LAUSR

A 38-year-old male with chronic myeloid leukaemia (CML) of 11 years duration presented with fatigue and night sweats. He had been non-compliant with imatinib treatment for one year. His full blood count showed normocytic anaemia (haemoglobin concentration 93 g/l), leucocytosis (white blood cells, 74.5 9 10/l), basophilia (6 9 10/l) and marked eosinophilia (60.3 9 10/l) with atypical eosinophils containing basophilic granules (images, Wright’s stain, 9100 objective). Quantitative polymerase-chain-reaction for BCR-ABL1 (p210) showed 17.431% BCR-ABL1. A bone marrow aspirate differential count was concordant with the peripheral blood, revealing eosinophilia (65%), with atypia and no significant increase in blasts (3%). The bone marrow biopsy was hypercellular (90%). Conventional cytogenetic study revealed multiple cytogenetic abnormalities: 43~48,XY,+8,t (9;22)(q34;q11.2),del(17)(p11.2),i(17)(q10),+der(22)t(9;22) (q34;q11.2)[cp13]/46,XY[7]. Notably, the cytogenetic abnormalities included an extra Philadelphia chromosome, trisomy 8 and an isochromosome 17q, supporting the diagnosis of CML in accelerated phase. A fluorescence in situ hybridization panel for PDGFRA, PDGFRB and FGFR1 showed no rearrangement; however, 81.5% of nuclei had three copies of FGFR1, consistent with the presence of trisomy 8. The patient received dasatinib and hydroxycarbamide treatment, which improved the leucocytosis, but eosinophilia with atypia persisted and five weeks later his blood showed 20% blasts, compatible with CML in myeloid blast phase. He underwent induction treatment and received a stem cell transplant. At day 100 post-transplant there was, no eosinophilia, atypical eosinophils or increase in blast cells. Eosinophilia is common in CML, but marked eosinophilia with atypia as a dominant feature is rare and its prognostic significance is unknown. In this patient it was associated with disease progression.