Abstract
IN 1956, Scavo and Andres1, and later others2–4, reported that glycogen in megakaryocytes was decreased in chronic idiopathic thrombocytopenic purpura (ITP) with megakaryocytic hyperplasia before splenectomy. Also, some of these investigators1,2 showed that megakaryocytic glycogen increased after splenectomy and that the increase coincided with the appearance of budding megakaryocytes and numerous platelet masses in bone marrow. Jamra and Lorenzi5, however, following Daniell's6 system for semi-quantitating megakaryocytic glycogen, noted that in presplenectomy patients with ITP there was an increase in large coarse PAS positive glycogen granules and concluded that this histochemical finding might prove to be pathognomonic of ITP with megakaryocytic hyperplasia. Because of the importance of phosphorylase, required for the initiation of glycogenolysis, it was decided to determine if the large masses of glycogen in megakaryocytes in this condition might be cumulative secondary to a relative phosphorylase deficiency, that is, an acquired megakaryocytic phosphorylase deficiency glycogenosis.
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References
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HEADINGTON, J. Phosphorylase Activity in Megakaryocytes. Nature 209, 928–929 (1966). https://doi.org/10.1038/209928a0
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DOI: https://doi.org/10.1038/209928a0
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