Abstract
A patient with multiple myeloma was treated with several cycles of chemotherapy and developed monoclonal IgA rheumatoid factor. The monoclonal rheumatoid factor in this case reacted with 2 types of monoclonal antiidiotypic antibody derived from monoclonal rheumatoid factors in a patient with Sjögren’s syndrome and a patient with macroglobulinemia. Two possible mechanisms accounting for the developement of rheumatoid factor activity during a course of chemotherapy are discussed. The first possibility is that the rheumatoid factor or activity had been initially covered by an antiidiotypic antibody but was disclosed by the decreased production of this antibody following by the immunosuppressive therapy. The second possibility is that monoclonal IgA acquired rheumatoid factor activity by a point mutation resulting in a change in the molecular structure of the idiotype. © 1996, The Japan Society for Clinical Immunology. All rights reserved.
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Nishinarita, M., Kashiwazaki, S., & Sugai, S. (1996). Monoclonal rheumatoid factor in a patient with multiple myeloma after chemotherapy. Japanese Journal of Clinical Immunology, 19(5), 519–523. https://doi.org/10.2177/jsci.19.519
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