Persistent presence of nonclinical isotypes during treatment, in mobilized autografts, and after transplantation.

Patient 3 was diagnosed in February 1999 and followed until December 2000. He was treated with 4 cycles of combination chemotherapy, followed by high-dose melphalan and autologous blood stem cell support in July 1999. His disease was stable until May 2000, when his serum M protein began to rise. He was treated with dexamethasone from June 2000 until December 2000. He had a transient response to therapy, followed by progression in November 2000. Thalidomide was added in December 2000. The clinical isotype was IgA. Some samples were weakly positive for clinical isotype in strategy A (not shown) and strongly positive for rearranged IgH VDJ in strategy D (not shown), supporting the suggestion that strategy D is considerably more sensitive than strategy A. Nonclinical isotypes were weakly detectable using strategy A but were readily apparent using strategy B as shown. All samples to the right of the vertical line were postautologous transplantation. D, response to dexamethasone therapy. Other abbreviations are as for Figures 2 and 3.