SCIENTIFIC PROGRAMME
SESSION I
HOW I TREAT
SMOLDERING MYELOMA
(SMM)
SESSION II
HOW I TREAT NEWLY
DIAGNOSED MULTIPLE
MYELOMA
SESSION III
FROM RISK
STRATIFICATION TO
RISK-BASED THERAPY?
DEBATE 1
SHOULD WE USE MRD
TESTING TO DETERMINE
THERAPY IN MULTIPLE
MYELOMA?
DEBATE 2
IS THERE A FUTURE ROLE
OF AUTOLOGOUS STEM
CELL TRANSPLANTATION?
SESSION IV
HOW I TREAT RELAPSED
MULTIPLE MYELOMA
DEBATE 3
SHOULD EVERY PATIENT
RECEIVE DARATUMUMAB
IN FIRST LINE?
ROUNDTABLE
MULTIPLE MYELOMA
FROM THE PERSPECTIVE
OF FDA/EMEA AND
FOUNDATIONS
SESSION V
YOU CAN’T BE IMMUNE
FOR IMMUNE THERAPY
ANYMORE
SESSION VI
OTHER PLASMA CELL
DYSCRASIAS
KEYNOTE LECTURES
THE FUTURE OF
MULTIPLE MYELOMA
SELECTED ABSTRACTS
FOR AN ORAL
PRESENTATION
ABSTRACTS SELECTED
AS POSTERS
DISCLOSURES
A NEWLY DIAGNOSED PATIENT WITH UNUSUAL BLEEDING AND MULTIPLE MYELOMA,
POSTER 13
FOUND TO HAVE A BICLONAL GAMMOPATHY
M N Dilhani1, W D D Prasanni2, T Dissanayake3 and Senani Williams4
(1)1 Senior Registrar in Clinical Haematology, Department of Pathology, Faculty of Medicine, University
of Kelaniya, Colombo, Sri Lanka
(2)Diploma Trainee in Clinical Haematology,Colombo North Teaching Hospital Ragama, Colombo, Sri
Lanka
(3)Consultant Hematologist Colombo North Teaching Hospital Ragama, Colombo, Sri Lanka
(4)Professor of Hematology, Department of Pathology, Faculty of Medicine, University of Kelaniya,
Colombo, Sri Lanka
Introduction:
Multiple myeloma (MM) is a malignant proliferation of clonal plasma cells1 characterized by
monoclonal immunoglobulins (M-protein) in serum or urine and represents approximately 10 - 15% of
all hematological neoplasms2.
We describe a 56-year-old woman with low backache for 4 months without a history of trauma. She
denied any bleeding manifestations, recurrent infections or B symptoms, Examination was
unremarkable except pallor. FBC revealed severe anemia (Hb 4.4g/L) with normal white cells and
platelets. ESR was 160mm/1sthr. Blood picture showed macrocytes, marked rouleaux formation, and
few plasmacytoid lymphocytes. Serum creatinine (254 μmol/L, eGFR-19 ml/min/1.73m2) and calcium
(3.4mmol/L) were elevated. No lytic lesions were seen in skeletal survey. Bone marrow examination
revealed 70% plasma cell infiltration. Amyloid deposits were not seen on Congo Red stain. Serum
protein electrophoresis showed IgG lambda monoclonal band (34.7 g/L) in beta region with
background immunoparesis. Serum immunofixation revealed two monoclonal bands - a prominent
IgG/ƛ band with a separate ƛ band without an associated heavy chain. Serum free light chain assay at
diagnosis revealed - ƙ- 47.13 mg/L, ƛ- 13,964 mg/L, ƙ/ƛ - 0.0034, with involved/uninvolved ratio- >100.
These confirmed a biclonal gammopathy in this patient. She was in ISS disease stage III. (ß2
microglobulin- 24.57 mg/L)
She developed an intramuscular haematoma in the right buttock the day after the marrow biopsy
though, no bleeding, swelling or evidence of infection was reported at the site of biopsy. Hb dropped
from post-transfusion value 8.1g/ dL to 6.9 g/dL. Platelets remained normal (180,000/μL). An isolated
prolongation of APTT (65.4 sec) was noted. Mixing studies demonstrated correction of patient’s APTT
with normal plasma and cryoprecipitate. No long-acting inhibitor was demonstrated. As the patient
had no personal or family history of bleeding, an acquired coagulation factor deficiency was
considered. Specific factor assays were unavailable.
Haemoglobin was corrected with transfusions. Pain and haematoma settled with treatment with FFP
and cryoprecipitate. Specific myeloma therapy was initiated with high dose dexamethasone,
bortezomib, and cyclophosphamide (VCD). Patient achieved a partial response at the end of first cycle.
(paraprotein level 18.9 g/L. Free ƙ -11.45 mg/L, Free ƛ -107.37 mg/L; ƙ/ ƛ ratio 0.11. Serum creatinine
and calcium normalized with improvement of APTT.
Discussion
Majority of patients with myeloma present with a single M- protein. Rarely patients have simultaneous
presence of two distinct M-proteins, which could be either from a single clone, or two separate clones
("biclonal gammopathy"). This phenomenon has not been found to carry an adverse prognostic factor
among those patients reported in literature3. Similarly, our patient also has responded well to the first