black patients with hepatocellular carcinoma was tested for HBsAg using a polyclonal radioimmunoassay, and first and second generation monoclonal radioimmunoassays designated M1‐RIA and M2‐RIA. These monoclonal radioimmunoassays have a lower limit of detection of about 55 and 15 pg of HBsAg‐associated epitopes per ml of serum. Correlations were made with other hepatitis B virus serologic markers such as anti‐HBc and anti‐HBs, using polyclonal radioimmunoassays. We found 47.5% (105/221) of the patients were HBsAg positive by conventional polyclonal radioimmunoassay; all of these patients were also reactive by monoclonal radioimmunoassay. Of the 116 polyclonal radioimmunoassay‐negative patients, 4 (3.4%) were reactive by M1‐RIA. These four patients were all positive for anti‐HBc and/or anti‐HBs antibodies. There were 106 of 112 patients negative for HBsAg by polyclonal radioimmunoassay and M1‐RIA available for testing by the M2‐RIA; 11 (10.4%) were found to be positive only by this test. Thus, with the use of M1‐ and M2‐RIAs, the number of hepatocellular carcinoma patients negative for HBsAg by polyclonal radioimmunoassay was reduced by 14% in this population. More importantly, of the 11 M2‐RIA‐positive patients, six demonstrated anti‐HBc and/or anti‐HBs antibodies whereas the remaining five had no serologic evidence of recent or past hepatitis B virus exposure. Finally, of the 21 patients in this series with no markers of hepatitis B virus infection using polyclonal radioimmunoassay and M1‐RIA, five (24%) were reactive for HBsAg‐associated epitopes by M2‐RIA. Taken together, these findings may be due in part to the detection of HBsAg in immune complexes, particularly in those patients with anti‐HBc and anti‐HBs. However, in hepatocellular carcinoma patients with no hepatitis B virus serologic markers, the M2‐RIA may have been reactive due to low levels of antigen expression co‐existing with an inadequate or lack of a host immune response to HBcAg and HBsAg, variable expression of hepatitis B virus gene products or to a “hepatitis B‐related virus”.