Rare synchronous co-existence of acute myeloid leukemia and hairy cell leukemia in a same patient
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LETTER TO THE EDITOR
Rare synchronous co-existence of acute myeloid leukemia and hairy cell leukemia in a same patient Xiaofeng Shi 1,2 & Qian Jiang 1 & Haiyan You 1 & Yichen Liu 1 & Min Chen 1 & Tiantian Li 1 & Jie Peng 1 & Rong Huang 1 & Jingan Liu 1 & Yilin Zhu 1 & Xiaodong Xi 3 Received: 25 August 2020 / Accepted: 9 September 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Dear Editor, A 78-year-old male patient was admitted into our hospital complained with fatigue, weak and dizzy. Soybean-sized lymph nodes could be palpable under left armpit. No hepatosplenomegaly was found in computed tomography scan (Fig. 1d). The blood test showed white blood count 1.4 × 109/L, hemoglobin 41 g/L, platelet count 25 × 109/L, lactate dehydrogenase 81 U/L, and β2-microglobulin 2.3 mg/L. Bone marrow smear showed 58% blasts with large nuclei and obvious nucleoli and 15% abnormal lymphocytes whose cytoplasmic margins were irregular with a frayed appearance (Fig. 1a, b). Bone marrow biopsy showed hyperplasia with increased myeloid blasts and abnormal lymphocytes (Fig. 1c). Bone marrow aspiration was smooth, and various volumes of bone marrow were collected successively, 0.1 mL for smear, 4 mL with heparin as anticoagulant for flow cytometry test, 4 mL with heparin for chromosome test, and last 4 mL with heparin for gene mutation test. The flow cytometry results showed that the mononuclear cells from bone marrow could be divided into two groups. Group A accounting for 66.2% bone marrow mononuclear cells expressed myeloid marks, such as CD34, CD117, CD33, CD13, CD123, and HLA-DR, and group B accounting for 10.25% expressed lymphoid marks, such as CD123, CD22, CD20, CD19, cCD79a,
* Xiaofeng Shi [email protected] * Xiaodong Xi [email protected] 1
Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, People’s Republic of China
2
The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, People’s Republic of China
3
State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
CD11c, CD103, CD25, cKappa, and HLA-DR (Fig. 1e). Further immunophenotype analysis confirmed that the CD19 ++ cells partially expressed CD23 and strongly expressed CD200. Chromosome karyotype was normal. Leukemia-associated 43 fusion genes were negative. Some typical leukemia-associated gene mutations were detected by exon sequencing. The mutation ratio was 40% for SRSF2 (c.284C>A, p.P95H), 1% for BRAF (c.1799T>A, p.V600E), 38.5% for IDH1 (c.394C>T, p.R132C), 5.4% for ASXL1 (c.1773C>A, p.Y591X), 41.2% for TET2 (c.5944_5948delTCCAC, p.T1983Nfs*30), 8.8% for NRAS (c.125A>G, p.K42R), and 52% for NOTCH3 (c.499C>T, p.P167S). The mutation of BRAFV600E was confirmed again using PCR showing missense mutation c.1799T>A (Fig. 1f). Acute myeloid leukemia (AML) is a myeloid malignant hematological disorder. In this patient, myeloblasts accounted for 58% of marrow cells. Gene sequencing confirmed mult
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