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Methimazole Induced Total Myeloid Aplasia with Delayed Recovery Despite Granulocyte Colony Stimulating Factor (G-CSF): Marrow Progenitor Recovery Kinetics

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Abstract

An eighteen-year-old female with Graves thyrotoxicosis presented with methimazole-induced agranulocytosis and total myeloid aplasia. The bone marrow at presentation showed complete absence of myeloid precursors and striking plasmacytosis. 16 days later, myeloid precursors were still absent morphologically; however bone marrow flow cytometry and cell culture detected an improvement in myelogenesis, which was soon followed by clinical recovery of agranulocytosis. Neutrophil recovery was delayed until day 22 after cessation of methimazole despite G-CSF use, consistent with a direct toxic effect on committed myeloid cells. Our findings suggest that cell culture and flow cytometric evaluation of bone marrow myeloid progenitors can be used as a guide to anticipate neutrophil recovery.

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Acknowledgments

Supported by Georgie Ginopolis Chair award to Y Ravindranath. We are thankful to Michael U. Callaghan, MD for his help with the figures.

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Correspondence to Tania Sarker.

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Sarker, T., Özgönenel, B., Gadgeel, M. et al. Methimazole Induced Total Myeloid Aplasia with Delayed Recovery Despite Granulocyte Colony Stimulating Factor (G-CSF): Marrow Progenitor Recovery Kinetics. Indian J Hematol Blood Transfus 32 (Suppl 1), 214–218 (2016). https://doi.org/10.1007/s12288-015-0595-1

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  • DOI: https://doi.org/10.1007/s12288-015-0595-1

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