茵陈蒿汤联合维生素C对母儿ABO溶血的临床研究

目的 分析针对母儿ABO血型不合溶血疾病患者采用茵陈蒿汤、维生素C联合用药治疗的疗效。方法 收集患母儿ABO血型不合溶血病的80例孕妇,将其随机分成两组:对照组40例,以维生素C、苯巴比妥用药治疗;观察组40例,在对照组治疗基础上加用茵陈蒿汤治疗。观察两组治疗后的IgG抗体效价疗效与新生儿黄疸、新生儿溶血症发生情况。结果 观察组治疗后的抗体效价总有效率为92.50%,高于对照组的52.50%,差异具有统计学意义（P＜0.05）。观察组的新生儿黄疸、新生儿溶血症发生率分别为7.50%、0,低于对照组的17.50%、5.00%,差异具有统计学意义（P＜0.05）。结论 母儿ABO血型不合溶血疾病患者采用茵陈蒿汤、维生素C联合用药治疗,可获良好的疗效,避免新生儿溶血症的出现,值得借鉴。     

母孕期血清抗体与新生儿ABO溶血症50例分析

目的为了探讨母孕期血清抗体与新生儿ABO溶血症程度的关系。方法对夫妇血型不合者在母孕中期曾测定血清IgG抗A、抗B抗体者≥64时追踪其新生儿ABO溶血症发生情况,共50例作了调查分析。结果50例其中有3例抗体很高分别为512、1024、2048均没有发生新生儿ABO溶血症。母子血型相同有14例,母子血型不合有36例。36例母子血型不合中有19例新生儿发生ABO溶血症,发生率为52.78%。母血型不合19例中母产前抗体滴定度≥64者有6例占17.14%,其中新生儿发生ABO溶血症为3例占50%母产前抗体滴定度128-≥256者有30例占83.33%,其中新生儿发生ABO溶血症为16例占53.33%。在母子血型组合中O-A血型组合明显多于O-B血型组合为1.57∶1。结论O-A血型组合较O-B血型组合易发生ABO溶血症,孕母血清抗体水平的高低其新生儿发生ABO溶血症的程度不成正比关系。     

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.     

新生儿ABO溶血病相关母亲因素分析

目的观察分析孕妇血清IgG抗A（B）效价、妊娠次数及年龄因素与新生儿溶血病的相关性。方法检测母婴血型不合孕妇血清IgG抗A（B）效价,分别统计不同IgG抗A（B）效价的孕产妇中发生因ABO血型不合所致的新生儿溶血病的比率,并比较不同妊娠次数、不同年龄段的孕妇发生新生儿溶血的比率。结果孕妇不同血清IgG抗A（B）效价时、不同妊娠次数时及孕妇的不同年龄段时发生新生儿ABO溶血病的比率之间均有统计学差异（P〈0．05）,随着孕妇血清IgG抗A（B）效价的增高、妊娠次数的增加及孕妇年龄的增加,新生儿ABO溶血病的发病也增多。结论为保障母婴安全,减少新生儿溶血病的发生率,有条件时检测孕妇血清IgG抗A（B）效价,并尽量减少妊娠次数及避免高龄怀孕。     

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。     

维族与汉族新生儿溶血症的比较分析

母婴血型不合所致新生儿溶血病是围产儿发病和死亡的原因之一,是一种与血型遗传有关的同种被动免疫性疾病,母体内的免疫抗体(如ABO或Rh血型抗体),可通过胎盘进入胎儿血液循环,造成新生儿发生溶血并可产生高胆红素血症.而有关新生儿溶血病血液细胞学特征性改变的相关报道为数甚少[1].本文就新疆地区维族与汉族新生儿溶血症,生化及血细胞指标间分析和探讨.现报道如下.     

抗体筛查在门诊产科常规检测中预防HDN的应用价值——附1例抗-M引起的新生儿溶血病

正新生儿溶血病(Hemolytic disease newborn,HDN)是指母胎血型不合所致的胎儿或新生儿免疫性溶血性疾病。在我国以ABO血型不合者占多数,Rh血型不合者较少,其他如MN、Kell血型系统尤其罕见[1]。有报道称ABO新生儿溶血病占85.3%,Rh新生儿溶血病占14.6%,而MN系统溶血病仅占0.1%[2]。在工作中首次发现1例单纯由Ig G抗M     

夫妇ABO血型不合产前抗体检查的临床意义

新生儿溶血病是一种血型抗原免疫后产生的溶血性贫血,在胎儿、新生儿都可以发病。目前在每个人体内已发现的14个血型系统79个血型抗原中发生新生儿溶血病的,以ABO系统为最多,其次为Rh系统,其他如MN系统等少见的血型不合也可以引起本病。产前夫妇血型不合的抗体检查是及早发现和     

519例O型血孕妇血清中IgG抗A抗B效价测定分析

新生儿溶血病（HDN）是指母婴血型不合，母血中胎儿红细胞的免疫抗体IgG通过胎盘进入胎儿血循环，发生同种免疫反应而引起的不同程度溶血。造成死胎、流产、早产等，在我国以ABO血型不合导致的新生儿溶血最为常见，本资料对我院妇产科门诊O型血孕妇行ABO血型抗体的检测，Rh血型检测，对IgG抗A、抗B高效价者进行了产前积极治疗，效果满意。     

80例新生儿黄疸的临床分析

我院1998年1月至1999年9月住院的新生儿黄疸占同期住院新生儿的65.5%。本文对资料完整的80例进行分析。本组病例主要来源于爱婴区，无1例发生核黄疸，仅1例门诊收住的ABO血型不合溶血症发生核黄疸。本组黄疸原因的排序是：溶血、感染并列第一，其次是原因不明，红细胞增我症,其他因素和窒息缺氧。本组黄疸病例胆红素高于危险阈25例，仅1例高达693.55μmol/L时出现核黄疸。提示：（1）实行母婴同室，及早发现病理性黄疸，是一个值得普及的对策；（2）48小时内出现的黄疸要高度警惕ABO血型不合溶血症及早期新生儿感染。（3）重新制定新生儿高胆红素血症诊断标准是很有必要的。     

Severe hemolytic disease of the newborn in a group B African-American infant delivered by a group O mother

Maternal-fetal ABO incompatibility is a common hematological problem affecting the newborn. In general, hemolysis is minimal and the clinical course is relatively benign, rarely causing the escalating levels of hyperbilirubinemia and significant anemia commonly associated with Rh hemolytic disease of the newborn (HDN). The incidence of HDN ranges from one in 150 births to 1:3000 births, depending on the degree of anemia and level of serum bilirubin. The etiology of ABO hemolytic disease of the newborn (ABO-HDN) is complex because anti-A and anti-B antibodies are composed mainly of IgM. Since only IgG antibodies cross the placenta, those pregnant women with high levels of IgG anti-A,B, anti-A, or anti-B with an ABO incompatible fetus will be the ones to give birth to an infant with ABO-HDN. We describe a case of a B/Rh positive term newborn born to an O/Rh negative African-American mother demonstrating aggressive hemolysis and a robust response of the bone marrow. This case was successfully managed with phototherapy and simple RBC transfusion without the need for exchange transfusion.     

Neonatal screening of glucose-6-phosphate dehydrogenase deficiency in umbilical cord blood

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most frequent enzyme deficiency. It is a sex-linked genetic disease concerning mostly african, mediterranean and far-eastern populations. The main clinical expression is a hemolytic anemia which can be acute or chronic. During the neonatal period the disease may manifest as neonatal jaundice. We have been asked by the neonate department to set up a blood screening test for this deficiency. We have therefore developed a test using umbilical cord blood. The assay of G6PD has been automatised and red blood cell aspartate-amino-transferase (ASAT) chosen as a reference enzyme to evaluate the age of red blood cells. Normal values of G6PD, ASAT and G6PD/ASAT ratio have been calculated from 235 cord samples. Genetic frequency of this deficiency in 2002 was 6% in male and 1% in female newborns.     

还原型谷胱甘肽治疗G-6-PD缺陷并新生儿高胆红素血症

目的观察还原型谷胱甘肽治疗新生儿红细胞葡萄糖-6-磷酸脱氢酶缺陷性高胆红素血症的疗效。方法对100例因G-6-PD缺陷导致高胆红素血症的新生儿加用还原型谷胱甘肽静滴,并与对照组比较观察疗效。结果治疗组与对照组治疗后胆红素、降幅及光疗时间比较,P〈0.01,差异有非常显著性。结论还原型谷胱甘肽对G-6-PD缺陷性新生儿黄疸具有良好的辅助治疗效果。     

镰状细胞病合并G6PD缺陷症五例临床分析

目的总结5例血红蛋白S病（HbS）各类实验数据,为临床提供实验诊断,预防新生儿的严重并发症。方法血常规检测,全自动血红蛋白电泳,G6PD/6PGD直接比值法,G6PD/6PGD全自动生化仪日立7600检测G6PD缺陷症。结果检测5例HbS患者,发现合并a地贫1例,4例合并G6PD缺陷症。结论 Hb电泳区带定量是诊断HbS的重要方法。镰变试验是鉴别HbS与HbD的确诊试验。G6PD缺陷症在非洲裔HbS患者中有较高的发生率,如果同时合并2种遗传病会加重贫血症状。     

Glucose-6-phosphate dehydrogenase deficiency in Mali. Epidemiology and pathological aspects

I,858 semi quantitative G6PD determinations were done in Mali (mostly in the Point G Hospital, in Bamako). 15.7% of the men and 4.5% of the women had a G6PD deficiency. The age did not affect the incidence of the disease. G6PD deficiency was more frequent among the Sonrais than among the other ethnic groups tested. It did not occur more frequently among subjects having the sickling trait of AC hemoglobinopathy but no G6PD was found among subjects having a major hemoglobinopathy (SS or SC). Severe hemolytic anemia was rather infrequent among adults subjects. Hemolysis was induced by drugs--such as dapsone or niridazole--but it was usually mild and time-limited.     

微柱凝胶技术应用于新生儿溶血病的实验室诊断

目的采用微柱凝胶技术进行新生儿溶血病（HDN）的实验室诊断分析。方法对1627例新生儿进行血型血清学分析,包括母婴血型、直接抗人球蛋白试验、血清游离抗体试验、热放散试验、ABO血型系统以外的抗体鉴定试验。结果 1627例病例中确诊为HDN的有163例,其中母-婴血型为O-A及O-B的最多,共占97.55%。确诊为HDN血清学结果中放散试验和游离抗体试验同时阳性最多,占76.07%。诊断为HDN可疑病例血清学结果中,直接抗人球蛋白试验阳性率最多,占79.55%。在出生后3～7d内确诊HND的患儿数最多,占66.26%。ABO血型系统以外的抗体鉴定试验阳性有6例,其中5例诊断为RhHDN。结论红细胞抗体释放试验、直接抗人球蛋白试验和血清游离抗体试验是早期诊断HDN的有效方法。HDN检出率与所采用的实验方法和采血时机有很大关系。     

Impaired glutathione metabolism in hemolytic anemia

During the delivery of oxygen by erythrocytes, highly reactive oxygen species such as superoxide anion arise. The presence of reactive species damages the cell constituents. Glutathione (GSH) functions to repair cells when they are attacked by oxidative stress. GSH is synthesized in erythrocytes and glutathione disulfide (GSSG) is transported outside the cells to maintain a high GSH/GSSG ratio. The redox cycle of GSH by glutathione reductase and glutathione peroxidase is closely related to G6PD. Hereditary enzyme deficiency related to GSH metabolism, with hemolytic anemia has been reported. G6PD deficiency causes hemolytic anemia due to insufficiency of the redox cycle of GSH. Deficiency of GSH synthesizing enzymes or glutathione reductase also causes hemolysis. Pyrimidine 5'-nucleotidase deficiency causes hemolytic anemia even when there is a high concentration of GSH. Accumulation of nucleotides in red cells causes inhibition of G6PD activity.     

Hereditary hemolytic disorders among the Ashram school children in Mayurbhanj district of Orissa

Hemoglobinopathy and allied hemolytic disorders are important genetic and public health problems in Orissa. These cause high degree of hemolytic anemia, morbidity and mortality in the vulnerable populations. A total of 465 Ashram School children aged 6-15 years belonging to Bathudi, Bhumiz, Kolha and Santal tribes in six localities of Mayurbhanj district of Orissa were screened for hemoglobinopathy, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, ABO and Rhesus blood groups serology and any other hereditary condition. The sickle cell trait (Hb AS) was detected in Santal (1.0%), Bathudi (1.0%) and Bhumiz (0.9%) tribals. No case of homozygous sickle cell disease was detected among the tribes of Mayurbhanj district. The beta-thalassemia trait was detected in Santal (8.0%), Kolha (2.0%), Bhumiz (1.7%) and other tribal (3.8%) students. Sickle cell hemoglobinopathy and beta-thalassemia are prevalent in this district among the tribes, but the frequency is very low. The prevalence of G-6-PD deficiency is considerably high (7.7-9.8%) among the tribes of Mayurbhanj district in Orissa. Out of total 43 G-6-PD deficient subjects, there were 32 males, 9 heterozygote females and 2 homozygous females. This shows that the antimalarial drugs should be administered with caution as these cause hemolytic anemia, sometimes fatal also. The distribution of ABO and Rhesus blood groups shows the preponderance of B blood group (33.8%) over O (29.6%) and 2.1% cases of Rhesus negativity were detected among the Bathudi tribe. This pattern is consistent with the characteristic features of tribal populations in India.     

Present status of understanding on the G6PD deficiency and natural selection

G6PD deficiency is a common hemolytic genetic disorder, particularly in the areas endemic to malaria. Individuals are generally asymptomatic and hemolytic anemia occurs when some anti-malarial drugs or other oxidizing chemicals are administered. It has been proposed that G6PD deficiency provides protection against malaria. Maintaining of G6PD deficient alleles at polymorphic proportions is complicated because of the X-linked nature of G6PD deficiency. A comprehensive review of the literature on the hypothesis of malarial protection and the nature of the selection is being presented. Most of the epidemiological, in vitro and in vivo studies report selection for G6PD deficiency. Analysis of the G6PD gene also reveals that G6PD-deficient alleles show some signatures of selection. However, the question of how this polymorphism is being maintained remains unresolved because the selection/fitness coefficients for the different genotypes in the two sexes have not been established. Prevalence of G6PD deficiency in Indian caste and tribal populations and the different variants reported has also been reviewed.