PMC3647705_01
BM biopsy, high magnification (x 40) shows prominent myeloid proliferation (a); elements with myelomonocytic morphology expressing CD33 (b) and CD68RPGM1 (c) are prevalent. Dysplastic granulocytopoiesis and megakaryocytopoiesis are evident. Cells with undifferentiated immature morphology or blast equivalent as monoblast or promonocytes are very rare.
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BM with large amount of monocytes and myeloid precursor such as promonocytes and cells with immature morphology featuring atypical nuclear anomalies, finely dispersed chromatin, small evident nucleoli and scant cytoplasm. Those cells are CD34 negative but express CD68KP1 and CD68RPGM1 (data not shown). The percentage of immature precursor through the entire BM biopsy has been estimated at about 15 - 20% of all hematopoietic cells. These findings were consistent with the diagnosis of chronic myelomonocytic leukemia- type2 (a). Insert b is a Gomori stain which shows a delicate bone marrow fibrosis, grade-1.
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A hematological diagnostic revision was performed with histopathological diagnosis of CMML with 15% of blasts in the BM (Figure 2a,b).
BM after azacitidine therapy reveals myelodysplastic features: dismegakariocytopoiesis and disgranulocytopoiesis are evident; rare erytroid islands with dyserythropoietic morphology are also detected (a). Cells with immature-blastic morphology are rare (less than 5%). Insert b: Gomori stain shows a diffuse and strong (grade-2) BM fibrosis.
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After the fourth azacitidine course, PB counts significantly improved, and the monocytosis disappeared; BM trephine biopsy showed the near full disappearance of blast cells but progression of the fibrosis (Figure 3a,b). Apart from the persistence of JAK2 V617F mutation, the analysis of most common alterations found in t-MDS/AML showed only an IDH2 R172K mutation. After the fourth azacitidine course, PB counts significantly improved, and the monocytosis disappeared; BM trephine biopsy showed the near full disappearance of blast cells but progression of the fibrosis (Figure 3a,b).