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Abstract：
Thrombocytopenia 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.
摘要：
血小板减少症是多种造血系统疾病的常见病,然而,导致血小板计数低的机制的细节仍然难以捉摸.巨核细胞是一系列负责血小板产生的祖细胞。骨髓中巨核细胞的改变是导致各种疾病中血小板减少的致病因素。根据43例血小板计数低的血液病患者偶然遇到的巨核细胞的超微结构分析，电子显微照片显示，异常巨核细胞在特发性血小板减少性紫癜中占主导地位，再生障碍性贫血,和骨髓增生异常综合征；自噬，凋亡，巨核细胞的细胞损伤是再生障碍性贫血的突出特征。另一方面,分化差的巨核细胞在急性巨核细胞白血病（AMKL）中占主导地位，尽管在非AMKL急性白血病中可见受损的巨核细胞。本文记录了与血小板减少症相关的巨核细胞的超微结构改变，并揭示了特定血液疾病的独特特征。对强调膜融合蛋白的未来研究途径发表了评论。
