A RARE CASE OF SIMULTANEOUS PRESENTATION OF MULTIPLE MYELOMA AND ACUTE
POSTER 8
MYELOID LEUKAEMIA: A CASE REPORT
Ines dos Santos Marques, Rui Bergantim, Eliana Aguiar and Fernanda Trigo
Centro Hospitalar Universitário São João, Porto, Portugal
Introduction: Concomitant occurrence of acute myeloid leukaemia (AML) and multiple myeloma
(MM) is a rare event. Aetiology, disease management, and treatment remains unclear for this
particular occurrence.
Case presentation: A 63-year-old man, Caucasian, performance status 1, with previous medical
history of Parkinson’s disease and acute myocardial infarction, was referenced by abnormal findings
in routine analysis. He was asymptomatic and physical examination was unremarkable. Complete
blood count was WBC:1.42x109/L (neutrophils=250), Hb:11.3g/dL and PLT:112x109/L. Vitamin deficits
and reactive causes of pancytopenia were excluded. Myelodysplasia was suspected and the patient
underwent bone marrow (BM) examination. BM aspirate revealed hypocellularity with mild
trilineage dysplasia and 11% plasma cells (PC). FISH on abnormal PC showed amp1q21 (12%PC).
Histology of bone biopsy was consistent with myelodysplastic syndrome (MDS), and monoclonal
interstitial plasmacytosis (IgA/λ), which did not allow differential diagnosis between MM (most likely
hypothesis) and monoclonal gammopathy. Serum creatinine, electrolytes and calcium were all
normal. Serum protein electrophoresis showed M-spike:18.9g/L and the serum immunofixation
revealed a monoclonal IgA/λ band. Quantitative immunoglobulin analysis revealed: IgG:739mg/dL,
IgM:30mg/dL, IgA:1450mg/dL, B2-microglobulin normal, λ-light chain:563mg/dL, κ-light
chain:171mg/dL, with serum free κ/λ ratio:3.2. Skeletal X-ray did not report lytic lesions. Thus, it was
assumed concurrent indolent MM and MDS with multilineage dysplasia.
During 1-year, the patient remained asymptomatic and without progression criteria. After this
period, presented worsening of Hb and WBC counts. BM aspirate revealed 13%PC and 25.6%myeloid
blasts, suggesting progression of MDS to AML. Karyotype was 46,XY,del12(p13)2/20
cells/46,XY18/20 cells and FLT3-, NMP1-. Considering the patient performance status and disease
severity, azacitidine was selected as the most adequate therapeutic option. At the 6th cycle, a partial
response was obtained: 8%myeloid blasts at smear of aspirated BM, the karyotype was normal and
the patient became independent of transfusional support. The treatment has been continued, and
the patient maintained haematological response without progression of indolent MM in the
subsequent 18-months.
Conclusion: This report presents a patient diagnosed with AML concurrent with MM, who has no
previous exposure to chemotherapy. A plausible explanation would be that MM is a slow evolving
disease with a resultant decrease in immune surveillance, and incipient leukemic clones might
present concurrently. Although the therapeutic option is uncertain, it should be started as soon as
possible given the aggressiveness of acute leukaemia. Azacitidine was considered for this patient and
showed a good response. More cases should be investigated to assess the therapeutic management
of patients with AML concurrent with MM.