1985
DOI: 10.1056/nejm198505023121807
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An Antibody Cytotoxic to Megakaryocyte Progenitor Cells in a Patient with Immune Thrombocytopenic Purpura

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Cited by 77 publications
(36 citation statements)
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“…During maturation, MK express CD41/CD61 and CD42b/CD42a on their surfaces, 6,7,26 so it is likely that the binding of antiplatelet autoantibodies could inhibit MK maturation [27][28][29] and interfere with platelet release. During endomitosis, the ploidy of diploid (2N) MK precursors increases 30 and each of these mature MK is able to release thousands of platelets 31 by extending proplatelets.…”
Section: Discussionmentioning
confidence: 99%
“…During maturation, MK express CD41/CD61 and CD42b/CD42a on their surfaces, 6,7,26 so it is likely that the binding of antiplatelet autoantibodies could inhibit MK maturation [27][28][29] and interfere with platelet release. During endomitosis, the ploidy of diploid (2N) MK precursors increases 30 and each of these mature MK is able to release thousands of platelets 31 by extending proplatelets.…”
Section: Discussionmentioning
confidence: 99%
“…[4][5][6] The reduced platelet production rate might be mediated by the action of antiplatelet antibodies, which can bind to megakaryocytes in the bone marrow. [7][8][9] Recent in vitro studies support this concept showing that human megakaryocyte colony formation and proplatelet formation is inhibited 10 and that a reduced expansion of megakaryocytic progenitors can be observed especially in the presence of certain antiplatelet glycoprotein antibodies. 11 However, despite the evidence of a reduced platelet production in several ITP patients, numbers of megakaryocytes in the bone marrow are usually normal or increased.…”
Section: Introductionmentioning
confidence: 99%
“…In addition to an immune mechanism, therefore, other factors likely contributed to the severe thrombocytopenia observed in this case including splenic platelet sequestration, sepsis-associated marrow suppression and hemophagocytosis. The marked reduction in bone marrow megakaryocytes may be consistent with an autoimmune syndrome in view of the fact that cytotoxic autoantibodies directed against megakaryocyte precursors have been demonstrated in patients with acquired pure megakaryocytic aplasia [26,27] and immunosuppressive treatment has been successful in this disorder [28]. The lack of response to prednisone and IVIg argues against an immune mediated mechanism; however, up to 30% of ITP patients are refractory to steroids [29] and up to 25% have an inadequate response to IVIg [30,31].…”
Section: Discussionmentioning
confidence: 96%