A 47-year-old male patient was hospitalized with a complaint of high fever which persisted for 2 months in spite of various antibiotics therapy. On admission his spleen was palpable 8cm below the costal margin. The peripheral blood showed RBC 470×10
4/mm
3, Hb 13.0g/d
l, WBC 3,300/mm
3, and platelet 27.3×10
4/mm
3. WBC differential count demonstrated 1.0% myelocytes, 4.5% metamyelocytes, 12.5% band forms, 4.0% segmented neutrophils, 18.0% eosinophils, 20.0% basophils, 8.5% monocytes and 44.5% lymphocytes. NAP score was 137. A bone marrow aspirate revealed a normal M/E ratio and a slight maturation disturbance in granulocytic series with 5.2% of blastic cells. Cytogenetic analysis of the bone marrow cells revealed a karyotype of 46, XY, t(8q-; 22q+), t(9q+; 22q-) in almost all metaphases examined. Because of persistent high fever and gradual progress of neutropenia, he was placed on prednisolone 30mg daily which made him afebrile on the next day, and thereafter WBC counts began to rise gradually. About 9 months after the onset of therapy, WBC counts estimate over 3×10
4/mm
3 with a typical pattern of CML, and a bone marrow aspirate showed intense granulocytic hyperplasia. Bone marrow cytogenetic studies at this time revealed the presence of Ph
1 chromosomes alone with a disappearance of t(8q-; 22q+). Since then, he was put on dibromomanitol therapy, and has been in complete remission for about 3 years.
It could be concluded that our case are CML preceded by so-called clinical blastic crisis, because there was no evidence suggestive blastic transformation hematologically, and t(8q-; 22q+) was an additional chromosomal abnormality frequently seen in blastic phase of CML. Some discussions were made in concern with published reports describing few cases who developed typical CML shortly after VP therapy from ALL.
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