Collision diffuse large B cell lymphoma and myeloid sarcoma in the liver
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LETTER TO THE EDITOR
Collision diffuse large B cell lymphoma and myeloid sarcoma in the liver Andrea Marra 1
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& Giovanni Martino & Nando Scarpelli & Vincenzo Perriello & Roberto Limongello & Stefano Ascani
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Received: 10 June 2020 / Accepted: 14 August 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Dear Editor, A 75-year-old Caucasian woman was diagnosed with chronic myelomonocytic leukemia (CMML type-1; 2017 WHO criteria [1]) with > 2% peripheral blood blasts and > 5% bone marrow (BM) blasts; CMML carried a normal karyotype and was molecularly defined by subclonal JAK2V617F mutation (variant allele frequency, VAF: 5%); prognostically, the disease was included within CMML low-risk category (score: 1), according to MD Anderson Prognostic scoring system [2]. At the time, the patient was in good clinical conditions with none remarkable comorbidities. Blood counts showed absolute monocytosis (but a normal absolute white blood cell count, WBC), mild macrocytic anemia, and moderate thrombocytopenia; she underwent routine follow-up with any treatment intervention. Four years later, she experienced pronounced weight loss (~ 10% of body weight in 3 months), asthenia, and a gradual onset of right-upper-quadrant pain associated with hepato-/splenomegaly. Blood counts showed marked leukocytosis (WBC count, 29.360/μL) with neutrophilia (absolute neutrophil count, 23.200/μL), macrocytic anemia (Hb 10.1 g/dL, MCV 108 fL), and a normal platelet count. Biochemical profile evidenced elevated lactate dehydrogenase (LDH, 885 U/I) and hyperuricemia (11.6 mg/dL); liver function tests (LFT) were unremarkable. Laboratory testing for EBV, HBV, HCV, and HIV was negative. Chronic alcohol abuse was not referred. On physical examination, the liver was palpable at 2 cm below the right costal margin and the spleen at 2 cm below the left costal margin. A 18FAndrea Marra and Giovanni Martino contributed equally to this work. * Andrea Marra [email protected] 1
Institute of Hematology and Centre of Haemato-Oncology Research (CREO), University and Hospital of Perugia, Perugia, Italy
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Department of Onco-hematology, Hospital of Spoleto, USL Umbria 2, Spoleto, Italy
fluorodeoxyglucose positron emission tomographycomputed (PET) scan (Fig. 1a) evidenced two distinct metabolically active lesions, respectively, involving the liver (standardized uptake value [SUV], 16.5) (Fig. 1a, red-arrow) and the spleen (SUV, 17.8) and a diffuse slight-to-moderate bone marrow (BM) glucose uptake. A biopsy specimen obtained from the hepatic lesion showed a diffuse infiltration by largesized, pleomorphic neoplastic lymphoid cells with conspicuous nucleolus (Fig. 1b, 100x; inset in 1b, 400x) that were CD20+ (Fig. 1d, 100x), CD10-, BCL6-, BCL2-, c-MYC+ (20%), and Ki67+ (80–90%). Epstein-Barr encoding region (EBER) in situ hybridization was negative, as well as FISH analysis for MYC-IgH rearrangement. Notably, the specimen revealed also the presence of medium-sized neoplastic myeloid cells, with convolute nuclei and small nucleo
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