Blood Res 2017; 52(1):
Published online March 27, 2017
https://doi.org/10.5045/br.2017.52.1.62
© The Korean Society of Hematology
1Department of Laboratory Medicine, School of Medicine, Kyung Hee University, Seoul, Korea.
2Department of Pathology, School of Medicine, Kyung Hee University, Seoul, Korea.
3Department of Hematology-Oncology, School of Medicine, Kyung Hee University, Seoul, Korea.
Correspondence to : Tae Sung Park. Department of Laboratory Medicine, Kyung Hee University, 23 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea. 153jesus@hanmail.net
A 71-year-old woman was admitted to the hospital for fever of unknown origin. The patient had a medical history of hypertension, osteoporosis, and iatrogenic Cushing's syndrome due to adrenal insufficiency. The initial complete blood count (CBC) showed a hemoglobin level of 9.5 g/dL, white blood cell count (WBC) of 5.41×109/L, and platelet count of 278×109/L. On peripheral blood smear, mild rouleaux formation was also observed. Diffuse osteoporosis and multiple compression fractures of the thoracolumbar spine were observed in a series of X-ray scans, and monoclonal gammopathy (Immunoglobulin [Ig] G kappa type, 1.5 g/L of M-protein in serum) was confirmed using serum immunofixation electrophoresis (IFE). Serum calcium and creatinine levels were normal. On bone marrow (BM) aspiration, 14.8% plasma cells with eccentric nuclei and basophilic cytoplasm were observed. The patient was diagnosed with PCM, and treated with 13 cycles of conventional melphalan and prednisolone (MP) therapy for 2 years.
Pancytopenia was observed before the 14th cycle of MP therapy, and the patient was admitted for further evaluation. The CBC consistently revealed pancytopenia (hemoglobin level 9.7 g/dL, WBC 0.84×109/L, platelet count 38×109/L). As a peripheral blood smear showed 16% abnormal promyelocytes and immature cells (Fig. 1A), BM examination was conducted, followed by cytogenetic and molecular analyses using BM specimens. The BM aspirate showed 74% abnormal promyelocytes with bilobed nuclei, densely packed large granules, and Auer rods. The proportion of plasma cells was counted up to 2.6% (Fig. 1B). Some plasma cells were positive for kappa on immunohistochemical staining. Monoclonal peak was continuously observed on serum IFE, showing IgG and kappa type monoclonal gammopathy, 0.8 g/L of M-protein in serum. Chromosome analysis using a BM sample revealed a karyotype of 46, XX, t(15;17)(q22;q12) in 18 out of 23 metaphase cells examined (Fig. 2A). Fluorescence in situ hybridization (FISH) analysis using a dual color dual fusion
t-APL is closely related to topoisomerase II inhibitor administration [2]. The mechanism underlying the occurrence of t-APL associated with topoisomerase II inhibitor is the existence of “hot spots” in the
This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (2014R1A1A1002797).
Microscopic examination of peripheral blood (PB) and bone marrow (BM)
Table 1 Cases of therapy-related acute promyelocytic leukemia in patients with plasma cell myeloma.
Abbreviations: ASCT, autologous stem cell transplantation; CT, chemotherapy; Ig, immunoglobulin; MM, multiple myeloma; MP, melphalanprednisolone therapy; ND, not described; RT, radiation therapy; VAD, doxorubicin+vincristine+cyclophosphamide; VP16, etoposide.
Blood Res 2017; 52(1): 62-64
Published online March 27, 2017 https://doi.org/10.5045/br.2017.52.1.62
Copyright © The Korean Society of Hematology.
Hyunjung Gu1,#, Young Jin Kim1,#, Woo-In Lee1, Juhee Lee2, Hwi-Joong Yoon3, and Tae Sung Park1*
1Department of Laboratory Medicine, School of Medicine, Kyung Hee University, Seoul, Korea.
2Department of Pathology, School of Medicine, Kyung Hee University, Seoul, Korea.
3Department of Hematology-Oncology, School of Medicine, Kyung Hee University, Seoul, Korea.
Correspondence to: Tae Sung Park. Department of Laboratory Medicine, Kyung Hee University, 23 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea. 153jesus@hanmail.net
A 71-year-old woman was admitted to the hospital for fever of unknown origin. The patient had a medical history of hypertension, osteoporosis, and iatrogenic Cushing's syndrome due to adrenal insufficiency. The initial complete blood count (CBC) showed a hemoglobin level of 9.5 g/dL, white blood cell count (WBC) of 5.41×109/L, and platelet count of 278×109/L. On peripheral blood smear, mild rouleaux formation was also observed. Diffuse osteoporosis and multiple compression fractures of the thoracolumbar spine were observed in a series of X-ray scans, and monoclonal gammopathy (Immunoglobulin [Ig] G kappa type, 1.5 g/L of M-protein in serum) was confirmed using serum immunofixation electrophoresis (IFE). Serum calcium and creatinine levels were normal. On bone marrow (BM) aspiration, 14.8% plasma cells with eccentric nuclei and basophilic cytoplasm were observed. The patient was diagnosed with PCM, and treated with 13 cycles of conventional melphalan and prednisolone (MP) therapy for 2 years.
Pancytopenia was observed before the 14th cycle of MP therapy, and the patient was admitted for further evaluation. The CBC consistently revealed pancytopenia (hemoglobin level 9.7 g/dL, WBC 0.84×109/L, platelet count 38×109/L). As a peripheral blood smear showed 16% abnormal promyelocytes and immature cells (Fig. 1A), BM examination was conducted, followed by cytogenetic and molecular analyses using BM specimens. The BM aspirate showed 74% abnormal promyelocytes with bilobed nuclei, densely packed large granules, and Auer rods. The proportion of plasma cells was counted up to 2.6% (Fig. 1B). Some plasma cells were positive for kappa on immunohistochemical staining. Monoclonal peak was continuously observed on serum IFE, showing IgG and kappa type monoclonal gammopathy, 0.8 g/L of M-protein in serum. Chromosome analysis using a BM sample revealed a karyotype of 46, XX, t(15;17)(q22;q12) in 18 out of 23 metaphase cells examined (Fig. 2A). Fluorescence in situ hybridization (FISH) analysis using a dual color dual fusion
t-APL is closely related to topoisomerase II inhibitor administration [2]. The mechanism underlying the occurrence of t-APL associated with topoisomerase II inhibitor is the existence of “hot spots” in the
This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (2014R1A1A1002797).
Microscopic examination of peripheral blood (PB) and bone marrow (BM)
Table 1 . Cases of therapy-related acute promyelocytic leukemia in patients with plasma cell myeloma..
Abbreviations: ASCT, autologous stem cell transplantation; CT, chemotherapy; Ig, immunoglobulin; MM, multiple myeloma; MP, melphalanprednisolone therapy; ND, not described; RT, radiation therapy; VAD, doxorubicin+vincristine+cyclophosphamide; VP16, etoposide..
Microscopic examination of peripheral blood (PB) and bone marrow (BM)