TRANSFUSION TRIAL TO PREVENT PLATELET ALLOIMMUNIZATION

同种异体免疫是难治性的主要原因之一。 接受血小板输注治疗。这可能导致显著的 发病率和道德性。血小板不能耐受的处理通常是 无效；因此，预防血小板难治性 最好是这样。已经尝试了几种方法来减少 血小板输注中的同种异体免疫，包括使用：人类白细胞抗原配型 血小板、单一供者血小板、缺乏白细胞的血小板，以及 免疫抑制疗法，如对接受者的治疗 环孢素或输注紫外线治疗的血小板 辐射。尽管人类白细胞抗原I类抗体经常牵涉到 作为血小板不稳定的一个原因，它们不能解释不良 所有同种异体免疫患者的血小板反应。只是一个相对的 次要作用被归因于血小板特异性和/或药物依赖性 血小板中的抗体难治性，目前尚无系统研究 调查了他们在这个问题上的潜在作用。这一发现是在 1988年新的血小板同种异体抗原，如BR a和Bak B，以及 两性霉素B和万古霉素与血小板关系的研究进展 耐火性强烈表明有必要进行全面的测试 分析难治性患者血清中所有可能的抗血小板药物 抗体。因此，建议进行调查，以减少 同种异体免疫和随后的血小板不稳定的发生率 通过使用单一捐赠者减少捐赠者暴露的数量 白血球耗尽的血小板和红细胞。二十- 每年将有四名新诊断的ANLL患者进入 随机试验。进一步建议制定一种敏感和 检测因以下原因引起的血小板不稳定的特异性实验室检测 同种异体免疫。将使用的检测方法包括单抗- 特异性抗原捕获酶联免疫吸附试验、免疫荧光、蛋白A花环 形成、51Cr释放和淋巴细胞毒作用。

Alloimmunization is one of the major causes of refractoriness associated with platelet transfusion therapy. This can lead to significant morbidity and morality. Management of platelet refractoriness often is not effective; thus, prevention of platelet refractoriness is preferable. Several approaches have been attempted to reduce alloimmunization to platelet transfusion including use of: HLA matched platelets, single donor platelets, leukocyte-poor platelets, and immunosuppressive therapies, such as treatment of recipients with cyclosporine or transfusion of platelets treated with ultraviolet irradiation. Although HLA class I antibodies are frequently implicated as a cause of platelet refractoriness, they do not account for poor platelet responses in all alloimmunized patients. Only a relatively minor role has been ascribed to platelet-specific and/or drug-dependent antibodies in platelet refractoriness and no systematic study has investigated their potential role in this problem. The discovery in 1988 of new platelet alloantigens, such as Br a and Bak b, and the recent association of amphotericin B and vancomycin, with platelet refractoriness strongly suggest the need for a comprehensive test to analyze serum from refractory patients for all possible anti-platelet antibodies. Therefore, an investigation is proposed to reduce the incidence of alloimmunization and subsequent platelet refractoriness by reducing the number of donor exposures through use of single donor platelets and red cells that have been depleted of leukocytes. Twenty- four patients with newly diagnosed ANLL will be entered yearly in the randomized trial. It is further proposed to develop a sensitive and specific laboratory test to detect platelet refractoriness due to alloimmunization. The assays to be used include monoclonal antibody- specific antigen capture ELISA, immunofluorescence, protein A rosette formation, 51 Cr release and lymphocytotoxicity.