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Dear EditorThe authors claim that they identified a patient with AML (subtype; acute megakaryocytic leukemia, AMKL) who presented with a peripheral blast count of 47% but an elevated platelet count of 519×109/L.The blasts were myeloperoxidase (MPO)+and contained Auer rods (not described in the literature). In Fig. 1 these cells displayed typical agranular blasts and a rare granular blast and easily recognized MPO+blasts. Nonspecific esterase was negative by butyrate staining (many megakaryocytes are strongly+using an alpha naphthyl acetae reaction).By flow cytometry the blasts were CD7, CD11c, CD13, CD33, CD117, cytoplasmic MPO, HLA-DR+ but negative for CD34 (which can be absent in myeloblasts). The only antigen detected for a megakaryocyte lineage was CD41a.The high platelet count could easily have produced a false+reaction with respect to the CD41 antibody by adhering to the myeloblasts. Cytospin immunofluorescence can differentiate platelet adhesion by showing punctuate reactivity vs. the diffuse reactivity of a true positive [1]. Moreover, there is no mention of additional platelet antigens for flow cytometry such as CD61 and CD42 (glycoprotein 1b). These antigens are often all positive when there is platelet adhesion, whereas in true cases of AMKL, one or more will be missing. Additionally, no histologic immunostains were done to confirm the presence of numerous megakaryocytes such as CD61 and/or Factor 8.The authors state that the use of backgating to show double positivity for MPO and CD41 was performed; however, the histograms are not indicative of that conclusion. The backgating clearly demonstrates inclusion of cells not confined to the myeloid progenitor cell region by CD45 and SSC.The reference of Tallman et al. [2] is misrepresented. There were two patients who had MPO positivity in that study and one had CD14 positivity and was classified as acute monocytic leukemia and the other was considered a diagnostic dilemma and not AMKL with MPO. The reference by Majhi et al. [3] with MPO positive myeloblasts concerned a child with leukemic transformation of myelofibrosis and not de novo AMKL.There was no mention of fibrosis or reticulin stains in this report. Although they stated that all genetic testing was negative, JAK2 can disappear in cases of leukemic transformation of myeloproliferative neoplasms such as essential thrombocythemia. A list of all genetic testing including CALR could be helpful to distinguish de novo AMKL from leukemic transformation as well. In conclusion, we are not convinced that this case was of megakaryoblastic origin and likely was AML with maturation.Most sincerely,John M. Bennett, M.D.Department of Pathology, University of Rochester, 601 Elmwood Ave, Box 626, Rochester, NY 14642, USATel: +1-585-275-4915Fax: +1-585-276-2390E-mail: john_bennett@urmc.rochester.eduDenise A. Wells, M.D.Hematologics, Inc. Seattle, WA 98121, USAE-mail: dwellsmd@hematologics.com

Re: Lee H, et al. An Unusual Case of Myeloperoxidase-Positive Acute Megakaryoblastic Leukemia. Ann Lab Med 2015;35:466-8