78例ABO新生儿溶血病筛查结果分析

目的总结我院ABO新生儿溶血病诊断经验。方法选取712例新生儿黄疸患儿及母亲血样,常规鉴定ABO血型、患儿血清学三项试验、母亲血清IgG抗-A（B）抗体效价,同时对产妇年龄、流产次数、新生儿黄疸发生的时间进行调查。结果明确ABO母婴血型不合新生儿溶血病78例,产妇年龄分布30岁以下共63例（80．8％）,有流产史共68例（87．2％）,新生儿黄疸发生3天内发生共51例（65．4％）。其中O—A型48例,O—B型30例,发病患儿母亲血清IgG抗-A（B）抗体效价1：16共0例（0％）,1：32—64共9例（11．5％）,1：128—512共56例（72．8％）,≥1：1024共13例（16．7％）。新生儿溶血病血清学放散试验阳性78例（100％）,游离试验阳性50例（64．1％）,直抗试验阳性30例（38．5％）。结论为预防ABO新生儿溶血病的发生,对孕妇做产前的ABO血型和血清IgG抗-A（B）抗体效价筛查极有必要,尤其是曾有生产史、流产史的孕妇,同时及时做新生儿黄疸的检查。     

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。     

IgM及IgG抗c^—致新生儿溶血病1例报道

由于Rh血型不合引起的新生儿溶血病(Rh HDN)屡见报道,均以抗D较为多见,而因抗c引起发生的新生儿溶血病(HDN)报道较少,就近我院发现1例IgM及IgG抗c致新生儿溶血病,现报告如下.     

新生儿ABO溶血病170例临床分析

我院新生儿科病房自 1998年 10月～ 2 0 0 2年 4月共收治新生儿ABO溶血病 170例 ,均经非换血疗法治愈 ,无胆红素脑病发生。所以临床应提高ABO溶血病的早期诊断率 ,及早进行干预和治疗 ,减少其后遗症的发生。临床资料一、一般资料 :170例均为本院产科出生 ,男 89例 ,女 81例 ;足月儿 16 4例 ,早产儿 6例 ;住院日龄 <2 4h 2 9例 ,～ 4 8h10 8例 ,～ 72h 33例 ;第 1胎 6 4例 ,第 2胎 78例 ,第 3胎 2 1例 ,第 4胎 4例 ,第 5胎 2例 ,第 6胎 1例。二、诊断标准及方法 :新生儿皮肤黄染出现早 ,进展快 ,程度重者做血清学检查。先确定母婴ABO血型…     

新生儿ABO溶血病10年病例回顾分析

我国新生儿血型不合溶血病主要为ＡＢＯ血型不合所致 ,以往传统方法待出现病理性黄疸后查母子血型 ,证明ＡＢＯ血型不合 ,再做直接抗入球蛋白试验 ,诊断过晚而造成重度黄疸增多。自开展溶血三项检查以及静脉应用免疫球蛋白以来 ,ＡＢＯ溶血病发现早 ,治疗早 ,黄疸轻 ,降低了高胆红素血症的发生率 ,从而减少了听力智力及神经系统等的后遗症。临床资料一、对象 :我院新生儿科自 1990年 1月 - 2 0 0 0年 12月10年住院ＡＢＯ溶血新生儿。其中Ａ组 1990年 1月 - 1998年 12月 ,2 4例 ,占同期产科出生儿的 0 .175 %。Ｂ组 1999年1月 - 2 0 0 0年 12…     

新生儿溶血病产前诊断与基因定型分析

目的 探讨母婴ＡＢＯ／Ｒｈ血型不合产前诊断的有效策略。方法 对ＡＢＯ／Ｒｈ血型不合孕妇,在孕期进行免疫抗体动态监测,并采用基因定型技术产前鉴定Ｒｈ基因型。结果 ５例Ｒｈ阴性具有不良孕产史孕妇在本方案中及时得到有效处理,并对她们用基因定技术进行分析;ＡＢＯ系统新生儿溶血病占一红素血症患儿的１２．６％,Ｒｈ系统,ＨＤＮ占其中的４．９‰,本文还得到２２１９例孕妇产前血清ＩｇＧ抗Ａ（Ｂ）效价分布比率概况２     

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.     

围产因素对新生儿ABO溶血病影响的探讨

目的探讨围产因素对新生儿ABO溶血病的影响。方法已证实ABO溶血病患儿按平产分娩及围产因素(包括剖宫产,胎儿宫内窘迫、羊水污染、羊水少)分娩,分Ⅰ组及Ⅱ组,所有患儿入院前采取静脉血,通过BS-400全自动生化分析仪测黄疸指数、血清总胆红素(TB)、直接胆红素(DB)进行比较。结果两组指标TB、DB采用HellingT2多元系统分析法,取Holelling-lawley Tvace统计量,所得P值=0.0287(P(0.05),说明Ⅰ组Ⅱ组两指标TB、DB的总体均值不同,两组有统计学意义。结论围产多种因素对新生儿ABO溶血病影响密切,需早期诊断,早期干预,动态观察黄疸指数,尽可能降低胆红素指数,使之处于一个较低水平,对于新生儿平稳渡过前7天高危期,降低神经系统后遗症起到了积极的作用。     

新生儿溶血病患儿母亲血清中IgG亚类水平的临床意义

目的:探讨IgG抗体亚类与新生儿溶血病发病的关系。方法:用ELISA法对89例有无新生儿溶血病新生儿母亲的血清及22例献血员的血清中IgG亚类进行定量分析。结果:发病患儿与不发病新生儿的血型及其母亲血清IgG抗体的效价均存在显著性差异(P<0.05)。IgG各亚类的水平在发病组、未发病组的母体及正常对照组之间,存在显著性差异(P<0.05)。结论:ABO血型系统中,母体血清中IgG1和IgG3的水平与新生儿溶血病的发病有关。     

ABO新生儿溶血病发病与O型血孕妇IgG抗体效价的相关分析

目的探讨黄疸患儿ABO新生儿溶血病(HDN)发病与"O"型孕妇孕期免疫性(IgG)抗体效价的相关性.方法分析60例黄疸患儿血型血清学检查及其母亲产前IgG抗A(B)效价检测结果等有关资料.结果黄疸患儿ABOHDN的发病与其母亲的免疫性抗体效价高低成正相关.结论产前检测夫妇ABO血型不合,特别是"O"型孕妇的IgG抗A(B)效价,对预防和治疗ABOHDN有积极意义.     

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。     

母儿ABO血型不合的治疗及母体血清抗体与新生儿黄疸的关系

目的 探讨母儿ABO血型不合的孕期治疗以及分娩前母体血清抗体效价与新生儿黄疸程度的关系。方法 回顾性分析62例母儿ABO血型不合患者的孕期治疗资料。62例患者采用中西医结合治疗，分为口服茵枝黄、静脉注射茵枝黄、静脉注射茵枝黄 免疫治疗组。测定治疗前后血清抗体效价下降以及新生儿血清胆红素值，采用SPSS10．0的Mann-Whitney检验。对3组治疗前后的抗体效价变化值进行两两比较的统计分析，采用SPSS10．0的直线回归(1inear regression)对分娩前母体血清抗体效价与新生儿血清胆红素值进行相关分析。结果 免疫治疗组分别与口服组(P值：抗A0．010，抗B0．024)、静脉组(P值：抗A0．027，抗B0．011)相比，治疗前后抗体效价下降具有显著性差异；分娩前母体血清抗体效价与新生儿血清胆红素值无显著相关关系，[TBILr=0．082，P=0．812；DBTLr=0．300，P=0．370]。结论 母儿ABO血型不合患者。一旦发生溶血，其严重程度并不像其发病率一般与分娩前母体血清抗体效价显著相关。为降低发病率，宜在孕期积极治疗，可采用中西医结合治疗，必要时加用免疫治疗。     

723例O型血孕妇产前IgG抗-A（B）效价对新生儿红细胞致敏的研究

目的研究O型血孕妇产前IgG抗-A（B）血型抗体的效价对新生儿红细胞致敏情况,以预防新生儿溶血病的发生。方法采用抗人球蛋白法检测723例丈夫为非O型的O型血孕妇IgG抗-A或抗-B的ABO血型抗体效价,分娩时取脐静脉血做红细胞四项试验：血型、直接抗人球蛋白试验、游离抗体检测、释放试验。结果 723份血清中IgG抗-A（B）效价≥1∶64者有168例,异常检出率为23.24%;丈夫为A型、B型、AB型者,IgG抗-A（B）异常检出率分别为26.01%、20.13%、23.53%。当孕妇IgG抗-A（B）效价≤32时,新生儿血清学检验结果均为阴性,而效价为64、128、256、≥512新生儿脐血血清学检验结果阳性率分别为7.69%、64.29%、94.12%、100.00%。结论孕妇IgG抗-A（B）效价与新生儿红细胞致敏呈正相关,是产前预报母子血型不合而引起HDN的有效方法。可及早发现,及时治疗,减少由于母婴血型不合引起的溶血病发生。     

Early detection of RhD status in pregnancies at risk of hemolytic disease of the newborn

The aim of this work was to investigate the presence of the RHD gene in fetal cells obtained from amniotic fluid. We studied 65 samples of amniotic fluid, 11 from RhD-negative mothers sensitized with anit-D alloantibodies. The fetal origin of the DNA was confirmed with the analysis of 1 VNTR locus and 3 STR loci in DNA samples from amniotic fluid and maternal blood. The RHD genotyping was performed in non-contaminated samples (n=62) using a multiplex polymerase chain reaction strategy that yields three amplification products from RhD-positive phenotypes (intron 4 of both RHCE and RHD genes and exon 10 of the RHD gene) and 1 DNA fragment from RhD-negative phenotypes (intron 4 of the RHCE gene). We genotyped 54 RhD-positive fetuses (8 from RhD-negative sensitized mothers) and 8 RhD-negative fetuses (3 from RhD-negative sensitized mothers). The fetal DNA genotyping allows the diagnosis, from a single amniocentesis, of fetuses at real risk of hemolytic disease of the newborn. When the fetus is determined to be RhD-negative invasive procedures can be avoided. Received: 17 October 2001 / Accepted: 26 May 2002     

Haemolytic disease of the fetus and newborn: advancements in precision and prevention

In pregnant patients, the impact of blood type and the presence of red blood cell antibodies influence the course of the pregnancy and the health of the fetus and newborn infant. Throughout history, haemolytic disease of the fetus and newborn has played a fundamental role in the discovery of the blood group antibodies and their cognate antigens. The mid‐1900s were noted for the advent of Rh immunoglobulin. Now, the technological advancements in diagnosis and treatment of haemolytic disease of the fetus and newborn have provided the critical tools needed to support mothers with affected pregnancies. The knowledge of blood typing has been further refined with the explosion of understanding about blood group genes, particularly in the RH blood group. Genomic blood group typing, improvements in ultrasound technology and transfusion medicine progress have advanced the field. The care of women with potentially affected pregnancies has never been more robust. Despite this, the risk to the fetus is significant, and prevention strategies for maternal alloimmunization deserve continued attention.     

Placental Transport of Maternal Immunoglobulin G in Pregnancies at Risk of Rh (D) Hemolytic Disease of the Newborn

PROBLEM: The following questions were addressed: Is the placental transport of immunoglobulin (Ig)G, IgG1, and IgG3 diminished in pregnancies at risk of hemolytic disease of the newborn? Is the placental transport of IgG, IgG1, and IgG3 correlated with the hemoglobin concentration in the fetus and AutoAnalyzer (AA) quantitations of maternal anti-D? METHOD OF STUDY: IgG concentrations were determined retrospectively in 41 paired fetal/maternal (f/m) samples in 31 Rh (D) alloimmunized pregnancies. IgG1 and IgG3 concentrations were determined in those 23 cases in which the results of fetal hemoglobin concentration and quantitations of maternal anti-D were available. The results were compared with values found in normal pregnancy and correlated with maternal anti-D AA quantitations and fetal hemoglobin concentrations. RESULTS: Fetal IgG, IgG1, and IgG3 concentrations, and the corresponding fetomaternal ratios in Rh (D) alloimmunized pregnancies, increased with gestational age according to the following formulas (obtained by simple regression): Fetal IgG = ?8.846 + 0.491.gestational age (GA), (R² = 0.544); fetal IgG1 = ?10.021 + 0.46GA, (R² = 0.463); fetal IgG3 = ?0.865 + 0.039GA, (R² = 0.327); f/m IgG = ?1.006 + 0.054?GA, (R² = 0.557); f/m IgG1 = ?1.876 + 0.085GA, (R² = 0.654); f/m IgG3 = ?0.199 + 0.026GA, (R² = 0.146). CONCLUSIONS: The placental transport of IgG, IgG1, and IgG3 in women with Rh (D) immunizations is not diminished compared with normal pregnancy. However, AA quantitations of anti-D are inversely correlated with f/m IgG ratio, f/m IgG1 ratio, and fetal IgG and IgG1 concentrations (P = 0.002, P = 0.004, P = 0.02, and P = 0.02 respectively). The placental transport of IgG3 is significantly higher in pregnancies at risk of hemolytic disease of the newborn compared with IgG3 concentrations in normal pregnancy.     

Correlation between the structure of IgG and its Fc-fragment and their ability to interact with staphylococcal protein A

Interaction between 7S monomers of rabbit IgG, dimers of molecules of this protein, IgG with disulfide bond ruptured in the hinge region of the molecule, and various fragments of IgG molecules, on the one hand, and protein A ofStaphylococcus aureus, on the other hand, were investigated by the passive hemagglutination inhibition test. Only the Fc-fragment of the rabbit IgG molecule obtained with papain was shown to bind protein A. Activity of the Fc-fragment on a molar basis was shown to be only one-sixth of that of native IgG. After repair of the disulfide bond between the chains in the hinge region of the IgG molecule, its ability to bind protein A was reduced by two-thirds. The binding activity of IgG was increased on a molar basis twelvefold as a result of its spontaneous dimerization. It is concluded from the results that the structural organization of the Fc-fragment of the IgG molecule correlates with its ability to interact with protein A.Laboratory of Immunochemistry, N. F. Gamaleya Institute of Epidemiology and Microbiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR P. A. Vershilova.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 89, No. 3, pp. 318–320, March, 1980.     

新生儿Rh溶血病的检查分析及预防

目的检查分析15例新生儿Rh溶血病及发生原因，预防新生儿Rh溶血病的发生。方法采用盐水法检测患儿和其父母Rh血型，用新生儿溶血病血型血清学检查检测新生儿Rh溶血病，用Rh抗原谱细胞鉴定孕妇血清、患儿血清和红细胞抗体放散液中的Rh系统抗体。结果15例Rh溶血病患儿中由抗D引起的溶血病有8例，由抗D和Rh其他系统抗体联合引起的有2例，共10例，占66．7％；由抗E引起的有3例，由抗E和抗C联合引起的1例，占26．7％；由抗C引起的1例，占6．7％。15例患儿母亲都曾有生产或流产或输血史。结论为预防新生儿Rh溶血病的发生．对产前尤其是对曾有过生产史、流产史或输血史的孕妇作产前夫妇Rh血型和孕妇Rh免疫性抗体筛查极有必要。     

Rh阳性个体RHD杂合性分析

目的 分析中国汉族Rh(D)阳性个体的RHD杂合性,讨论Rh阴性妇女产前Rh同种免疫预防策略.方法 血清学检测31 115名汉族捐血者的Rh(D)表型,分析Rh(D)阳性个体的RHD杂合率;对其中3628名随机Rh阳性个体采用PCR方法直接测定RHD合子型,计算杂合率与前者比较.结果 31 115名捐血者中采用间接抗人球蛋白试验(indirect antiglobulin test,IAT)确认99名个体为Rh(D)阴性(0.318%),d基因频率0.056 41,D基因频率0.943 59,Dd杂合型0.106 45(10.6%),考虑IAT检测D放散型为Rh(D)阴性,计算后实际Dd杂合型为0.090 32(约9.0%);PCR测定3628名Rh阳性个体RHD合子型测定显示DD纯合型3383人(93.2%),Dd杂合体245名(6.8%),由于无效RHD等位基因的PCR结果为阳性(D),重新分析后实际携带1条功能性RHD基因的杂合性个体约7.4%.提示中国汉族Rh(D)阴性妇女当配偶为Rh(D)阳性时,子女Rh(D)阴性的比率约3.7%～4.5%.结论 中国新生儿Rh同种免疫预防进行侵入性胎儿Rh(D)血型预测意义不大,或可直接假定新生儿为Rh(D)阳性进行产前检查和同种免疫防护.

Abstract：

Objective To investigate the RHD zygosity of Rh(D)-positive Chinese Hans in order to study the mother-fetus Rh isoimmunization prophylaxis. Methods Rh(D) blood group of 31 115 donors were serotyped, and the RHD zygosities were analyzed, or determined through a PCR method for 3628 donors of Rh(D)-positive individuals. Results Among the 31 115 donors, 99 were tested Rh(D)-negative by indirect antiglobulin test (IAT) (0. 318%). The d frequency was 0. 056 41, D was 0. 943 59, and Dd heterozygosity was 0. 106 45 (10.6%). However the rate was 0.090 32 (about 9.0%) after excluding DEL (IAT-negative). For the 3628 PCR tested donors, 3383 were DD (93. 2%), 245 were Dd (6.8%). After excluding nonfunctional RHD alleles, 7. 4% of the donors were carrying one functional RHD. It showed that an Rh(D)-negative Chinese Hah woman gives an Rh(D)-negative child at a rate of 3.7%-4. 5% when her husband is Rh (D)-positive. Conclusion Fetus Rh (D)-genotyping may be unnecessary for Chinese Hans if invasive operation was needed for prenatal diagnosis. The Rh prophylaxis could be chosen assuming an Rh(D)-positive fetus.     

Association analysis of a polymorphism of the monoamine oxidase B gene with Parkinson's disease in a Japanese population

The polymorphic allele of the monoamine oxidase B (MAO-B) gene detected by polymerase chain reaction (PCR) and single-stranded conformation polymorphism (SSCP) was associated with Parkinson's disease (PD) in Caucasians. We characterized this polymorphic allele, allele 1, of the MAO-B gene using direct sequencing of PCR products. A single DNA substitution (G-A), resulting gain of Mae III restriction site was detected in intron 13 of the MAO-B gene. The allele associated with PD in Caucasians was twice as frequent as in healthy Japanese, but the association of the allele of the MAO-B gene was not observed in Japanese patients with PD. © 1995 Wiley-Liss, Inc.