Acute Lymphoblastic Leukemia in the Course of Polycythemia Vera: A Case Report and Review of Literature

Abstract

Introduction Polycythemia vera (PV) is one of the most common forms of myeloproliferative neoplasms. Acute myeloid leukemia secondary to PV is well reported, and the mechanism has been clarified to some extent. Only a limited number of cases have been reported about the development of acute lymphoblastic leukemia (ALL) in the course of PV, and the possible underlying mechanism has not been explored well. Case presentation A 75-year-old patient who developed ALL 3 years after he was diagnosed with PV. The presence of remarkable splenomegaly, typical immunophenotyping of the peripheral blood and increased expression of serum fibrosis markers indicated the existence of extramedullary hematopoiesis which may ascribe to myelofibrosis. After the treatment of dosage-modulated chemotherapy, the patient got complete remission. Conclusion The JAK2 mutation may the underlying factor that contributes to the development of ALL, and the existence of MF may indicate the progression to postpolycythemic MF, which may be a risk factor for the accelerated transformation.

Acute Lymphoblastic Leukemia Transformation in Polycythemia Vera: A Rare Phenomenon

“…Of note is that the latter is not observed in adult patients with ALL. Overall, as far as we know, 11 cases of post-PV ALL have been reported [5,9,[11][12][13][14][15][16][17], but only three patients including the present case received HU and/or phlebotomy alone for PV [11,12]. Details were shown in Table 1.…”

Expression of CD markers in JAK2V617F positive myeloproliferative neoplasms: Prognostic significance

“…For example, coexpression of CD10 and terminal deoxynucleotidyl transferase (TdT) in PV patients represents the disease progression toward ALL. 124 , 125 The expression of CD23 and CD5 in these patients can be indicative of a mature B-cell lymphoid neoplasm. 126 Similarly, simultaneous expression of CD19 and CD5 could be a poor prognostic factor for progression to CLL in these disorders.…”

Platelet donor database: a study on the specialist donor database for the patients with alloimmune thrombocytopenia in the Chinese population and the assessment of completeness

“…To the Editor: Due to the immunogenicity of the platelet antigens, especially blood group antigen (such as ABO antigens), human leukocyte antigen (HLA), human platelet antigen (HPA), and CD36 (platelet glycoproteins IV), which can produce corresponding alloantibodies through immune factors such as blood transfusion, pregnancy, and drugs, the immune reaction of the platelet antigens and antibodies in patients will lead to various types of alloimmune thrombocytopenia, including the immune platelet transfusion refractoriness, post-transfusion purpura, and fetal/neonatal alloimmune thrombocytopenia. [1][2][3][4] Platelet transfusion is an effective approach to treat alloimmune thrombocytopenia. Antigen-negative platelets (platelets lacking certain antigens that do not react with the alloantibodies in vivo) are the keys to avoid related alloimmune reactions and achieve satisfactory treatment outcomes of platelet transfusion.…”

“…[3] Among the 265 published and unpublished cases of tested and identified platelet antibody specificity in our laboratory from 2007 to 2019, there were 231 cases of anti-HLA (89.17%, 231/265), 22 cases of anti-CD36 (8.30%, 22/265), five cases of anti-HLA combined withanti-CD36 (1.89%, 5/265), three casesofanti-HPA-3a (1.13%, 3/265), two casesofanti-HLA combined with anti-HPA-5b (0.75%, 2/265), one case of anti-HPA-5b (0.38%, 1/265), andone caseofanti-HLA combined with anti-HPA-3a (0.38%, 1/265) alloantibodies involvedin the occurrence of alloimmune thrombocytopenia in the Nanning area. [2][3][4] Based on the analysis of the characteristics of HLA-A and -B gene polymorphisms and the cross-reactive groups (CREGs) of the population in the Nanning area (7001 samples detected), the HPA-1-17w gene polymorphisms of the population in the Nanning area (4243 samples detected), and the incidence rate of CD36 deficiency in individuals and ABO blood group distribution characteristics of the apheresis platelet donors in the Nanning area (5081 samples detected), a PDD consisting of the database of donors with known HLA, HPA, and CD36 deficiency was constructed. All the samples were random and unrelated individuals.…”