European journal of haematology · 2006
Peripheral blood haematopoietic progenitor cells in patients with beta thalassaemia major receiving desferrioxamine or deferiprone as chelation therapy.
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Vlachaki Efthimia, Ioannidou-Papagiannaki Elissavet, Tziomalos Konstantinos, Haralambidou-Vranitsa Styliani, Perifanis Vassilios, Klonizakis Ioannis, Athanassiou-Metaxa Miranda
Аннотация
OBJECTIVES: The main adverse effect of deferiprone is the development of neutropenia, which occurs via an unknown mechanism. We aimed to gain insight into the pathogenesis of deferiprone-induced neutropenia by assessing the peripheral blood haematopoietic progenitor cells.
METHODS: Sixteen patients with beta thalassaemia were studied; nine (Group A) were receiving desferrioxamine and seven (Group B) deferiprone. Ten healthy individuals comprised the control group (Group C).
RESULTS: Granulocyte-erythrocyte-monocyte-megakaryocyte colony forming units were significantly more in Groups A and B compared with Group C. Granulocyte-macrophage colony forming units (CFU-GM) were significantly more in Group B compared with Group C. Macrophage colony forming units were significantly less in Group B compared with Group C. Granulocyte colony forming units (CFU-G) were significantly more in Group A compared with Group C. We found a trend in the difference in the number of CFU-G between patients' groups (P = 0.123). Adding serum from patients receiving deferiprone to cultures of controls resulted in a maturation arrest of the granulocytic lineage.
CONCLUSION: Our findings point to a maturation arrest at the level of CFU-GM as a potential mechanism of deferiprone-induced neutropenia.
METHODS: Sixteen patients with beta thalassaemia were studied; nine (Group A) were receiving desferrioxamine and seven (Group B) deferiprone. Ten healthy individuals comprised the control group (Group C).
RESULTS: Granulocyte-erythrocyte-monocyte-megakaryocyte colony forming units were significantly more in Groups A and B compared with Group C. Granulocyte-macrophage colony forming units (CFU-GM) were significantly more in Group B compared with Group C. Macrophage colony forming units were significantly less in Group B compared with Group C. Granulocyte colony forming units (CFU-G) were significantly more in Group A compared with Group C. We found a trend in the difference in the number of CFU-G between patients' groups (P = 0.123). Adding serum from patients receiving deferiprone to cultures of controls resulted in a maturation arrest of the granulocytic lineage.
CONCLUSION: Our findings point to a maturation arrest at the level of CFU-GM as a potential mechanism of deferiprone-induced neutropenia.