Transient atypical monocytosis mimic acute myelomonocytic leukemia in post-chemotherapy patients receiving G-CSF: report of two cases
Department of Pathology, Hematopathology/Molecular Pathology Laboratories, New York University School of Medicine, New York, NY 10016, USA.Clinical & Laboratory Haematology (Impact Factor: 1.3). 11/2004; 26(5):359-62. DOI: 10.1111/j.1365-2257.2004.00628.x
Granulocyte colony-stimulating factor (G-CSF) is now widely used in patients with malignant disorders receiving intensive chemotherapy to increase leukocyte count and to upregulate phagocyte function during neutropenia. Monocytosis associated with G-CSF has been reported in anecdotal literature. We report two cases of pseudoleukemia secondary to G-CSF administration. Both patients initially presented with myelodysplastic syndrome with chromosome 7 abnormalities that evolved into acute myeloid leukemia. Case one had deletion 7q while case two initially had monosomy 7 and subsequently developed a balanced translocation between the short (p) arm of chromosome 1 and long (q) arm of chromosome 15. Following the induction chemotherapy and G-CSF administration, both of these patients developed pseudoleukemia. Patient 1 had white blood cell (WBC) count of 26 x 10(9)/l with 72% monocytes, while patient two had WBC of 14.1 x 10(9)/l with 30% monocytes. In both patients the monocytosis resolved after the discontinuation of G-CSF therapy. In summary, patients treated with G-CSF should be followed closely. In those cases with pseudoleukemia discontinuation of the drug with no supplemental chemotherapy is probably enough to control the atypical monocytosis.
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ABSTRACT: Trephine bone marrow biopsy is a frequent routine investigation, particularly important in cases with an unsuccessful aspirate. In addition to a representative trephine biopsy length and quality, the patient's clinical history is of critical importance. Especially drug-induced bone marrow changes are often difficult to interpret without prior knowledge of exposure to respective agents. Since some of these changes mimic malignancies, this can lead to serious misinterpretations. Drugs in general can induce a wide spectrum of bone marrow reactions. Immunosuppressants such as Azathioprine and Methotrexate cause morphological bone marrow changes that can not be distinguished from myelodysplastic syndromes, while cytokines and growth factors induce an overall increase in cellularity and, in particular, a left shift of myelopoiesis with increased myeloblasts and monoblasts, mimicking acute myeloid leukaemia. Moreover, drugs with immuno-allergic- (such as Allopurinol, Carbimazole, Crabamazepine, Clozapine, non-steroidal anti-rheumatics, Phenytoin, Sulfonamides) or direct myelotoxic potential can lead either to T-cell-mediated bone marrow stem cell destruction with the morphological pattern of aplastic anaemia, to direct toxic or immunological burst- or colony-forming units' destruction with isolated erythro- or myelopoietic hypoplasias or to other changes such as eosinophilia, (haemo)phagocytosis, T-cell lymphocytosis (which can be very severe, resembling lymphoma/leukaemia), perivascular plasmacytosis, siderosis or stromal oedema. In summary, clinical information on drug exposure is at least as important as a good quality biopsy for comprehensive histology-based bone marrow diagnostics, helping to avoid not only misinterpretation but also expensive additional examinations. KeywordsBone marrow-Trephine biopsy-Pitfalls-Drug-induced changesmemo - Magazine of European Medical Oncology 10/2010; 3(3):132-135. DOI:10.1007/s12254-010-0215-6
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