新生儿溶血病Rh血型免疫性抗体检测的分析

目的:探讨母婴Rh血型不合免疫性抗体的特异性及其效价对新生儿溶血病(HDN)的影响。方法:采用血型血清学检测技术对母婴进行ABO及Rh血型鉴定,对15例母婴Rh血型不合HDN患儿的血标本进行直接抗球蛋白试验、抗体游离试验和抗体放散试验,采用间接抗球蛋白试验对患儿及其母亲的血清进行ABO以外血型不规则抗体筛选、特异性鉴定及效价测定。结果:在15例Rh HDN患儿中检出抗-D 4例(26.7%),抗-E 6例(40.0%),抗-cE 3例(20.0%),抗-Ce 2例(13.3%);Rh血型免疫性IgG抗体效价为1∶8～1∶128。结论:产前对孕妇夫妇进行ABO、Rh血型鉴定及Rh血型免疫性抗体筛查及特异性鉴定,产后对患儿及时进行检测诊断和治疗,对减少HDN患儿的受害程度和保证优生优育均有重要的临床意义。     

1627例新生儿红细胞抗体筛查和鉴定试验的分析

目的红细胞血型抗体（即不规则抗体）筛查和鉴定试验在新生儿溶血病中的意义。方法采用微柱凝胶技术对1627例新生儿进行ABO、Rh血型定型、直接抗人球白试验、游离抗体测定、放散试验,红细胞血型抗体筛查试验,检测出6例有ABO以外的抗体,进一步用盐水、聚凝胺法、抗球蛋白试验进行抗体鉴定。结果6例红细胞血型抗体筛查阳性,进一步抗体鉴定,检测出抗-D4例,抗-E1例,抗-c1例。结论根据红细胞血型抗体的特性,可为患儿选择无相应抗原的血液进行换血和治疗。     

母婴血型不合HDN患儿致敏红细胞的抗体特异性

目的:调查母婴血型不合新生儿溶血病(HDN)患儿致敏红细胞的抗体特异性,比较不同抗体致敏新生儿红细胞所致HDN的血型血清学特征.方法:对黄疸新生儿,鉴定母婴血型,做新生儿红细胞直接抗球蛋白试验(DAT),检测母婴血浆及新生儿红细胞放散液中可致敏新生儿红细胞的血型抗体以诊断HDN.结果:血型血清学诊断为HDN的252例患儿中,致敏红细胞的抗体分别为:抗-A 40例、抗-B 40例、抗-A 抗-AB 92例、抗-B 抗-AB 65例、抗-AB 4例、抗-A 抗-M 1例、抗-M 3例、抗-c 1例、抗-cE 1例、抗-E3例、抗-D 2例;由ABO血型抗体及抗-M所致HDN者DAT多为阴性或弱阳性,由Rh血型抗体致HDN者DAT均为强阳性,ABO、Rh血型抗体及抗-M致HDN患儿红细胞热放散液中致敏红细胞的抗体效价均高于血浆游离抗体.结论:被调查的HDN患儿绝大多数由来自O型母亲的IgG抗-A、抗-B及抗-AB所致,其次为抗-M及抗-E,由抗-D引起的HDN呈逐步减少的趋势.     

黄疸患儿血清学检测时间对诊断新生儿溶血病的影响

目的对黄疸患儿进行血型血清学检测分析,并探讨血清学检测时间对诊断新生儿溶血病的影响。方法选择2014年1月~5月临床送检母亲为O型、出生1~10d的高胆红素血症黄疸患儿血标本212例,进行患儿红细胞直接抗人球蛋白试验、血清游离抗体试验、红细胞抗体放散试验。结果 212例患儿中,直接抗人球蛋白试验阳性4例(1.9%),游离抗体试验阳性24例(11.3%),放散试验阳性33例(15.6%),未检出ABO以外抗体;出生1~3d、4~7d的新生儿血清学检测阳性率明显高于7d以上的阳性率,放散试验阳性患儿总胆红素明显高于阴性患儿,差异有统计学意义(P0.05)。结论黄疸患儿血清学检测时间与新生儿溶血病检出率密切相关,早期检测,早期确诊,能够为新生儿溶血病的治疗争取时间,对防止胆红素脑病、减低新生儿溶血病后遗症的发生具有重要意义。     

新生儿溶血病红细胞血型免疫性抗体的特异性分析

目的:观察母婴血型不合新生儿溶血病(HDN)红细胞血型免疫性抗体的检出率及其特异性.方法:采用试管法和微柱凝胶法对母婴血标本进行ABO、Rh血型鉴定及不规则抗体筛查,对有黄疸症状的新生儿血标本进行直接抗人球蛋白试验、抗体游离试验、抗体放散试验、抗体特异性鉴定及其效价测定.结果:在298例由红细胞血型免疫性抗体引起的HDN患儿中,检出抗A 62例(20.8％),抗B 65例(21.8％),抗A+抗AB 87例(29.2％),抗B+抗AB 6例(2.0％);抗M4例(1.3％),抗N1例(0.3％);抗D4例(1.3％),抗E7例(2.3％),抗cE 3例(1.0％).由ABO及MN血型免疫性抗体引起HDN者,直接抗人球蛋白试验多为弱阳性,由Rh血型免疫性抗体引起HDN者,直接抗人球蛋白试验多为强阳性;微柱凝胶法的凝集强度高于试管法;HDN患儿出生后24 h内阳性检出率为91.5％.结论:HDN血型免疫性抗体的特异性主要为ABO系统的抗A、抗B、抗AB,其次为Rh系统的抗E、抗D、抗cE及MN系统的抗M、抗N.     

41例新生儿溶血病患者血型血清学检测结果分析

目的：探讨不同的免疫性血型抗体与新生儿溶血病的关系,为新生儿溶血病提供诊断依据。方法采用微柱凝胶技术对41例新生儿溶血病的患者进行ABO血型、Rh(D)血型、直接抗人球蛋白、游离、放散和不规则抗体筛查及抗体鉴定试验,确定患者体内是否有免疫性IgG抗体及IgG抗体特异性。结果41例新生儿溶血病患者中,ABO血型不合者38例,占92.68%,其中由免疫性IgG抗原A抗体引起者21例,由免疫性IgG抗原B抗体引起者17例。Rh血型不合者3例,占7.32%,其中2例由抗-D引起,1例由抗-E引起。41例新生儿溶血病的患者中,直接抗人球蛋白试验阳性者20例,阳性率为48.78%,游离试验阳性者36例,阳性率为87.80%,放散试验阳性者41例,阳性率为100%。结论母婴血型不合的新生儿溶血病主要发生于ABO血型系统,以母亲为O型,患者为A型或B型最为常见;放散试验对新生儿溶血病的诊断最有价值。     

IgGA(B)抗体与新生儿溶血病关系的探讨

目的探讨IgGA(B)抗体与新生儿溶血病的关系。方法对2693例新生儿黄疸症状的患儿作ABO、Rh(D)血型检查,直接抗人球蛋白试验、游离抗体测定及放散试验。结果在2693例患儿中母婴ABO血型不合所致新生儿溶血病有334例,母婴O/A所致的HDN为161例,O/B所致的HDN为171例,A/ABHDN1例,B/ABHDN1例。结论对新生儿黄疸患儿及时进行ABOHDN血型血清学检测,有助于早期诊断及时诊治。     

新生儿溶血病ABO血型免疫性抗体检测分析

目的:探讨血型免疫性IgG抗体对母婴ABO血型不合新生儿溶血病的影响.方法:采用抗人球蛋白法、微柱凝胶法对临床有新生儿高胆红素血症的患儿进行血型血清学检测,对母婴ABO血型不合的患儿血标本进行直接抗人球蛋白试验、抗体游离试验和抗体放散试验,检测免疫性IgG抗体的特异性.结果:在476例临床有新生儿高胆红素血症的患儿中,由母婴ABO血型不合引起的新生儿溶血病为59.5%(283/476).其中直接抗人球蛋白试验阳性率为31.4%(89/283),抗体游离试验阳性率为79.5%(225/283),抗体放散试验阳性率为100%(283/283);在283例ABO新生儿溶血病中,由IgG抗A引起者占48.1%(136/283),由IgG抗B引起者占51.9%(147/283).结论:ABO血型为A型或B型的分布与新生儿溶血病的发病率无显著性差异.     

IgG抗-D致新生儿溶血病七例分析

目的 了解IgG抗-D抗体与新生儿溶血病关系。方法 采用盐水法检测患儿和其父母Rh血型，采用直接抗人球蛋白试验、游离抗体试验、放散试验检测ABO以外的抗体，采用微柱凝胶间接抗人球蛋白试验进行抗体鉴定。结果 通过母婴血型血清学检查，检出IgG抗-D7例。结论 一旦证实有IgG抗-D，及时为新生儿溶血病患儿选择相合的血液进行换血和综合治疗，其疗效显著。     

抗球蛋白试验及抗体放散试验在脐带血检验的应用研究

为了早期诊断新生儿溶血病 (HDN) ,本文随机对本院妇产科的 90 8例新生儿脐带血做了抗球蛋白 (coombs)试验和抗体放散试验。结果 :在母子ABO血型不相配合的 2 2 2例新生儿脐带血中 ,有 2 5例直接Coombs试验或抗体放散试验阳性 ,以母子血型O -A(B)组合为主。经跟踪检验 ,这 2 5例阳性的患儿中有 15例 (6 0 % )发生高胆红素血症 ,直接Coombs试验(DAT)和抗体放散试验与间接Coombs试验 (IAT)在HDN诊断方面有很好的相关性。结论 :脐带血Coombs试验和抗体放散试验是早期诊断HDN的有效方法 ,应进一步推广使用     

1 350 例新生儿溶血三项试验的血清学检测分析

目的:探讨由母婴血型不合引起的新生儿溶血病(HDN)的血型分布及其溶血三项试验在HDN 诊断中的价值。方法:对2014 年1 月到2016 年1 月临床送检的O 型或Rh 阴性的产妇脐带血标本及高胆红素血症的新生儿血液标本用微柱凝胶检测卡进行溶血三项试验,并对结果进行统计学分析。结果:(1)1 350 例标本中,母婴血型不合者占918 例,确诊为HDN 的有569 例, 阳性率为62.0%。569 例HDN 三项试验结果为:直抗试验阳性率为27.9% (159/569),游离抗体试验阳性率为86.5%(492/569),抗体释放试验均为阳性。其中直抗阴性+游离阳性+释放阳性的组合与其他各组合相比有统计学差异(P<0.05)。(2)918 例血型不合标本中,ABO HDN 阳性率为73.8%(551/747),Rh HDN 阳性率为10.5%(18/171),两者差异有统计学意义(P<0.05)。(3)747 例ABO 血型不合标本中,A 型阳性率为80.0% (280/350),B 型阳性率为68.3% (271/397),两者差异有统计学意义(P<0.05)。(4)171 例Rh 血型不合标本中,Rh D 阳性率为17.7% (14/79),Rh E 阳性率为6郾8%(4/59),Rh C 阳性率为0(0/33),三者差异有统计学意义(P<0.05)。结论:抗体释放试验敏感度最高,是判定HDN 最有力的证据。母婴ABO 血型不合引起的HDN 发生概率明显高于Rh 不合,A 型血患儿发生HDN 的概率明显高于B 型血患儿,Rh D 不合引起的HDN 发生概率明显高于Rh E 和Rh C。     

新生儿Rh溶血病的检查分析与晚期贫血

目的对11例Rh新生儿溶血病血清抗体进行分析。方法采用直接抗人球蛋白试验、游离抗体试验、放散试验检测ABO以外的抗体，采用微柱凝胶间接抗人球蛋白试验进行抗体鉴定。结果11例新生儿Rh溶血病中检出抗-D7例，抗-E3’例，抗-E、C1例，其中1例抗-E新生儿溶血病患儿发生了晚期贫血。结论根据不规则抗体的类型，及时为新生儿溶血病患儿选择相合的血液进行换血和综合治疗，其疗效显著。同时提醒大家要注意新生儿溶血病患儿有发生晚期贫血的可能。     

Anti-Jk3 with no clinical evidence of HDN

A sample was submitted to a reference lab from a 27-year-old Asian female, gravida 4 para 1, for antibody identification. Anti-Jk3 with an IgM component was identified. Subsequently, the antibody was eluted from the infant's cord and venous red blood cells. Normal bilirubin and hematocrit levels ruled out hemolytic disease of the newborn (HDN). Anti-Jk3 has been implicated in two cases of mild HDN. In this case, this noncomplement-binding antibody caused a positive direct Coombs test without clinical signs of HDN.     

流式细胞术在母婴血型不合新生儿溶血病检测中的应用

目的建立流式细胞仪检测母婴血型不合新生儿溶血病（HDN）的方法。方法对临床送检的115例拟诊新生儿溶血病标本以流式细胞仪进行直接抗人-IgG试验、血清游离抗体检测及红细胞放散液抗体检测3项试验，选择FITC标记的单克隆二抗作为与红细胞特异性抗体结合的抗体。同时以试管抗球蛋白法进行3项试验作为对照，比较两方法的差异。结果建立了以流式细胞仪检测新生儿溶血病的实验方法：细胞采集比例为54．5％；阴性阈值2％；流式法对ABOHDN和RhHDN的检测阳性率分别为86％和100％。试管法检测阳性率分别为50％和100％。结论流式法具有敏感性高，特异性强，结果易判定，客观、标准等优点，为新生儿溶血病检测提供了一种可靠的诊断依据。     

母儿ABO血型不合孕妇血清IgG抗体效价与新生儿溶血的相关性分析

目的探讨母亲孕期血型血清学的IgG抗体效价与新生儿ABO溶血病(HDN)的关系。方法选取2005年1月～2009年12月在我院分娩的2168例ABO血型不合孕妇及其新生儿为研究对象。以分娩前孕妇最后一次IgG抗A(B)效价值为标准,效价≥1∶64者列为研究范围。新生儿HDN则观察溶血3项筛查指标及其红细胞、血红蛋白、网织红细胞等。结果 2168例ABO血型不合孕妇中血清IgG抗体效价1∶64有710例,1∶128有800例,1∶256有519例,效价≥1∶512有171例。HDN发病患儿共529例。2次及以上妊娠孕妇的抗A、抗B抗体效价值大于1次妊娠者,差异有显著性,P<0.05;年龄30-40岁组孕妇的抗A和抗B抗体效价高于21-29岁组,差异有显著性,P<0.05;母亲IgG抗A或抗B抗体效价与新生儿ABO溶血的发生率相关,r=0.8119,P<0.05。结论孕妇血清中血型免疫性抗体IgG是引起HDN的主要原因,且随着IgG抗体效价的增高,HDN的发病率也增高,但不是HDN发病的唯一因素,妊娠次数的增多、年龄增大、不良生育史等因素可加重IgG抗体效价对HDN的发生。     

Direct enzyme linked antiglobulin tests (ELAT) for detecting in-vivo sensitized erythrocytes: evaluation of screening for ABO incompatibility of newborn

ABO incompatibility of the newborn is one instance where immune hemolysis may present with a negative direct antiglobulin test (DAT) and therefore a simple sensitive test for detecting sensitization would be useful in this clinical situation. To evaluate the usefulness of ELAT in detecting in-vivo sensitized red cells, 1608 maternal-baby pairs were screened for ABO incompatibility over a period of 10 mth. Of 251 ABO-incompatible babies, there were 49 (19.5%) with positive DAT, but an additional 67 (26.7%) were ELAT positive. These were eluate positive as well, indicating that the increased number with sensitized cells as shown by ELAT is due to detection of in-vivo sensitized cells. The positive predictive value for ABO hemolytic disease of the newborn (HDN) is 48%, which is two times that of DAT. Calculating the difference of the absorbance from baseline (delta OD) may give an indication of degree of sensitization which together with the maternal antibody titre would aid us in the estimation of antigen dosage on the baby's red cells and in the appraisal of the role of antigen dosage in HDN.     

Significant ABO hemolytic disease of the newborn in a group B infant with a group A2 mother

ABO hemolytic disease of the newborn (HDN) occurs almost exclusively in infants of blood group A or B who are born to group O mothers because IgG anti-A or -B occurs more commonly in group O than in group A or B individuals. We report a case in which clinically significant ABO-HDN occurred in a group B neonate from anti-B of a group A2 mother. The IgG anti-B titer was much higher (256) than that found in a group A1 mother/infant control group (相似文献   

After 70 years,serological RhD determination remains a challenge: DNA to the rescue

After ABO system antigens, RhD is the most clinically significant blood group antigen. This is reflected in its high immunogenicity and potential to cause haemolytic transfusion reactions (HTR) and severe haemolytic disease of the newborn (HDN). Thus, correct determination of the RhD antigen is essential for a safe transfusion strategy and adequate indications of anti‐D immunoglobulin prophylactic administration. The RhD determination challenge started in 1939 with a case history of fatal HDN and HTR in a mother who was transfused with her husband′s blood. Subsequent findings of an antibody reacting with 80% ABO compatible red blood cells (RBCs) in the serum of the afflicted woman lead to the hypothesis that the mother was lacking an antigen present on the father's and fetal RBCs and that her production of a corresponding antibody was responsible for both HDN and HTR. This hypothesis was proven to be correct. The following year, the effort to determine the origin of a causal antigen coincided with an animal immunization experiment where a similarly reacting antibody developed by injecting Rhesus monkey RBCs into rabbits and guinea‐pigs, as well as with another publication of HTRs after ABO compatible blood transfusions in patients with antibodies of apparently identical specificity. This first challenge in the ‘pre‐DNA’ era was slightly erroneously named in humans as the anti‐Rhesus antibody, and 20 years later, the animal antibody was designated anti‐LW. Meanwhile, the complexity of Rh group of antigens increased and several genetic models were suggested to explain it: Rh‐Hr single gene, three genes C, D and E and finally a two locus model (which a few years later was shown by molecular analysis to be the accurate one). At the beginning, serological determination of RhD was performed using human anti‐D, first by direct agglutination (IgM), later also using the Coombs’ test (IgG). Weak D antigens were a challenge at the time: the term ‘D^U’ (now obsolete) was used for those antigens negative in direct agglutination and positive in the Coombs’ test. Weakening of the D antigen could be caused indirectly by the ‘position effect C in Trans’ or directly (mutations in the RHD gene, usually point mutations coding for amino acids in transmembranous and intracellular parts of the polypeptide). Extremely weakened D antigens are called D_el, and these are serologically detected only by adsorption/elution tests (multiple genetic mechanisms). The next challenge came in the 1960s, with the observation of qualitative D variants – partial D antigens. The first cases were detected after the development of allo‐anti‐D in D‐positive individuals – immunized against that part of the D protein missing in their D epitope mosaic. Mutual reactivity of anti‐D from these individuals with different partial D antigens established the basis for their classification. The increase in partial D types accelerated dramatically after the development of the mouse hybridoma technique and the production of numerous different monoclonal anti‐Ds. According to patterns of reactivity of different partial Ds after two international workshops, the number of D epitopes reached 30. DNA techniques subsequently helped refine discrimination between partial D types. The number of described D antigen variants will surely rise after this ISBT congress and Working Party meeting. A further increase can be anticipated once NGS will provide new information and more data will come from large Asian and African populations and the polymorphic complexity of RhD and the whole Rh system will expand.     

全自动血型仪检测ABO血型正反定型不符原因分析及处理策略

目的 探讨在鉴定ABO血型中全自动血型仪正反定型不符的原因,并探寻解决对策。方法 对2017年10月~2018年8月遂宁市中心医院血型仪检测的298例ABO血型正反定不符的标本进行分析,同时结合试管法、抗人球蛋白实验、吸收放散实验、不规则抗体鉴定结果及病史资料分析定型不符的原因并进行归类。结果 298例正反定型不符标本准确鉴定后归纳分为4类:可被纠正类型（标本、人员操作、试剂和仪器原因）占24.16%;抗原原因占7.38 %,其中包括抗原减弱以及ABO亚型;抗体减弱占31.88%,包括抗体合成不足（如婴幼儿）,抗体缺失（如老年人和肿瘤患者）,意外抗体等;其他原因占36.58%,主要包括自身免疫性溶血性贫血、冷凝集素综合症、高球蛋白血症等。结论 鉴定血型前标本质量控制、仪器定期的保养维护以及试剂红细胞的更换可以有效减少正反定型不符,抗体合成不足、自身免疫性疾病以及冷凝集素综合症是导致ABO正反定型不符的主要原因。建议院方根据可能原因进行相关确认实验,准确鉴定ABO血型从而保证患者输血安全。