PB2112 COEXISTENCE OF MONOCLONAL B‐ CELL POPULATION IN PATIENTS WITH NEWLY DIAGNOSED MULTIPLE MYELOMA; INCIDENCE, IMMUNOPHENOTYPING AND CLINICAL CHARACTERIZATION
Authors: Y. Cohen, I. Cohen, C. Perry, I. Avivi, S. Kay, Y. Herishanu
Journal: HemaSphere (2019)

Background: Clustering of B‐cell malignancies in families, and recently described genetic correlations between multiple myeloma (MM) and chronic lymphocytic leukemia (CLL) (Went M et al; Blood Cancer Journal 2018) suggest shared biological pathways influencing the development of these malignancies. Since we began applying multiparameter flow cytometry (FACS) analysis of 8‐color panel for plasma cell dyscrasia (PCD), we observed several cases of newly diagnosed multiple myeloma (NDMM) with a co‐existing monoclonal B‐cell clone. Herein, we retrospectively review the incidence of this phenomenon and describe phenotypic and clinical characteristics. Aims: To investigate patients with NDMM and a co‐existing monoclonal B‐cell population. Methods Hospital records of all consecutive patients who underwent FACS analysis of bone marrow aspirates between January 2016 and September 2018 were reviewed and NDMM, active or smoldering, according to IMWG criteria, were identified. Cases of Waldenstrom's macroglobulinemia and lymphoplasmacytic lymphoma were excluded. FACS analysis included a PCD panel comprising CD45, CD138, CD38, CD27, CD56, CD19, and CytoKappa/Lambda. Cases that were found to have a monoclonal B‐cell population were further evaluated by a lymphoid screening tube (LST) and a B‐cell chronic lymphoproliferative disorders (BCLD) panel as proposed by EuroFlow™. Demographics, clinical characteristics, and outcomes of patients were documented from the hospital records. Results: Out of 160 consecutive FACS analyses of patients with NDMM, 13 cases (8.1%) had a coexisting monoclonal B‐cell population. In most cases, the monoclonal B‐cells had a CLL‐like phenotype (n = 8, 61.5%), whereas in the rest they were CD5‐negative (n = 5, 38.5%), with mean percentage of the monoclonal B‐cells of 5.7% (±1.7) out of all leukocytes. Patients with MM and co‐existing monoclonal B‐cells had a mean age of 72 years (range: 46‐86), 6 had smoldering and 7 had active myeloma and none of them had lymphadenopathy or splenomegaly. Involved immunoglobulin was IgG (n = 7), IgA (n = 3), IgM (n = 1) and undetected/unavailable (n = 2). PCD involved light chain was Kappa in 9 and Lambda in 4 patients. Involved free light chain level median was 332 mg/L (range 34‐9310) and M‐SPIKE median was 2.3 g/dL (range 0‐8.1). Plasma cells light chain subtype was concordant with that of the monoclonal B‐cells in 8 patients (61.5%). Hemoglobin median was 11.8 g/dL (range: 7.4‐14), absolute lymphocyte counts median was 1.7 × 10 9 /L (1.1‐4.3). CRAB symptoms included lytic or focal lesions (n = 5), anemia (n = 5), renal failure (n = 1). Five of the 6 patients who received anti‐myeloma therapy responded. At a median follow‐up time of 9 months, none of the patients developed expansion of their B‐cell clone or progressed to an overt clinical lymphoproliferative disorder and 11 (80%) patients remain alive. Summary/Conclusion: We describe for the first time presence of a B‐cell monoclonal population in 8.1% of patients with NDMM. The clone is mostly with a CLL‐like phenotype, and did not expand or require therapy. While this incidence is slightly higher than expected, it may still be merely a coincidence reflecting prevalence of monoclonal‐B cell lymphocytosis in older population; alternatively, it may be caused by shared genetic drivers. Further investigations, including longer follow‐up and correlative molecular studies, are required.