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Case Report Haematological Malignancies Plasmacytic Post-transplant Lymphoproliferative Disorder – Case Report Jir i Hanousek, 1 Jakub Radocha, 1 Ondrej Soucek, 2 Lenka Pliskova, 3 Katerina Kamaradova, 4 Alzbeta Zavrelova 1 and Pavel Zak 1 1. 4th Department of Internal Medicine – Haematology, University Hospital Hradec Kralove and Charles University in Prague, Faculty of Medicine in Hradec Kralove, Hradec Kralove, Czech Republic; 2. Institute of Clinical Immunology, University Hospital Hradec Kralove and Charles University in Prague, Faculty of Medicine in Hradec Kralove, Hradec Kralove, Czech Republic; 3. Institute of Clinical Biochemistry, University Hospital Hradec Kralove and Charles University in Prague, Faculty of Medicine in Hradec Kralove, Hradec Kralove, Czech Republic; 4. The Fingerland´s Department of Pathology, University Hospital Hradec Kralove and Charles University in Prague, Faculty of Medicine in Hradec Kralove, Hradec Kralove, Czech Republic W e present a case of a 43-year-old Caucasian female with acute myeloid leukaemia (AML), who developed Epstein-Barr virus (EBV) positive post-transplant lymphoproliferative disorder (PTLD) of duodenum, with plasma cell differentiation after second haematopoietic stem cell transplantation. The patient was given rituximab and CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone); however, these were only temporarily effective, and the patient passed away 36 days after PTLD was diagnosed. PTLD with plasma cell differentiation is a rare type of PTLD, and there are no strict treatment guidelines. Keywords Plasmacytoma, post-transplant lymphoproliferative disorder, PTLD, haematopoietic stem cell transplantation, HSCT Disclosure: Jiri Hanousek, Jakub Radocha, Ondrej Soucek, Lenka Pliskova, Katerina Kamaradova, Alzbeta Zavrelova and Pavel Zak have nothing to disclose in relation to this article. No funding was received in the publication of this article. Ethics: All procedures were followed in accordance with the responsible committee on human experimentation and with the Helsinki Declaration of 1975 and subsequent revisions, and informed consent was received from the patient involved in this case study. Authorship: All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship of this manuscript, take responsibility for the integrity of the work as a whole, and have given final approval to the version to be published. Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. Received: 1 February 2017 Accepted: 2 May 2017 Citation: European Oncology & Haematology, 2017;13(1):80–2 Corresponding Author: Jiri Hanousek, IV. interni hematologicka klinika, Sokolska 581, Hradec Kralove, 500 05, Czech Republic. E: 80 Post-transplant lymphoproliferative disorder (PTLD) is a severe complication of haematopoietic stem cell transplantation (HSCT). Most of the PTLDs originate from B-cells. Overall, 60–80% of PTLDs are associated with Epstein-Barr virus (EBV); this can vary depending on PTLD type and time of onset after HSCT. 1,2 The majority of the general population is infected by EBV during their life, but an immunocompetent host mounts a swift immune response that controls proliferation of EBV infected B-cells. EBV then resides only in resting memory B-cells in latent form. 3 The balance between latently infected B-cells and immune surveillance is disrupted after a patient receives HSCT. An increase in the number of infected B-cells (almost always of donor origin) may develop into PTLD. 4–6 PTLDs are divided into three stages of evolution: early lesions, polymorphic PTLDs and monomorphic PTLDs. Monomorphic PTLDs are mostly derived from B-cells, but can also be of T-cell origin, and resemble aggressive non-Hodgkin lymphomas. 5 PTLD resembling diffuse large B-cell lymphoma (DLBCL) is the most common. 7 Rituximab, an anti CD20 monoclonal antibody, can be used effectively to treat them. 8,9 Other types of PTLD are rare and only 4% of them show plasma cell differentiation. 7,10 We would therefore like to present our patient with PTLD of duodenum with plasma cell differentiation. Case report A 43-year-old Caucasian female was diagnosed with MLL/PTD- and FLT3/ITD-positive acute myeloid leukaemia (AML) in June 2013. She was given “3+7” induction chemotherapy regimen (cytarabine 100 mg/m 2 for 7 days and daunorubicin 90 mg/m 2 for 3 days) followed by consolidation chemotherapy high-dose cytarabine (HiDAC) in July 2013. She achieved complete remission (CR) with negative minimal residual disease (polymerase chain reaction [PCR] for MLL/PTD gene). She underwent allogeneic HSCT with 10/10 sibling donor (sister) in September 2013, using a conditioning regimen of busulfan 3.2 mg/kg for 4 days, fludarabine 30 mg/m 2 for 5 days and rabbit derived anti-thymocyte globulin (r-ATG [Thymoglobulin; Sanofi, Paris, France]) 3 mg/kg for 1 day, with tacrolimus and mycophenolate mofetil as immunosuppression. She remained in CR for 14 months but relapsed in November 2014. She was then given Flag-Ida chemotherapy (fludarabine 30 mg/m 2 for 5 days, cytarabine 2 g/m 2 for 5 days and idarubicin 12 mg/m 2 for 3 days) and again achieved CR. Donor lymphocyte infusion (DLI) was administered (5x10 5 CD3+ cells/ kg in December 2014 and 1x10 6 CD3+ cells/kg in April 2015). Despite this, the disease relapsed (molecular relapse) in August 2015. The patient received one cycle of low dose cytarabine while waiting for a suitable unrelated donor. Through September and October 2015 sequential stem cell transplantation was performed (HiDAC chemotherapy and then conditioning with treosulfan 12 mg/kg for 3 days, fludarabine 30 mg/m 2 for 6 days and r-ATG [Thymoglobulin] 3 mg/kg for 2 days) with 9/10 human leukocyte antigen (HLA) mismatched unrelated male donor (DQB1 mismatch). TOU C H ME D ICA L ME D IA