Multiple Myeloma and Chronic Myelogenous Leukemia; an Uncommon Coexistence in 2 Patients, with Literature Review

Case Report

Ann Hematol Oncol.2015;2(3): 1030.

Multiple Myeloma and Chronic Myelogenous Leukemia; an Uncommon Coexistence in 2 Patients, with Literature Review

Pessach I, Bartzis V, Tzenou T, Roumelioti M, Palaiologou D, Nikolaou E, Konstantis S, Bitsani K, Panayiotidis P and Kyrtsonis MC*

Haematology Section of the First Department of Propaedeutic Internal Medicine, Laikon University Hospital, Greece

*Corresponding author: Marie-Christine Kyrtsonis, Haematology Section of the First of Department Propaedeutic Internal Medicine, Laikon University Hospital, Agiou Thoma 17, Athens 11527, Greece

Received: December 11, 2014; Accepted: February 24, 2015; Published: February 26,2015


The coexistence of Multiple Myeloma (MM) and Chronic Myelogenous Leukemia (CML) is an extremely uncommon event that has only been reported in very few cases. Here, we present 2 new cases of concurrent MM and CML. The case of 63 year old woman with CML, who was treated with imatinib mesylate and subsequently developed MM 6 years after the diagnosis of CML, and the case of a 68 year old man with MM, who was treated with radiation therapy and chemotherapy and subsequently developed CML 4 years and 7 months after the diagnosis of MM. The relationship between CML and MM, is also discussed.

Keywords: Multiple myeloma; Chronic myeloid leukemia; Cell transformation


Multiple Myeloma (MM) is a malignancy of lymphoid origin, characterized by monoclonal proliferation of malignant plasma cells in the bone marrow microenvironment, monoclonal protein in serum and/or urine and associated organ dysfunction [1]. The diagnosis is based on the presence of at least 10 % bone marrow infiltration by clonal plasma cells that are usually secreting a monoclonal immunoglobulin in addition with or without end organ damage manifestations [1-3]. Chronic Myeloid Leukemia (CML) is a clonal disorder of myeloid origin characterized by a chromosomal reciprocal t(9;22) (q34;q11) translocation, the Philadelphia (Ph) chromosome [4]. The crucial pathogenetic consequence of this translocation is the creation of a chimeric BCR/ABL fusion protein, resulting in a constitutively active tyrosine kinase with high proliferative potential [5,6].

Therefore, the respective malignant cells in MM and CML are completely different, being lymphoplasmacytic and myeloid cells, accordingly. The occurrence of MM and CML in the same patient, either at diagnosis or with one or the other disease pre-existing, is a rare event that has previously been reported in a limited number of case reports in the literature [7–25], and the question of the origin of these 2 malignancies in such patients, remains unanswered.

In this report, we reviewed previously published cases, and presented 2 more patients with concurrent MM and CML.

Patient 1

A 63 year old woman was referred to our hospital in October 2002 because of leukocytosis. She had a history of hepatits A, hysterectomy for benign fibroids (1996), and colon cancer (1999) in complete remission after surgical resection and chemotherapy. She had no symptoms and no clinical findings.

Peripheral blood analysis revealed white blood cell count of 17.8x109/l, (64% segmented neutrophils, 7% basophils, 4% myelocytes, 2% metamyelocytes, 3% band forms, 18% lymphocytes, and 2% monocytes). Haemoglobin was 12.8gr/dl, and platelets were 339x109/l. Neutrophil Alkaline Phosphatase (NAP) was 128, and Lactate Dehydrogonase (LDH) elevated (765U/L). Bone Marrow (BM) aspirate and biopsy were typical of CML; BM karyotype showed Philadelphia (Ph) chromosome in 18 out of 20 metaphases. Molecular analysis by quantitave reverse transcription-polymerase chainreaction (qRT-PCR) detected the chimeric BCR-ABL messenger RNA, confirming the diagnosis of CML.

The patient was started on imatinib mesylate at standard dose (400mg/day) and achieved complete hematologic and cytogenetic response at 3 months and complete molecular response at 9 months after treatment initiation. Two years after, and although she was still under imatinib treatment, qRT-PCR became positive for BCR-ABL transcripts, and BM karyotype revealed Ph chromosome in 1 out of 20 metaphases; BM biopsy showed additionally 5-8% κ light chain restricted plasma cell infiltration, while a small M-spike was present on serum protein electrophoresis, serum immunofixation showed an IgGκ monoclonality and quantitative Immunoglobulin (Ig) measurements were within normal range; Monoclonal Gammopathy of Undetermined Significance (MGUS) was diagnosed. Imatinib mesylate dosage was increased to 600mg/day, resulting again in a complete molecular response.

While under follow-up and regular CML evaluation with BM karyotypes and BCR-ABL quantification, and although she remained in complete molecular CML remission, her karyotype presented in 2005 an additional abnormality del (7)(q32) and two more in 2006 [t(1;7)(q32;q21) and t(2;7)(q33-35;q21)]. At that time BM examination showed 12% infiltration by clonal plasma cells (Table 1). As she had no MM-related symptoms, the diagnosis of asymptomatic MM (AMM) was made.

Citation: Pessach I, Bartzis V, Tzenou T, Roumelioti M, Palaiologou D, et al. Multiple Myeloma and Chronic Myelogenous Leukemia; an Uncommon Coexistence in 2 Patients, with Literature Review. Ann Hematol Oncol. 2015;2(3): 1030. ISSN:2375-7965