Development of a second monoclonal immunoglobulin G in a patient with late manifestation of myeloma.

Abstract

Abstract In 1961 routine serum protein electrophoresis revealed the presence of monoclonal IgG in a patient who presented no clinical symptoms of myeloma. The paraprotein was of type G4/K. For five more years the patient remained in excellent general condition, and there was no change in the serum protein findings. In 1966 the occurrence of a second monoclonal γ‐globulin band was noticed in serum protein electrophoresis and the coexistence of two IgG paraproteins of types G4/K and G1/L was established. The serum titer for Gm(1) was 1: 8 192 as compared to a titer of 1: 64 in 1961. Titers for Gm(3) and Gm(5) had remained normal or low. In 1967 there was rapid development of polysymptomatic‐myeloma. Serum levels of myeloma protein increase. continuously and, in late 1969, the patient's serum was found to contain 6 400 mg% of none but G1/L type monoclonal IgG. There was no more evidence of G4/K paraprotein. The undiluted serum was negative for Gm(3) and Gm(5), but the Gm(1) titer had risen to 1: 32 768. At that time the patient's clinical condition had become critical. She suffered from multiple pathological fractures, developed anemia and antibody deficiency syndrome, and expired in spring 1970. After a 5‐year asymptomatic history of “benign” G4/K type paraproteinemia the occurrence of clinical myeloma together with a shift to G1/L type paraproteinemia is postulated to be a second disease due to proliferation of a second “malignant” plasma cell clone.