Marked increase of normal blast morphologically mimicking leukemic clone in acute lymphoblastic leukemia patient following G-CSF therapy

Abstract

In some of the anecdotal literature, atypical cells including blastic cells mimicking original leukemic cells were observed after the administration of granulocyte colonystimulating factor (G-CSF) in post-chemotherapy patients [1–5]. An evolutional increase of monocytes and the scant appearance of immature myeloid cells, including myeloblasts in peripheral blood (PB) after the G-CSF treatment commonly occurred, but blastocytosis in PB resembling leukemia was not generally observed. G-CSF-associated blastocytosis is troublesome and causes confusion in management of the underlying disease [3]. Although in almost all of the previous reports, myeloblastosis after chemotherapy for acute myelocytic leukemia (AML) mimicked a recurrence of underlying myelocytic leukemia, some odd cases, such as leukoerythroblastosis in AML [4] and myeloblastosis in acute lymphoblastic leukemia (ALL) [5] were described. Our present case is the first report of lymphoid blastocytosis in ALL after the treatment of G-CSF. A 38-year-old woman diagnosed with Ph acute lymphoblastic leukemia (ALL) received consolidation therapy with high dose methotrexate (1 g/m, day 1) and cytarabine (3 g/m 9 2/day, day 2–3) after first achieving complete remission (CR). She was treated with G-CSF by day 12 after chemotherapy. On day 15, immature cells that morphologically resembled lymphoblasts (Fig. 1) increased to 33% in peripheral blood, although her lowest leukocyte count was 200/lL. She was thus considered to have possibly suffered a relapse. However, the blast did not express lymphoid markers presenting on her original leukemic clone (CD19, CD10, CD22 and CD34), but immature myeloid markers including CD13, CD33, CD34, HLA-DR and c-kit. In addition, bone marrow (BM) aspiration on the same day revealed no evidence of the involvement of blast clones. After several days, we observed that the blasts had been entirely replaced by normal myeloid blasts (Fig. 2). G-CSF has the potentiality of stimulating rapid leukemic cell proliferation in vivo [6]. In consequence of chemotherapy for acute leukemia, blastocytosis is a problematic and confusing issue to differentiate with disease recurrence and hematopoietic recovery. The usual response to G-CSF represents an increase recovery of immature monocytes after chemotherapy [3]. Thus, the diagnosis is considered more difficult to make. However, in our case, the proliferating cells after chemotherapy had lymphoid morphology but immature myeloid surface markers. This is the first case to reveal that transient atypical immature cells mimic not only acute myeloid, but also lymphoblastic leukemia. O. Imataki (&) H. Ohnishi Division of Hematology, Department of Internal Medicine, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan e-mail: oima@med.kagawa-u.ac.jp