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Curr Opin Hematol. 2012 Nov;19(6):469-74. doi: 10.1097/MOH.0b013e328358f86c.
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Toward a prophylaxis against fetal and neonatal alloimmune thrombocytopenia: induction of antibody-mediated immune suppression and prevention of severe clinical complications in a murine model.针对胎儿和新生儿同种免疫性血小板减少症的预防:在小鼠模型中诱导抗体介导的免疫抑制和预防严重临床并发症。
Transfusion. 2012 Jul;52(7):1446-57. doi: 10.1111/j.1537-2995.2011.03480.x. Epub 2012 Jan 17.
3
Human platelet antigen allele frequencies and new mutations on platelet glycoprotein genes in the Chinese Han population.中国汉族人群血小板抗原等位基因频率及血小板糖蛋白基因的新突变
Transfus Med. 2011 Oct;21(5):330-7. doi: 10.1111/j.1365-3148.2011.01081.x. Epub 2011 Jun 9.
4
Reconsidering fetal and neonatal alloimmune thrombocytopenia with a focus on screening and prevention.重新考虑胎儿和新生儿同种免疫性血小板减少症,重点关注筛查和预防。
Expert Rev Hematol. 2010 Oct;3(5):559-66. doi: 10.1586/ehm.10.49.
5
Molecular insight into human platelet antigens: structural and evolutionary conservation analyses offer new perspective to immunogenic disorders.深入了解人类血小板抗原:结构和进化保守性分析为免疫性疾病提供新视角。
Transfusion. 2011 Mar;51(3):558-69. doi: 10.1111/j.1537-2995.2010.02862.x. Epub 2010 Aug 30.
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Genotyping for human platelet alloantigen polymorphisms: applications in the diagnosis of alloimmune platelet disorders.人类血小板同种抗原多态性的基因分型:在同种免疫性血小板疾病诊断中的应用
Semin Thromb Hemost. 2008 Sep;34(6):539-48. doi: 10.1055/s-0028-1103365. Epub 2008 Nov 28.
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Fetal/neonatal allo-immune thrombocytopenia (FNAIT): past, present, and future.胎儿/新生儿同种免疫性血小板减少症(FNAIT):过去、现在与未来
Obstet Gynecol Surv. 2008 Apr;63(4):239-52. doi: 10.1097/OGX.0b013e31816412d3.
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Management and outcome of 200 cases of fetomaternal alloimmune thrombocytopenia.200例胎儿-母体同种免疫性血小板减少症的管理与结局
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9
Advances in the management of alloimmune thrombocytopenia.同种免疫性血小板减少症的管理进展
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应用序列特异性引物聚合酶链反应检测 998 名台湾献血者的人类血小板抗原等位基因。

Human platelet antigen alleles in 998 Taiwanese blood donors determined by sequence-specific primer polymerase chain reaction.

机构信息

Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, No. 1 Chang-Te Street, Taipei 10048, Taiwan.

出版信息

Biomed Res Int. 2013;2013:973789. doi: 10.1155/2013/973789. Epub 2013 Jun 20.

DOI:10.1155/2013/973789
PMID:23865077
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3705808/
Abstract

Polymorphism of human platelet antigens (HPAs) leads to alloimmunizations and immune-mediated platelet disorders including fetal-neonatal alloimmune thrombocytopenia (FNAIT), posttransfusion purpura (PTP), and platelet transfusion refractoriness (PTR). HPA typing and knowledge of antigen frequency in a population are important in particular for the provision of HPA-matched blood components for patients with PTR. We have performed allele genotyping for HPA-1 through -6 and -15 among 998 platelet donors from 6 blood centers in Taiwan using sequence-specific primer polymerase chain reaction. The HPA allele frequency was 99.55, and 0.45% for HPA-1a and -1b; 96.49, and 3.51% for HPA-2a and -2b; 55.81, and 44.19% for HPA-3a and -3b; 99.75, and 0.25% for HPA-4a and -4b; 98.50, and 1.50% for HPA-5a and -5b; 97.75 and 2.25% for HPA-6a and -6b; 53.71 and 46.29% for HPA-15a and -15b. HPA-15b and HPA-3a, may be considered the most important, followed by HPA-2, -6, -1, -5, and -4 systems, as a cause of FNAIT, PTP, and PTR based on allele frequency. HPA-4b and HPA-5b role cannot be excluded based on their immunogenicity. A larger-scale study will now be conducted to confirm these hypotheses and to establish an apheresis donor database for the procurement of HPA-matched apheresis platelets for patients with PTR.

摘要

人类血小板抗原(HPAs)的多态性导致同种免疫和免疫介导的血小板疾病,包括胎儿-新生儿同种免疫性血小板减少症(FNAIT)、输血后紫癜(PTP)和血小板输注无效(PTR)。HPA 分型和人群中抗原频率的知识对于为 PTR 患者提供 HPA 匹配的血液成分尤为重要。我们使用序列特异性引物聚合酶链反应(PCR)对来自台湾 6 个血液中心的 998 名血小板供者进行了 HPA-1 至 HPA-6 和 HPA-15 的等位基因基因分型。HPA 等位基因频率为 99.55%和 0.45%,分别为 HPA-1a 和 HPA-1b;96.49%和 3.51%,分别为 HPA-2a 和 HPA-2b;55.81%和 44.19%,分别为 HPA-3a 和 HPA-3b;99.75%和 0.25%,分别为 HPA-4a 和 HPA-4b;98.50%和 1.50%,分别为 HPA-5a 和 HPA-5b;97.75%和 2.25%,分别为 HPA-6a 和 HPA-6b;53.71%和 46.29%,分别为 HPA-15a 和 HPA-15b。根据等位基因频率,HPA-15b 和 HPA-3a 可能被认为是导致 FNAIT、PTP 和 PTR 的最重要因素,其次是 HPA-2、-6、-1、-5 和 -4 系统。根据其免疫原性,不能排除 HPA-4b 和 HPA-5b 的作用。现在将进行更大规模的研究,以验证这些假设,并为 PTR 患者建立一个 HPA 匹配的单采血小板采集的供体数据库。