A 57 -year-old male truck driver presen ts For evaluation of chest pain and dyspnea on minimal exertion. Patien t reports gradually worsening generalized Fatigue over the precedi ng 3 mon ths. Examination reveals splenomegaly. Laboratory workup shows leukocyte count of 32.000/pl. hemoglobin of 9.7 g/dl. and platelet count of 1 3LJ .0001 pl. Peripheral blood smear reveals increased number of homogeneously ap-pearing leukocytes as shown below.
Testing for BCI-ABL translocation is negative. and a bone marrow aspira te is hypercel-lular and shows 2% myeloblasts. A diagnosis of CMML is made, and the patient is treated with oral etoposide for the next 18 months with near normalization of h is peripheral blood counts and decreased splenomegaly. On a rou tine follow-up, the pa-tient is noted to have increased leukocyte count of LJ 5 .800/,LLL. hemoglobin of 8.2 g/dl. and platelet count of 2 LJ , OOO/,LLL. Peripheral blood smear is shown below.
What is the most likely explanation of the new clinical picture?
- Progression to myelofibrosis (MF)
- Etoposide-induced toxicity
- Progression to acute myelomonocytic leukemia (AMML)
- De novo acute lymphoblastic leukemia (ALL)
- Transformation to chronic myeloid leukemia (CML)
Medicine
C. Peripheral blood smear now exhibits a different picture compared with the one observed at diagnosis with predominance of monocytoid cells with increased nuclear-to-cytoplasmic ratio and fine chromatin and nucleoli. This picture is consistent with transformation to AMML. CMML is a myeloproliferative/myelodysplastic syndrome with a variable survival. Two large case series of CMML reported a median survival of 12 and 18 months respectively. The most important factor determining survival is the percentage of blasts in the bone marrow and blood, with transformation to acute leuke-mia reported in approximately 20% to 40% of patients.
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