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dc.contributor.authorEyden, Brian P
dc.contributor.authorRu, Y. X.
dc.contributor.authorDong, S. X.
dc.contributor.authorLiu, J.
dc.contributor.authorLiu, X. F.
dc.date.accessioned2022-05-26T08:35:13Z
dc.date.available2022-05-26T08:35:13Z
dc.date.issued2021en
dc.identifier.citationEyden B, Ru YX, Dong SX, Liu J, Liu XF. Ultrastructural alterations of megakaryocytes in thrombocytopenia: A review of 43 cases. Vol. 3, Blood Science. Ovid Technologies (Wolters Kluwer Health); 2021. p. 107–12.en
dc.identifier.pmid35402843en
dc.identifier.doi10.1097/bs9.0000000000000093en
dc.identifier.urihttp://hdl.handle.net/10541/625274
dc.description.abstractThrombocytopenia is a frequent occurrence in a variety of hematopoietic diseases; however, the details of the mechanism leading to low platelet count remain elusive. Megakaryocytes are a series of progenitor cells responsible for the production of platelets. Alterations in megakaryocytes in the bone marrow are a causative factor resulting in thrombocytopenia in varied diseases. Based on ultrastructural analysis of incidentally encountered megakaryocytes in 43 patients with blood diseases marked by low platelet counts, electron micrographs demonstrated that aberrant megakaryocytes predominated in idiopathic thrombocytopenic purpura, aplastic anemia, and myelodysplastic syndrome; autophagy, apoptosis, and cellular damage in megakaryocytes were a prominent feature in aplastic anemia. On the other hand, poorly differentiated megakaryocytes predominated in acute megakaryoblastic leukemia (AMKL) although damaged megakaryocytes were seen in non-AMKL acute leukemia. This paper documents the ultrastructural alterations of megakaryocytes associated with thrombocytopenia and reveals distinctive features for particular blood diseases. A comment is made on future avenues of research emphasizing membrane fusion proteins.en
dc.language.isoenen
dc.relation.urlhttps://dx.doi.org/10.1097/bs9.0000000000000093en
dc.titleUltrastructural alterations of megakaryocytes in thrombocytopenia: A review of 43 casesen
dc.typeArticleen
dc.contributor.departmentDepartment of Histopathology, Christie NHS Foundation Trust, Manchester, UKen
dc.identifier.journalBlood Scienceen
dc.description.noteen]
refterms.dateFOA2022-06-29T09:33:30Z


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