62例血小板输注无效患者的交叉配型及HLA抗体分析

目的对广州地区血小板输注无效患者进行两种不同试验方法的交叉配型并检测人类白细胞抗原（HLA）抗体特异性。方法对62名临床不同疾病类型血小板输注〉2次的患者分别做流式细胞血小板交叉配型（Flow—XM）试验和经典补体依赖微量淋巴细胞毒交叉配型（NIH．CDC）试验,并进行群体反应性抗体（PRA）分析。结果62例血小板输注无效患者通过NIH．CDC试验,得出血小板配型阳性标本22例,阳性率为35．48％;Flow-XM试验比NIH—CDC试验阳性检出率高,为70．97％,两种配型结果的阳性率比较差异有统计学意义（P〈0．01）。分析配型阳性患者的HLA抗体特异性,除2例为阴性外,其余都证实存在针对供者的HLA抗体。结论Flow—XM试验对于检测HLA抗体具有较高的灵敏度,值得推荐。     

复发性流产患者HLA及血小板特异性糖蛋白抗体GPⅡb/Ⅲa表达的初步研究

目的:探讨原因不明复发性流产(RSA)患者HLA抗体和血小板特异性糖蛋白(GPⅡb/Ⅲa)抗体的表达情况。方法:对299名复发性流产的患者血浆中HLA抗体和GPⅡb/Ⅲa抗体进行检测,血小板抗体检测试剂盒(固相凝集法)筛查IgG抗体,Antigen Tray-LATM板检测HLA抗体,GTI公司PAK-PLUS检测试剂盒检测血小板特异性抗体,利用流式细胞仪技术进行GPⅡb/Ⅲa抗体的确证。结果:检测的299例RSA患者中,IgG抗体阳性26例,阳性率8.69%。26例IgG抗体阳性患者中,25例HLA抗体呈阳性。HLA-Ⅰ类抗体阳性占5.02%,HLA-Ⅱ类抗体阳性占1.33%,HLA-Ⅰ+Ⅱ类抗体阳性占2.01%;在26例RSA患者中,GPⅡb/Ⅲa抗体阳性4例(占15.38%),其中GPⅡb/Ⅲa阳性和HLA抗体均阳性3例(占11.54%),GPⅡb/Ⅲa抗体单独阳性1例(占3.85%)。结论:初步探讨了RSA患者HLA抗体和GPⅡb/Ⅲa抗体的分布情况,本研究为复发性流产患者血小板抗体的检测提供了初步的实验基础。     

联合分析血小板特异性抗体和瞬逝生物传感器技术检测血小板抗体的方法比较

目的 应用联合分析血小板特异性抗体(specificp platelet antibodies,SASPA)和瞬逝生物传感器技术(evanescent biosensor technology,EVA)分别检测血小板特异性同种抗体和自身抗体,对两者进行方法学比较.方法 收集94例存在HPA-1a、HPA-5b、HLA-I和自身抗体的患者血浆标本,制备血小板膜糖蛋白-血小板特异性抗体复合物,分别用SASPA和EVA方法对复合物进行检测,对SASPA检测所得平均荧光强度值(MFI)和EVA检测所得斜率值(Slope)作统计学分析和比较.结果 SASPA方法对HPA-1a、HPA-5b、HLA-I和自身抗体检测的敏感度分别为74.1％、86.9％、86.9％和40.9％,EVA方法的敏感度分别为88.9％、78.3％、60.9％和72.7％.人类血小板抗原(HPA)-1a抗体检测中,MFI与Slope表现为强相关性,相关性系数为r=O.95(P ＜0.05).结论 SASPA和EVA技术对传统的单克隆抗体特异性血小板抗原固定实验(MAIPA)作了继承和改良,SASPA方法可以用极少量的血小板同时检测多种血小板特异性抗体,提高了检测效率;EVA方法将血小板裂解后的实验时间缩短为10 min,极大地简化了操作过程,减少了检测时间.SASPA和EVA检测方法的建立对临床血小板免疫相关疾病的诊断和血小板输血领域的发展具有深远意义.     

326例孕妇HLA抗体检测结果分析

人类白细胞抗原（HkA）为移植抗原,具有高度多态性,分为HLA—Ⅰ、HLA-Ⅱ、HLA-Ⅲ三类,HIA为同种抗原,可以刺激机体产生HIA同种抗体。现代医学研究证明,HLA抗体与实体移植、输血、妊娠等密切相关,为探讨HLA抗体与妊娠的关系,笔者对326例孕妇进行HIA抗体检测,现将结果报告如下。     

两例罕见的血小板抗原HPA-21bw等位基因报告

目的:调查中国人群人类血小板抗原HPA-21w多态性.方法:采用聚合酶链反应-序列特异性引物法(PCR-SSP)基因分型技术,对广州汉族血小板献血者进行HPA-21w基因分型,并使用PCR扩增HPA-21w基因片段,进行DNA测序验证.结果:在200例受检者中发现2例HPA-21 a/b杂合子个体,DNA测序表明GPIIIa编码基因1960位G→A,导致GPIIIa膜糖蛋白第628位谷氨酸被赖氨酸所取代,产生HPA-21 bw抗原特异性.中国人群HPA-21 bw的等位基因频率为0.50％.结论:在中国人群首次检出HPA-21 bw等位基因,提示在血小板同种免疫症的诊断和血小板输注治疗中,该抗原具有免疫学意义.     

ELISpot:一种新的检测人类HLA-Ⅰ抗体的方法

目的建立一种新的检测人类HLA-Ⅰ类抗体方法--酶联免疫斑点法(ELISpot).方法以鼠B细胞系HB95为模型,建立一系列特异性ELISpot检测HLA-Ⅰ类抗体的参数,包括HLA抗原的来源、包被抗体最适宜浓度的选择、B细胞最适宜孵化时间,同时以经EBV转化的敏感NTP患者B细胞系为干扰因素,检验该方法的敏感性和特异性.结果以B细胞溶胞体作为HLA抗原来源,当抗原浓度为0.25mg/ml时,相同细胞密度下所获得的斑点频数均高于其它三种抗原浓度(0.125、0.5和1.0 mg/ml,P＜0.05);当包被抗体浓度为1.8 mg/ml、稀释度为1125时,相同孵育时间下所获得的斑点频数高于其它稀释浓度(1250、1500和11 000,P＜0.05);且在抗体稀释度相同情况下,B细胞孵育时间为24小时所获得的斑点最清晰、背景着色最浅、最容易被分析仪器识别.此外,当同时加入经EBV转化的人B细胞时,所获得的斑点频数与单纯加鼠B细胞相似,无明显差异(P＞0.05).结论当B细胞溶胞体作为HLA抗原且浓度为0.25 mg/ml、包被抗体浓度为1.8 mg/ml且稀释度为1125、B细胞孵育时间为24小时时,该ELISpot方法能特异地、敏感地、可信地检测人HLA-Ⅰ类抗体.     

黑龙江省满族人群血小板抗原1～17系统基因多态性的研究

目的 探讨黑龙江省满族人群人类血小板抗原(HPA)1～17系统基因多态性及其表达频率,建立HPA基因型资料库.方法 选择101例满族的健康无血缘关系的人群为研究对象,采用PCR-SSP技术,对HPA1～17共17个抗原系统34个等位基因进行分型,分别计算其基因频率、基因型频率.结果 黑龙江省满族人群HPA-1a、2a、3a、5a、6a、15a基因频率分别是0.99505、0.940595、0.549505、0.99505、0.9802、0.445545,HPA-4a、7a～14a、16a和17a均为1.0;HPA-1b、2b、3b、5b、6b、15b基因频率分别是0.00495、0.059405、0.450495、0.00495、0.0198、0.554455,未检测出HPA-4b、7b～14b、16b和17b.调查和分析的HPA基因组合型及其频率发现满族人群HPA基因有22种组合型,其中仅有3种基因组合型频率＞10％(42.57％),另外19种基因组合型的频率均＜10％(57.43％).黑龙江省满族HPA基因频率与黑龙江省汉族相比,HPA-3a、3b基因频率差异具有统计学意义(P＜0.05).结论 黑龙江省满族健康人群HPA1～ 17基因频率的分布与汉族人群相比有相似之处,也有本民族的自身特点.HPA-3,15系统具有高度多态性,在随机血小板输注中,供受者HPA-3、HPA-15系统不配合的机会分别为37.25％、37.20％,易发生血小板不配合而造成的同种免疫,是HPA配合性输注关注重点.     

海南岛黎族人血小板1～17抗原系统基因多态性研究

目的 调查海南岛黎族人群血小板抗原基因(human platelet alloantigens,HPA)1～17等位基因多态性,分析不同民族的差异,评估其在随机输血中供受者HPA不配合比例,为黎族人群临床血小板输注提供实验依据.方法 采用聚合酶链反应-序列特异性引物方法 对180名黎族人HPA-1～17抗原系统34个等位基因分型.结果 黎族人HPA的等位基因频率分别为:HPA-2a:0.9972,-2b:0.0028,-3a,0.4889,3b:0.5111,5a:0.9667,-5b:0.0333,-6a:0.9972,-6b:0.0028,-15a:0.4250,-15b:0.5750,其余HPA-1、-4、7、-14、-16、-17系统未检出相应HPA-b等位基因.结论 本研究结果 揭示了黎族人HPA-1～17基因型和等位基因频率分布概况,提示黎族人HPA基因频率分布具有黎族人独有的特点.在随机血小板输注中,HPA不配合的机会依次为:HPA-3为37.49%、HPA-15为36.93%、HPA-5为6.23%,只需检测供、受者HPA-3、-5、-15基因相合,就可基本达到血小板匹配性输注.     

海南岛黎族人血小板1～17抗原系统基因多态性研究

目的 调查海南岛黎族人群血小板抗原基因(human platelet alloantigens,HPA)1～17等位基因多态性,分析不同民族的差异,评估其在随机输血中供受者HPA不配合比例,为黎族人群临床血小板输注提供实验依据.方法 采用聚合酶链反应-序列特异性引物方法 对180名黎族人HPA-1～17抗原系统34个等位基因分型.结果 黎族人HPA的等位基因频率分别为:HPA-2a:0.9972,-2b:0.0028,-3a,0.4889,3b:0.5111,5a:0.9667,-5b:0.0333,-6a:0.9972,-6b:0.0028,-15a:0.4250,-15b:0.5750,其余HPA-1、-4、7、-14、-16、-17系统未检出相应HPA-b等位基因.结论 本研究结果 揭示了黎族人HPA-1～17基因型和等位基因频率分布概况,提示黎族人HPA基因频率分布具有黎族人独有的特点.在随机血小板输注中,HPA不配合的机会依次为:HPA-3为37.49%、HPA-15为36.93%、HPA-5为6.23%,只需检测供、受者HPA-3、-5、-15基因相合,就可基本达到血小板匹配性输注.     

海南岛黎族人血小板1～17抗原系统基因多态性研究

目的 调查海南岛黎族人群血小板抗原基因(human platelet alloantigens,HPA)1～17等位基因多态性,分析不同民族的差异,评估其在随机输血中供受者HPA不配合比例,为黎族人群临床血小板输注提供实验依据.方法 采用聚合酶链反应-序列特异性引物方法 对180名黎族人HPA-1～17抗原系统34个等位基因分型.结果 黎族人HPA的等位基因频率分别为:HPA-2a:0.9972,-2b:0.0028,-3a,0.4889,3b:0.5111,5a:0.9667,-5b:0.0333,-6a:0.9972,-6b:0.0028,-15a:0.4250,-15b:0.5750,其余HPA-1、-4、7、-14、-16、-17系统未检出相应HPA-b等位基因.结论 本研究结果 揭示了黎族人HPA-1～17基因型和等位基因频率分布概况,提示黎族人HPA基因频率分布具有黎族人独有的特点.在随机血小板输注中,HPA不配合的机会依次为:HPA-3为37.49%、HPA-15为36.93%、HPA-5为6.23%,只需检测供、受者HPA-3、-5、-15基因相合,就可基本达到血小板匹配性输注.     

Stratégies d’exploration de l’allo-immunisation plaquettaire pour la prévention et la prise en charge des inefficacités transfusionnelles plaquettaires

Platelet refractoriness is a serious complication for patients receiving recurrent platelet transfusions, which can be explained by non-immune and immune causes. Human Leukocyte Antigens (HLA) allo-immunization, especially against HLA class I, is the major cause for immune platelet refractoriness. To a lesser extent, allo-antibodies against specific Human Platelet Antigen (HPA) are also involved. Pregnancy, transplantation and previous transfusions can lead to allo-immune reaction against platelet antigens. After transfusion, platelet count is decreased by accelerated platelet destruction related to antibodies fixation on incompatible platelet antigens. New laboratory tests for allo-antibodies identification were developed to improve sensibility and specificity, especially with the LUMINEX^® technology. The good use and interpretation of these antibodies assays can improve strategies for platelet refractoriness prevention and management with a patient adapted response. Compatible platelets units can be selected according to their identity with recipient typing or immune compatibility regarding HLA or HPA antibodies or HLA epitope compatibility. Prospective studies are needed to further confirm the clinical benefit of new allo-antibodies identification methods and consensus strategies for immune platelet refractoriness management.     

Human platelet alloantigens (HPAs): PCR‐SSP genotyping of a UK population for 15 HPA alleles

Alloimmunization to human platelet alloantigens (HPAs) is responsible for neonatal alloimmune thrombocytopenia (NAIT), post‐transfusional purpura (PTP) and platelet transfusion refractoriness. HPAs may also have a role as histocompatibility antigens in transplantation as well as associations with cardiac disease. We have developed a polymerase chain reaction–sequence‐specific primer (PCR‐SSP) assay capable of detecting 15 HPA allelic variants. As part of the validation of the assay, 134 UK renal donors were genotyped to determine HPA allele frequencies in the UK population. The HPA allele frequencies obtained are consistent with those of the other European studies: GP1A*1 (HPA‐5a) and GP1A*2 (HPA‐5b), 0.914 and 0.086, respectively; GP1BA*1 (HPA‐2a) and GP1BA*2 (HPA‐2b), 0.925 and 0.075; GP2B*1 (HPA‐3a) and GP2B*2 (HPA‐3b), 0.627 and 0.373; GP3A*1 (HPA‐1a) and GP3A*2 (HPA‐1b), 0.840 and 0.161. The rare alleles GP2B*3 (HPA‐9bw) and GP3A*3 to *8 (HPA‐4b, ‐6b, ‐7bw, ‐8bw, ‐10bw and ‐11bw, respectively) were all absent. This comprehensive HPA genotyping assay allows rapid, accurate and reproducible results at low cost.     

Diagnosis and treatment of immunological platelet refractoriness by histocompatibility

Immunological platelet refractoriness occurs when polytransfused patients develop antibodies against donors’ HLA class I antigens, HPA (human platelet antigens) and few cases against both systems. Flow cytometry crossmatch with the patient serum against platelets from several donors can determine whether the refractoriness is or is not of immunological origin. Patients with moderate sensitization will be given transfusions from donors with a negative platelets crossmatch; those who are hypersensitized will need to have antibodies assessed against a reactivity panel (RP) for HLA class I and HPA. The patient must be typed for HLA and HPA in order to identify best donors. We have compiled a list of 500 donors registered at our blood bank with known HLA and HPA profiles. Pre-transfusion crossmatch is performed against donors selected virtually, transfusing those who are negative.We analyzed 75 patients with refractoriness, 67% (50/75) of whom had anti-HLA or anti-HPA antibodies and 56% (28/50) were hypersensitized, with RP ≥ 80%.The diagnosis of the immunological refractoriness and the compatibility between donor and recipient allowed efficient transfusions for all patients.     

Alloantibodies to human platelet glycoprotein antigens (HPA) and HLA class 1 in a cross section of Nigerian antenatal women

The prevalence of antibodies to human platelet antigens (HPA) and human leukocyte antigens (HLA) class 1 antigens among Nigerian pregnant women has not been reported in our country. This study was therefore aimed at screening the obstetric population for evidence of alloimmunization due to human platelet and HLA class 1 antigens. One hundred and forty four (144) pregnant women attending the obstetric clinic of Military Hospital, Port Harcourt, participated in the study. Their sera were tested for antibodies to HPA and HLA class 1 antigens using GTI PakPlus solid phase ELISA Kit. The total prevalence rate of antibody production was 60.5% (87 out of 144). Among the positive samples, 60 had platelet glycoprotein specific antibodies (41.7%) and 27 had HLA class 1 antibodies (18.8%). In 39.6% of the pregnant women, both platelet specific antibodies and HLA class 1 antibodies appeared. The prevalence of platelet specific glycoprotein antibodies were obtained as follows: GP 11b/111a 12 (8.3%), GP 1a/11a 35 (20.8%), GP Ib/IX 18 (12.5%) and GP IV 9 (6.3%). The prevalence of each platelet antibody subgroup was obtained as follows: anti-HPA-1a,-3a,-4a (4.2%), anti-HPA-1b,-3b,-4a (4.2%), anti-HPA-30 5a and anti-GP Ib/IX (12.5% each), anti-HPA-5b (8.3%) and anti-GP IV (6.3%). A high prevalence rate of human platelet arid cytotoxic antibodies has been observed in our obstetric population. There is need to establish platelet serology laboratory for the proper antenatal and postnatal management of pregnant mothers in this region.     

Human Leucocyte Antigens in blood transfusion

Human Leucocyte Antigen (HLA) genes and molecules have an important role in transplantation, aetiology of many autoimmune, non‐autoimmune and infection diseases. Due to the extremely high polymorphism of HLA genes and their different frequency distributions in various populations, an increasing probability of HLA non‐compatible blood products, tissues or organs usage exists. For that reason, the aim of this paper was to give a concise overview of the role of HLA antigens and antibodies in adverse reactions caused by administration of transfusion products. The HLA system can cause detrimental immune reactions in transfusion therapy (platelet immune refractoriness, febrile transfusion reaction, transfusion‐related acute lung injury and transfusion‐associated graft versus host disease). Anti‐HLA antibodies present in the patient are responsible for some of these reactions, while anti‐HLA antibodies or HLA reactive cells present in the transfused product are accountable for immune‐reactivity in other cases. In order to avoid or reduce the development of these transfusion‐related events, anti‐HLA antibody‐negative or compatible products should be used. This is increasingly facilitated by introduction of more sensitive and specific techniques to determine anti‐HLA antibodies and gene polymorphisms. In conclusion, the most common adverse reactions related to administration of incompatible HLA transfusion products are discussed. Basic information about HLA genes and antibodies as well as methods for their detection is also provided in order to give sufficient data for safe and efficient administration of transfusion products.     

Human platelet alloantigens (HPAs): PCR-SSP genotyping of a UK population for 15 HPA alleles.

Alloimmunization to human platelet alloantigens (HPAs) is responsible for neonatal alloimmune thrombocytopenia (NAIT), post-transfusional purpura (PTP) and platelet transfusion refractoriness. HPAs may also have a role as histocompatibility antigens in transplantation as well as associations with cardiac disease. We have developed a polymerase chain reaction-sequence-specific primer (PCR-SSP) assay capable of detecting 15 HPA allelic variants. As part of the validation of the assay, 134 UK renal donors were genotyped to determine HPA allele frequencies in the UK population. The HPA allele frequencies obtained are consistent with those of the other European studies: GP1A*1 (HPA-5a) and GP1A*2 (HPA-5b), 0.914 and 0.086, respectively; GP1BA*1 (HPA-2a) and GP1BA*2 (HPA-2b), 0.925 and 0.075; GP2B*1 (HPA-3a) and GP2B*2 (HPA-3b), 0.627 and 0.373; GP3A*1 (HPA-1a) and GP3A*2 (HPA-1b), 0.840 and 0.161. The rare alleles GP2B*3 (HPA-9bw) and GP3A*3 to *8 (HPA-4b, -6b, -7bw, -8bw, -10bw and -11bw, respectively) were all absent. This comprehensive HPA genotyping assay allows rapid, accurate and reproducible results at low cost.     

Avoidance of Certain Systematic Pitfalls in the Detection of HLA–DR Antibodies Defining Fine Specificities

A selective screening program has been established to identify rapidly and effectively the fine specificity of HLA-DR antibodies in pregnancy anti-HLA sera. Following initial HLA-A, B, C screening sera with extra- or multispecific reactions were selected and specifically tested after platelet absorption on isolated B- and T-lymphocyte populations of the serum donor's husband. Identification of the HLA-DR type of the husband, as well as screening and typing on HLA, A, B and -C typed heterozygous panel B cells led to a more precise characterization of the major specificity of a detected anti-HLA-DR serum. Multispecific anti-DR sera were defined and rendered operationally monospecific by titration.
Some critical steps in a reliable assessment of HLA-DR typing reagents could be worked out. Weak HLA-A, B antibodies, B-cell auto- and Lewis antibodies may cause positive reactivity preferentially or even selectively on B lymphocytes. Of particular importance was the hidden presence of HLA-C specific antibodies, since they cannot be absorbed out by stored platelets. In addition they are not readily detectable through screening on typed panel cells. Because of the frequently very high linkage disequilibrium between HLA-B and HLA-C alleles it is difficult to select appropriately dissecting panel cells. The two points demonstrated above gain even more weight when isolated T and B cell populations are used for HLA-DR typing, because HLA-C antibodies preferentially kill B cells. In this fashion contaminating HLA-C antibodies are not only difficult to detect but can mimic the presence of HLA-DR antibodies.     

Platelet Transfusion Refractoriness in Single-Unit Cord Blood Transplantation for Adults: Risk Factors and Clinical Outcomes

Platelet transfusion refractoriness (PTR) is frequently observed after allogeneic hematopoietic cell transplantation (HCT). However, the incidence of and risk factors for PTR, and impact of PTR on transplant outcomes after cord blood transplantation (CBT) have not been fully investigated. We retrospectively analyzed 185 adult patients who received single-unit CBT in our institute. The mean 16-hour corrected count increment (CCI) for the 5840 platelet transfusions was 3.68?×?10⁹/L. Among them, 3196 transfusions (54.7%) were associated with a PTR with 16-hour-CCI <4.5?×?10⁹/L. Results of multivariate analysis indicated that the following factors were significantly associated with decreased platelet transfusion responses: female sex with pregnancy history, male sex, the presence of HLA class I antibody, lower cord blood total nucleated cell dose, lower cord blood CD34⁺?cell dose, 3 locus HLA disparities, body temperature ≥38°C, C-reactive protein ≥10?mg/dL, cytomegalovirus reactivation, use of foscarnet, and use of liposomal amphotericin B. By contrast, graft-versus-host disease prophylaxis including methotrexate, ABO minor mismatch, use of ganciclovir, and use of linezolid were significantly associated with better platelet transfusion responses. PTR had a significant effect on poor neutrophil and platelet recovery, and overall mortality after CBT. These data suggest that early phase PTR may be predictive of engraftment and mortality after single-unit CBT for adults.     

HLA antigens and Graves' disease in Black South Africans

This study concerns the frequencies with which 36 HLA-A, -B and -C antigens occurred in 84 Black Africans with Graves' disease and in 311 Black controls. In the hyperthyroid patients significant reductions were found in the frequencies of HLA-B7 ( P <0.001, relative risk (RR) 0.33), HLA-Bw42 ( P <0.001, RR 0.32) and the HLA-B7-Bw42 crossreactive group (CREG) ( P <0.0001, RR 0.27), and in the frequencies of the phenotypic combinations HLA-A1, B7 ( P <0.001) and Aw30, B7-Bw42 ( P <0.001). HLA-B8 was increased in frequency ( P <0.01, RR 2.84). In patients without circulating antithyroglobulin or antimitichondrial antibodies the frequencies of HLA-A2 and B17 were increased when compared to those with antibodies or to the controls. In patients with and without clinically evident infiltrative ophthalmopathy the frequencies of HLA antigens were similar. In 62 Caucasian patients with Graves' disease, no antigens or phenotypic combinations occurred with increased or decreased frequency when compared to 278 controls.
Analysis of the frequencies of 9 HLA antigens and phenotypic combinations common in Caucasians but rare in Blacks revealed that only two antigens (A2 and B8) occurred with increased frequency in Black patients, suggesting that a contribution of Caucasian genes to the Black thyrotoxic subjects was unlikely.
Similarly, only one common Black antigen (A28) of 8 common antigens and phenotypic combinations, occurred in Caucasian patients with a frequency similar to that of Black controls. Thus it is unlikely that Black genes contributed to the lack of a significant increase of HLA antigens in the Caucasian thyrotoxic patients. The possession of HLA-B7-Bw42 CREG or related genes may be a protection against Graves' disease in Black Africans.     

Gene frequencies of the HPA-1 to 6 and Gov human platelet antigens in Thai blood donors

Human platelet alloantigens (HPA) are important in neonatal alloimmune thrombocytopenia (NAIT), posttransfusion purpura (PTP), platelet transfusion refractoriness, passive alloimmune thrombocytopenia, and transplantation-associated alloimmune thrombocytopenia. Thus, HPA genotyping is essential in diagnosis and treatment. We analyzed HPA-1 to 6 and Gov alleles, using PCR with sequence specific primers (PCR-SSP) in 500 Thai blood donors who had been HLA class I antigen typed. HPA-4a was present in all samples. HPA-1b, -2b, -5b, and -6b were rare, and HPA-4b was not found. HPA-3a and -3b showed frequencies of 56.0 percent and 44.0 percent, respectively. Gova and Govb showed frequencies of 49.1 percent and 50.9 percent, respectively. The prevalence rates of HPA-1 to 6 gene frequencies (GFs) were consistent with those of other Asian populations rather than those of Caucasians. We also report on the GFs of Gova and Govb, which also are comparable to those of Asian populations. Our results could establish a useful HPA- and HLA-matched plateletpheresis donor file and provide an improvement of platelet alloantibody detection in alloimmune thrombocytopenic patients, and, therefore, a more effective platelet transfusion program.