The United Network for Organ Sharing position on using donors with primary central nervous system malignancies.
The United Network for Organ Sharing position on using donors with primary central nervous system malignancies.
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器官共享联合网络对于使用患有原发性中枢神经系统恶性肿瘤的捐赠者的立场。
DOI：
10.1097/01.tp.0000148910.32618.7f
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发表时间：
2005
期刊：
影响因子：
6.2
通讯作者：
H. Kauffman
中科院分区：
文献类型：
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作者：
H. Kauffman
我们在这里报告一个不寻常的情况下，肝移植后抗CD 36（GP IV，纳卡）过敏，可能是从输血，并涉及血小板输注难治性（PTR）。一名47岁的日本男性，患有B型肝炎病毒相关肝硬化，于2001年接受了他52岁的兄弟的肝移植，他的兄弟有一个人类白细胞抗原（HLA）基因座错配（表1）。移植后，患者的血小板降至21010/L，并频繁输注血小板以将计数保持在可接受的水平。血小板数量在2 ~ 41010/L之间波动，输注后短暂升高至101010/L，表明输注随机供体血小板的反应较差。未观察到明显出血事件。抗CD 36同种抗体在移植前和移植后5天均为阴性，8天后首次检测到。到第8天，21名供体的血小板已输注。接受者给予免疫抑制剂，由于肝功能障碍，他克莫司（4 mg/天）在第7天改为泼尼松龙（5 mg/天）。抗体滴度从第8天的16上升到第22天的128。整个期间未检测到抗HLA或抗人血小板抗原（HPA）。受体和肝脏供体均为CD 36抗原阴性。患者有效地输注了来自CD 36阴性但HLA非选择性供体的血小板。第99天后，滴度降至16，血小板计数持续在约4 - 51010/L，无需频繁输血。在临床过程中没有明确的败血症或排斥反应的证据。抗CD 36滴度在CD 36阴性输血后逐渐下降，并在第232天消失。然而，血小板计数低并未完全消退。患者于第377天死于多器官功能衰竭。成人同种免疫性血小板减少症分为输血后紫癜、被动性同种免疫性血小板减少症、移植相关性同种免疫性血小板减少症和PTR。移植的实体器官含有乘客淋巴细胞，可以传播自身免疫性疾病或引发受体的同种免疫性疾病。同种免疫性血小板减少症是一种罕见的，但并不罕见，血小板减少症的原因。抗血小板特异性同种抗原的同种抗体，特别是白色人群中的HPA-1 a，可导致受者严重血小板减少症。
We report here an unusual case of a liver transplantation followed by anti-CD36 (GP IV, Naka) sensitization, probably from transfusion, and involving platelet-transfusion refractoriness (PTR). A 47-year-old Japanese man with hepatitis B virus-related liver cirrhosis received a liver transplant in 2001 from his 52-year-old brother with one human leukocyte antigen (HLA) locus mismatch (Table 1). After the transplantation, the patient’s platelets dropped to 21010/L, and platelets were transfused frequently to keep the count at an acceptable level. The number of platelets fluctuated between 2 and 41010/L with a transient rise to 101010/L after transfusion, indicating a poor response to transfusions of randomdonor platelets. No obvious bleeding episodes were observed. Anti-CD36 iso-antibody, which was negative before and 5 days after the transplantation, was first detected after 8 days. Platelets from 21 donors had been transfused by day 8. The recipient was administered immunosuppressants, and tacrolimus (4 mg/day) was changed to prednisolone (5 mg/day) on day 7 because of liver dysfunction. The titer of the antibody, which was16 on day 8, went up to 128 on day 22. No anti-HLA or anti-human platelet antigen (HPA) was detected throughout the period. The recipient and the liver donor were negative for CD36 antigen. The patient was transfused effectively with platelets from CD36 negative, but HLA nonselected, donors. After day 99 when the titer went down to 16, the platelet count persisted at approximately 4 to 51010/L without frequent transfusions. There was no clear evidence of sepsis or rejection during the clinical course. The titer of anti-CD36 declined gradually after CD36-negative transfusion and disappeared on day 232. Nevertheless, the low platelet count was not resolved completely. The patient died of multi-organ failure on day 377.Alloimmune thrombocytopenias in adults are classified into posttransfusion purpura, passive alloimmune thrombocytopenia, transplantation-associated alloimmune thrombocytopenia, and PTR. Transplanted solid organs contain passenger lymphocytes that can transmit autoimmune disease or initiate alloimmune disorders in recipients. Alloimmune thrombocytopenia is an uncommon, but not rare, cause of thrombocytopenia. Alloantibodies against platelet-specific alloantigens, in particular HPA-1a among white populations, can cause severe thrombocytopenia in recipients.