Abstract
The simultaneous appearance of B-CLL and MM in the same patient (pt) seems to be a rare phenomenon. In those cases - our experience included - 1. the myeloma exhibits an aggressive course, 2. with CLL-treatment, MM seems to emerge, 3. which, if well treated (e.g. high-dose chemotherapy [CTx] with autologous peripheral blood stem cell transplantation [auto-PBSCT]), may lead to a slower myeloma course, improved clinical condition and CLL disapearance. Here we report on the simultaneous (n=2) and successive (n=2) occurrence of CLL and MM in four pts, who were diagnosed at our center during the last year. We suggest that the occurrence of CLL and MM, when carefully monitored, may be more frequent than assumed so far. Case 1. This 64-year-old male was evaluated due to weight loss, leukocytosis, anaemia, foamy urine and increased creatinine. Kappa (k) Bence-Jones (BJ) proteinuria and elevated k-serum free light chains (SFLC) were found. A bone survey was normal, but BM biopsy showed infiltrates of plasma- (PC) and B-CLL-cells. Due to Rai 0 CLL and MM stage IIIB, the pt received 2 cycles of VAD followed by an auto-PBSCT. Thereby, he obtained a PR. Maintenance with thalidomide stabilized both diseases. Case 2. This 77-year-old male was simultaneously diagnosed with RAI 0 CLL and stage IIIB MM. Diagnostics revealed a lambda (l)-paraprotein, BJ-l-proteinuria and lytic bone lesions. The BM showed monoclonal l-LC-expressing PCs, and k-LC-CLL-cells. The pt received melphalan/prednisone (MP) and thereby obtaining SD. Case 3. This 62-year old pt was diagnosed with RAI II B-CLL. Two years later, he showed increased splenomegaly, anemia, elevated l-SFLC and dense CLL-BM-infiltrates. Chlorambucil/prednisone-CTx was initiated, but failed to improve his condition. Further evaluation due to renal impairment revealed multiple lytic lesions and monoclonal l-LC-expressing PCs, coexisting with remaining CLL infiltrates in his BM. Cyclophosphamide-CTx, 2 cycles of VAD and auto-PBSCT were performed and Bortezomib maintenance, improving the pt’s general condition, his PB counts and l-SFLC secretion. Despite these efforts, MM relapse occurred 5 months later with persisting absence of his preceding CLL and the pt eventually died due to myeloma progression. Case 4. This 73-year-old male was diagnosed with B-CLL, showing moderate splenomegaly, lymphocytosis, initially not requiring any therapy. Two years later, he showed a deteriorating clinical condition, multiple osteolytic lesions, anemia, hypercalcemia, monoclonal IgA paraprotein and k-BJ-proteinuria. A BM biopsy confirmed k-LC B-CLL- and k-PC-infiltrates. The diagnosis of stage IIIA IgA k-MM, and RAI II B-CLL led to MP-CTx that induced SD of his MM and CLL. In summary, our 4 pts had a median age of 69 years (range; 62–77) and showed a median time interval of their CLL and MM diagnosis of 11 months (0–31). All pts had stage III MM and renal impairment in 3/4, whereas CLL showed an indolent course. LCs of CLL and MM were different in all except one pt. Cytogenetic and genomic analyses are currently ongoing and will be reported at the meeting. We conclude that the elucidation of the coincidence of CLL and MM will allow to understand why and how often both occur and also, how they can be efficiently treated. The question of their clonal relationship should be answered via genomic analyses that will allow to gain further insight into the origin of both diseases.
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