ITP is characterized by autoantibodies to platelet glycoproteins that also bind megakaryocytes and megakaryocyte precursors in the bone marrow, thereby impairing megakaryocyte maturation and proplatelet release. In some patients inhibition of proplatelet release is extreme, in others it is only partial or minimal. Eltrombopag or other TPO-R agonists can stimulate megakaryocyte proliferation and maturation, but has no effect on proplatelet formation and release. Both in responders and nonresponders the bone marrow will show an increased number of megakaryocytes, which tend to be clustered and have a hypolobulated nucleus. The difference between responders and nonresponders is only functional: responders produce platelets, nonresponders do not. Professional illustration by Debra Dartez.

ITP is characterized by autoantibodies to platelet glycoproteins that also bind megakaryocytes and megakaryocyte precursors in the bone marrow, thereby impairing megakaryocyte maturation and proplatelet release. In some patients inhibition of proplatelet release is extreme, in others it is only partial or minimal. Eltrombopag or other TPO-R agonists can stimulate megakaryocyte proliferation and maturation, but has no effect on proplatelet formation and release. Both in responders and nonresponders the bone marrow will show an increased number of megakaryocytes, which tend to be clustered and have a hypolobulated nucleus. The difference between responders and nonresponders is only functional: responders produce platelets, nonresponders do not. Professional illustration by Debra Dartez.

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