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Akihito Fujimi [1] and Yasuhiro Nagamachi [1] and Naofumi Yamauchi [1] and Yuji Kanisawa [2]
Academic Editor: Marie-Christine Kyrtsonis
1, Department of Hematology, Sapporo Kiyota Hospital, Sapporo, Japan
2, Department of Hematology and Oncology, Oji General Hospital, Tomakomai, Japan
Received Sep 3, 2017; Revised Nov 13, 2017; Accepted Nov 21, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
Anaplastic myeloma is an extremely rare, but distinct, subtype of myeloma with poorly differentiated, pleomorphic, and significantly enlarged plasma cells [1–3]. The prognosis of anaplastic myeloma is extremely poor, with a mean survival of less than 3.5 months [2]. Another morphological variation of multiple myeloma described as multiple myeloma with cleaved, convoluted, or multilobated plasma cell nuclei has also been reported previously [4–13], having been frequently associated with plasma cell leukemia (PCL) [4–8] and with poor prognosis as well [6–10]. To date, the correlation between anaplastic myeloma and other morphological types of multiple myeloma has not been reported. Here, we present a case of secondary PCL, which morphologically transformed into multilobated plasma cell nuclei just 7 days after bortezomib and dexamethasone administration, and finally, transformed into anaplastic myeloma that simultaneously occurred with an expanded t(11;14) chromosomal abnormality.
2. Case Presentation
A 48-year-old man was diagnosed with multiple myeloma (IgG-k, Durie-Salmon IIIB, ISS III) in February 2008 and was treated with one course of high-dose dexamethasone as an induction therapy followed by TD (thalidomide and dexamethasone) therapy for the succeeding 4 months. G-banding chromosomal analysis at the initial diagnosis showed normal diploid cells. High-dose chemotherapy with autologous peripheral blood stem cell transplantation was not performed as stem cell mobilization failed despite the use of high-dose cyclophosphamide and granulocyte colony-stimulating factor. As a result, thalidomide 50 mg was continued for 8 months and then switched to MPT (melphalan, prednisolone, and thalidomide) therapy after disease progression. In December 2009, after seven courses of MPT therapy, the patient developed secondary PCL (Figure 1). The following laboratory results were obtained: white blood cell (WBC) count, 20.2 × 109/L (plasma cells, 79.5%); hemoglobin level, 11.4 g/dL; platelet count, 2.9 × 104/L; and IgG, 3,770 mg/dL in the peripheral blood. Chromosomal...