避免抗-Dia抗体漏检的临床分析与处理

目的鉴定1例不规则抗体导致的交叉配血不合。方法通过选择合适的抗体筛查细胞和谱细胞进行抗体鉴定检测不规则抗体,通过血清学及分子生物学手段检测红细胞表型。结果患者血清中同时存在IgG抗-E和IgG抗-Di~a抗体。抗-E抗体、抗-Di~a抗体效价分别是4和16。结论患者血清中的抗-E、抗-Di~a抗体是导致交叉配血不合的原因。合理选择抗体筛查细胞和谱细胞对输血前患者进行不规则抗体筛查和鉴定,是避免发生迟发型免疫性溶血性输血反应的重要保障。     

抗Dia合并抗E抗体致交叉配血不合的临床分析

目的：探讨交叉配血中抗 Dia 合并抗 E 抗体致配血不合的原因。方法对该院1例因抗 Dia 合并抗 E 抗体致多次配血不合的患者进行分析。通过血型鉴定、直接抗人球蛋白试验、不规则抗体筛查、吸收放散实验来确定患者的血型、可能的不规则抗体、细胞谱反应格局。结果患者血型正定型：抗 A 抗体（－）、抗 B 抗体（－）;反定型：Ac（＋＋＋＋）、Bc（＋＋＋＋）、RBC （－）、Oc（－）;Rh 血型定型：抗 c 抗体（－）、抗 C 抗体（＋＋＋＋）、抗 D 抗体（＋＋＋＋）、抗 e 抗体（＋＋＋＋）、抗 E 抗体（－）。直接抗人球蛋白试验（－）。患者血清中含有抗 E、抗 c 抗体。结论患者血清中的不规则抗体是导致交叉配血不合的重要原因。     

抗球蛋白试验在疑难交叉配血过程中的重要性分析

目的通过对患者输血前血样进行抗球蛋白试验检查,查找导致临床患者配血不合的原因,配合性输注,确保临床输血安全。方法通过不规则抗体筛选试验,检测患者血清中抗体性质。结果 61例交叉配血不合患者抗球蛋白试验结果显示,由温、冷性自身免疫性抗体及冷凝集素影响配血不合30例;ABO血型系统以外不规则抗体同种免疫性抗体31例,由Rh血型系统同种免疫性抗体导致配血不合占大多数,其中与抗-E抗体有关的患者17例,占由同种免疫性抗体引起配血不合的54.84%。结论患者体内产生的ABO血型系统以外不规则同种免疫性抗体或者温、冷性自身免疫性抗体及冷凝集素等几种因素的影响,是造成临床交叉配血不合的主要原因,Rh血型抗原的复杂性和多态性应引起临床的重视,Rh血型同型输注可降低输血不良反应的发生率。     

抗-E合并抗-Dia致疑难配血试验分析

不规则抗体是指除抗-A、抗-B红细胞以外的血型抗体。不规则抗体是导致溶血性输血反应、新生儿溶血病、疑难配血及血型鉴定困难的主要原因[1-2]。对献血员和患者进行抗体筛选,可避免因为找不到相合的血液给患者而延误治疗,因此抗体筛查试验在临床配血中非常重要。引起临床疑难交叉配血最常见的抗体是Rh血型系统的相关不规则抗体,该系统不规则抗体可单独存在,也可以联合其他抗体的形式存在。本实验室在工作中发现1例抗-E合并抗-Dia引起的交叉配血不合,现将试验分析过程报道如下。     

IgG抗-E、抗-c致配血不合原因分析

引起交叉配血不合的原因较多,主要有:(1)技术因素;(2)血清抗体因素;(3)红细胞抗原因素。究其原因:(1)实验操作不认真,标本张冠李戴,试剂管理紊乱,实验结果观察不仔细等人为因素;(2)患者反复输血、妊娠等产生的不规则抗体及自身免疫性疾病患者血清中自身抗体所引起的交叉配血不合;(3)血浆蛋白紊乱、冷凝集素及某些药物因素使红细胞聚集,干扰交叉配血结果,也可引起交叉配血不合[1-3]。现就1例长期反复输血患者配血时出现交叉配血不合进行原因分析,目的是避免由于交叉配血不合而延误对患者的输血救治。     

抗-A1、抗-Ce、抗-M引起交叉配血不合1例

临床输血工作中交叉配血不合多由不规则抗体引起，在多数情况下抗体性质比较单一，鉴定较为容易。笔者在工作中发现1例抗-A1、抗-Ce、抗-M引起的交叉配血不合患者．现报告如下。     

高效价低频抗-Mur漏检致疑难配血及其处理

目的 通过研究1例高效价低频抗-Mur漏检导致疑难配血的处理思路与方法，提高对MNS血型系统的认识，确保临床输血的安全。方法 对交叉配血主侧不合的献血者进行直接抗人球蛋白试验，检测患者血清的不规则抗体，更换不同的患者与该献血者及不同的献血者与该患者重复交叉配血，对不规则抗体常规筛查“阴性”的患者追加谱细胞检测并根据阳性反应格局来确定抗体的类型及特异性，测定抗体效价，运用荧光PCR法对患者MNS血型系统进行基因分型。结果 交叉配血主侧4+、次侧-,更换不同患者和献血者多次交叉配血结果均相合。该献血者直接抗人球蛋白试验为阴性。患者血清中存在(IgG+IgM)型抗-Mur, IgG抗体效价128,IgM抗体效价16,MNS血型系统基因分型结果为M(+)N(+)S(-)s(+)Mur(-)。结论 不规则抗体筛查细胞存在局限性，可导致抗-Mur等低频抗体的漏检。交叉配血主、次侧不合时，我们要多方寻找原因。即使不规则抗体筛查结果呈阴性，我们也需根据不同介质、实验条件，追加谱细胞进行抗体特异性鉴定以避免低频抗体的漏检，保障临床输血的安全性和有效性。     

35例疑难交叉配血患者血清中不规则抗体结果分析

目的了解临床患者血清中不规则抗体对交叉配血不合的影响。方法通过不规则抗体筛选试验,检测患者血清中抗体性质。结果 35例交叉配血不合患者血清中,抗-E抗体13例、抗-Ec抗体4例、IgG抗-D抗体1例、抗-Ce抗体1例、抗-c抗体1例、抗-e抗体1例、抗-M抗体4例、抗-Mur抗体1例、无规律ABO系以外不规则同种免疫性抗体9例。结论有多次输血史、妊娠史患者体内容易产生ABO系以外不规则抗体,而Rh血型系统同种免疫性抗体是造成临床配血不合的主要原因之一。     

抗-Ec合并抗-M抗体致疑难配血实验分析

不规则抗体是指ABO血型抗体以外的血型抗体,而有临床意义的不规则抗体会导致机体发生溶血性输血反应[1]。不规则抗体的出现是引起ABO血型鉴定困难和配血困难的主要原因,而其中最常见的是与Rh血型系统相关的不规则抗体,该系统不规则抗体可单独存在,也可以联合其他抗体共同存在。本课题组在工作中发现1例由抗-Ec合并抗-M抗体引起的正反定型不符及交叉配血不合,现将试验分析过程报道如下。     

多次输血产生抗-E、抗-c联合抗-Wra抗体致疑难配血一例

正临床患者在输血前进行不规则抗体筛查试验,不规则抗体是引起临床配血不合的主要原因。对于不规则抗体筛查阳性患者,需进行进一步的抗体鉴定,确定抗体特异性,然后选择相应抗原阴性的献血者红细胞进行输注,保障临床输血安全。本实验室发现一例抗-E、抗-c联合抗-Wra抗体导致配血不合,现报道如下。材料与方法1 标本来源患者何某,女,71岁,临床诊断T-细胞大颗粒淋巴细胞白血病,上呼吸道感染,重度贫血入院,Hb 24 g/L,     

745例患者疑难交叉配血检测结果分析

目的：回顾性分析本地区导致临床输血交叉配血不相合产生的原因,为预防溶血性输血反应,保障临床输血安全,拯救病人提供有效依据。方法：对2006-2013年番禺、南沙两区各医院因交叉配血困难而送检的标本745例检测结果进行血型鉴定、不规则抗体筛选和鉴定、交叉配血。结果：ABO血型不合引起的交叉配血不相合15例、血浆蛋白异常引起的交叉配血不相合33例,血型不规则抗体引起的151例。其中ABO血型不合引起配血不相合的A亚型12例,B亚型3例;不规则抗体引起配血不相合分别是：自身抗体57例,药物抗体7例,同种特异性抗体87例．分别为：抗-E31例、抗-cE12例、抗-c5例、抗-Ce1例、抗-M10例、抗-Mur9例、抗-E伴抗-Mur3例、抗-Le^a 5例、抗～Le^b 3例、抗-P16例、抗-Jk^b 2例。结论：本地区导致交叉配血不相合的原因主要是同种不规则抗体,异常血浆蛋白次之,最后是ABO亚型。同种不规则抗体以1Kh血型系统的抗体为主,抗-E比例最多;建议交叉配血试验不配合时,应考虑ABO血型定型是否错误,排除异常血清蛋白影响,开展不规则抗体筛选和鉴定,建立Rh系统数据库,选择相合的血液输注,预防免疫性输血反应,保障临床输血安全。     

低频率抗Mur抗体引起溶血性输血反应的调查研究

目的研究抗Mur抗体血型血清学特征，调查其在输血医学中临床意义。方法对2例患者的血清，与已知血型的试剂红细胞和4个已知Mur抗原，在盐水介质、低离子间接抗球蛋白介质，分析鉴定出其抗体的特异性。结果这2例患者与已知血型的试剂红细胞在多种反应介质中的反应结果显示患者血清中含有抗Mur抗体，患者血清与4个已知Mur抗原的反应证实该例抗体只与Mur抗原反应。结论该例同种抗体为特异性抗Mur抗体，在临床会引起溶血性输血反应。在东方人群中Mihenberger血型抗体常规筛选鉴定值得探讨。     

大量输注多种抗体红细胞但无不良反应的输血分析

目的分析一例临床配血不合的不明抗体的成分和来源,探讨大量输注配血不合红细胞而没有导致输血不良反应的原因。方法对患者血浆做血型鉴定、直抗、抗筛、抗体鉴定和抗体效价测定等血清学试验。结果患者血浆中同时存在效价高达1∶1024的抗-I为主的多种抗体,包括特异性抗体和药物抗体且已激活补体,造成配血不合。结论大量配血不合红细胞的输注并没有引起明显输血不良反应,临床输血应根据患者病情灵活调整输血方案。     

疑难交叉配血分析和对策

目的分析交叉配血不合的原因,探讨处理方法,寻求使患者有效、安全输血治疗的对策。方法采用凝疑胺介质和微柱凝胶抗人球蛋白方法交叉配血,选用多种抗体筛选细胞和谱细胞,进行抗体特异性鉴定,以吸收放散试验和2-巯基乙醇试验,鉴别自身抗体和同种特异性抗体。结果共收集231例交叉配血不合案例。其中交叉配血不合由不拱则抗体引起的102例、未捡出不规则抗体的59例、同时存在不规则抗体和自身抗体的70例。结论对于A、B、O、RhD同型输血引起的交叉配血不合,根据引起交叉配血不合的不同因素,采用合理的交叉配血流程与方法,可明显提输血疗效,减少输血不良反应。     

自制Coombs微柱凝胶卡的临床应用研究

目的探讨自制Sephadex-G50Coombs微柱凝胶卡应用于稀有血型抗体筛选和新生儿溶血病检测的可行性。方法以Sephadex-G50凝胶为载体,制备Sephadex-G50Coombs微柱凝胶卡。取无偿献血者血清与稀有血型(Mur)抗原阳性红细胞加入凝胶卡反应腔,37℃孵育后15min离心,观察结果。再取阳性反应者血清,用2-Me灭活IgM型抗体后,重复前述步骤,以确定是否含IgG型抗-Mur。取新生儿血液标本,进行直抗实验、游离抗体实验和放散液抗体检测实验。结果 2 600名无偿献血者中,检出1例IgM型抗-Mur。246例新生儿溶血病标本中,检出ABO溶血病210例,RhD溶血病5例,RhE溶血病2例,抗-M和抗-Jka引发的溶血病各1例。自制凝胶卡与进口凝胶卡检测结果一致。结论自制Sephadex-G50Coombs微柱凝胶卡与进口凝胶卡检测结果差异无统计学意义,且具有成本低、工艺简单的特点,可用于血型血清学临床实验。     

不规则抗体筛查在临床输血中的意义探讨

目的探讨通过抗体筛查和鉴定,发现有临床意义的不规则抗体,以避免不规则抗体引起的溶血性输血反应发生,并选择相合的血液,确保患者输血安全。方法采用微柱凝胶抗人球蛋白法检测978例神经外科择期手术需要输血患者的血清（浆）不规则抗体,结果阳性的标本再送南京市血液中心进行抗体特异性进一步鉴定。对不规则抗体筛查结果进行分析。结果 978例择期手术患者的不规则抗体筛查发现不规则抗体阳性6例,阳性率0.61%。筛检阳性的6例标本经南京市血液中心进行抗体特异性鉴定,发现在6例不规则抗体阳性患者中抗-E 3例、抗-D 1例、抗-cE 2例。对6例不规则抗体阳性患者提示少输或不输血,其中2例未输血,4例输注经南京市血液中心配合型血液,无1例发生溶血性输血反应。结论在输血前对受血者进行不规则抗体筛查可发现有意义的不规则抗体,以及选择和准备相适合的血液,防止溶血性输血反应。这对确保临床输血安全具有重要的意义。     

Anti-i cold agglutinins in a patient with Wiskott-Aldrich syndrome binding study with membrane glycosphingolipids

An unusual isohemagglutinin caused blood incompatibility in a patient with the Wiskott-Aldrich syndrome after nine transfusions. The patient's serum agglutinated erythrocytes of all the donors examined. The antibodies were cold agglutinins which agglutinated adult and cord erythrocytes equally. The binding of these antibodies to glycosphingolipids was analyzed by thin-layer chromatogram immunostaining and solid phase radioimmunoassay. The results indicate that the antibodies in the patient's serum bound specifically to lactonorhexaosylceramide and sialosyllactonorhexaosylceramide, glycolipids known to carry the i antigenic determinant. The antibodies did not bind to neolactotetraosylceramide, sialosylneolactotetraosylceramide or lactoisooctaosylceramide (I-active glycolipid). The patient's serum immunostained several components in the acidic glycolipids from OI erythrocytes. The antibody activity was predominantly present in IgG but the IgM showed similar binding specificity. Hemagglutination of OI erythrocytes with the patient's serum could be inhibited with lactonorhexaosylceramide. These results showed that the patient's antibodies recognized the i determinants carried by membrane surface glycolipids. The production of anti-i antibodies in the patient is intriguing in view of the decreased antibody response to carbohydrate antigens and deficient isohemagglutinins which have been generally observed in the Wiskott-Aldrich syndrome.     

Development of non‐ABO RBC alloantibodies in patients undergoing allogeneic HPC transplantation. Is ABO incompatibility a predisposing factor?

BACKGROUND: Data from the appearance of RBC antibodies other than ABO in patients undergoing HPC transplantation are limited. STUDY DESIGN AND METHODS: The incidence and specificity of non-ABO RBC alloantibodies are described in a series of 217 patients undergoing allogeneic HPC transplantation because of various hematologic malignancies. RESULTS: Eight patients (3.7%) developed 10 antibodies after transplant. None of these patients had previously been immunized. Seven patients had one RBC antibody and one patient had three RBC antibodies. Antibody specificity were anti-Jk(b) (2 patients), -Kell (2), -M (2), -Le(b) (1), and -D (1). Finally, two patients had a panagglutinin. The mean time between transplant and antibody detection was 23 days (range, 16-672). The source of the HPCs, the conditioning regimen administered, and the type of GVHD prophylaxis administered did not influence the rate of antibody formation. On multivariate analysis, ABO blood group incompatibility (p = 0.005) and patient's age (p = 0.02) were the only two variables significantly associated with the development of RBC alloantibodies. CONCLUSION: Patients undergoing allogeneic HPC transplantation are at risk of developing RBC-specific antibodies despite the immunosuppressive therapy administered. Antibody formation was more frequently observed in ABO-mismatched cases, which suggests a potential role of this incompatibility in facilitating antibody production.     

The risk of abbreviating the major crossmatch in urgent or massive transfusion

The risk of abbreviating the major crossmatch in urgent situations by issuing blood after an "immediate spin" phase was evaluated by a retrospective study of 82,647 crossmatches performed on serum from approximately 13,950 patients. Although the initial screening test for unexpected antibodies for all patients failed to show agglutination or hemolysis of the reagent red blood cells, agglutination was subsequently noted during at least one crossmatch performed for 148 of them. Further evaluation of these patients' serums indicated that most positive reactions were due to weakly reactive low thermal amplitude antibodies. Eight of the incompatible crossmatches were related to antibodies in the Kell, Kidd or Rh systems, and a ninth antibody, anti- E, was identified through subsequent evaluation of a cold antibody- induced crossmatch incompatibility. Issuance of blood in urgent situations after an "immediate spin" phase of the crossmatch, for patients whose red blood cells have been typed, and whose serums have been screened for unexpected antibodies, has a low level of risk.     

Serologic evidence that factor IX inhibitor in the plasma of hemophilia B patients detects factor IX on normal red cells

BACKGROUND: Patients with hemophilia B lack factor IX (F IX). These patients may become alloimmunized after the transfusion of F IX concentrates and may develop F IX inhibitors, which have been characterized as polyclonal IgG4 alloantibodies. Two cases in which F IX inhibitors caused difficulty in compatibility testing and antibody identification were encountered. It was hypothesized that, because F IX is present in normal plasma, it might be adsorbed by red cells in vivo and then be detected during antibody screening tests with serum containing F IX inhibitors. CASE REPORT: Sera from two African American half-brothers with hemophilia B were incompatible with all common and rare red cell phenotypes tested in the anti-human globulin test, but did not react with each other's red cells. The brothers' red cell antibodies were neutralized with both normal plasma and a commercially available F IX concentrate, which indicated that the red cell incompatibility was most probably caused by their F IX inhibitors. Red cells from an unrelated patient with hemophilia B and a very low titer of F IX inhibitor were tested against the half-brothers' sera and did not react. The compatible red cells from one of the half-brothers and the unrelated patient with hemophilia B adsorbed F IX from normal plasma or F IX concentrate after 37 degrees C incubation; this rendered them incompatible with the plasma containing F IX inhibitor from the other half-brother. CONCLUSION: F IX appears to be present on normal red cells and may be detected during compatibility and antibody identification procedures when serum or plasma containing F IX inhibitors is tested.