Chronic myeloid leukaemia initiating as acute lymphoid leukaemia.

Chronic Myeloid Leukaemia Initiating as Acute Lymphoid Leukaemia W. Walter Paolino Walter Paolino, Alessandro Levis, Luciano Caramellino and Franco Paolino, Ospedale Maggiore S. G. Battista e Città di Torino, Ente regionale, Torino (Italy) To the Editor In the last years some cases of chronic myeloid leukaemia (CML) initiating as acute lymphoid leukaemia (ALL) have been described [1, 3–5]. A similar case was observed by us. C. P., a 37-year-old woman developed phlebitis shortly after her third delivery (12-IV-1973). This resolved quickly. She then developed bilateral mastitis, followed by pallor and weakness. Blood examination (9-V) showed: RBC 2.5 X 1012/1, WBC 43 X 109/1, platelets 80 X10V1. On admission the patient showed generalized lymphadenopathy, marked splenomegaly, bilateral enlargement of the breasts, which contained hard, painful nodules, skin dimpling and blushing. The leucocyte count rose to 72 × 10V1, with 40% lymphoblast-like cells (fig. 1A), but there were also 2% myelocytes, 3% metamyelocytes and 2% basophils. The bone marrow was hypercellular with total replacement by PAS-positive lymphoblasts (fig. IB). After two courses of COAPshe entered complete remission: RBC 3.8 X 10* VI, WBC 4.5 X lO»/l with 72% neutrophils, platelets 240 X 10VI; bone marrow hypocellular with 3% blasts. The breast infiltration, lymphadenopathy and splenomegaly were resolved. In November, despite further treatment with COAP and POMP, she showed a CML-like picture: WBC 26 X lO»/l with 6% blasts, 18% granulocyte precursors; marrow hypercellular with 10% myeloblasts and 49% granulocyte precursors (fig. 1C, D). She had a good response to 6-MP: WBC 11 X 10V1 with 1% blasts, 6% granulocyte precursors, platelets 950 X 10VI; hypercellular bone marrow with myeloblasts 1% and granulocyte precursors 30%. In February she was readmitted because of meningeal involvement and splenomegaly. She was in haematological relapse with WBC 95 X 10V1 with 6% blasts and 74% granulocyte precursors. The lumbar puncture showed increased pressure and CSF sediment composed of many lymphoblast-like cells (fig. IE). The meningeal involvement resolved after intrathecal methotrexate and cranial irradiation. February 11 she was started on busulfan, but a few days later the breast infiltration recurred CML Initiating as ALL 57 Fig. 1. Blood (A) and bone marrow (B) at presentation; CSF sediment (C); blood (D) and bone marrow (E) in chronic myeloid phase; bone marrow (F) in terminal crisis. on the right side; a biopsy showed myeloid leukaemic infiltration. A cytogenetic study of the marrow revealed the Ph1 chromosome; the neutrophile alkaline phos-phatase score resulted low. After a few days the treatment was changed from busulfan to vincristine and prednisone owing to the changes in the blood picture: WBC 4 × 10V1 with 26% blasts; RBC 2.8 X 1012/1, platelets 14 X 10V1. The marrow showed 90% undifferen-tiated blasts (fig. IF). Despite the new treatment the blast count increased and the patient died on 20-ΓV-1974 of cerebral haemorrage.