新生儿高胆红素血症的病因分析

目的通过对我院新生儿高胆红素血症的病因分析,探讨不同时期感染、母乳和围产三大因素对新生儿黄疸的影响及其干预措施.方法将911例高胆红素血症患儿分为母婴同室前(Ⅰ组)和母婴同室后(Ⅱ组),并按其病因进行分类比较. 结果Ⅱ组和Ⅰ组相比,感染性黄疸发生率下降明显,母乳性黄疸和早产、低出生体重儿出现高胆红素血症的比率明显上升(P<0.005),有极显著性差异;病因不明的比率有所上升,但G6PD缺乏症的比率则呈下降趋势,两组对比,P<0.01;ABO血型不合溶血病比率仅呈轻微上升,两组对比无显著性差异.结论新生儿高胆红素血症的病因发生了明显的变迁,由母婴同室前的感染性黄疸为主演变为近年的母乳性黄疸为主,围产因素已成为影响新生儿高胆的重要因素之一,提示改善环境因素、预防感染是降低感染性黄疸的主要措施,对母乳喂养儿及合并围产因素的新生儿,生后即应进行血微量胆红素监测并进行早期干预和治疗.     

新生儿非结合性高胆红素血症遗传学特征及病因相关因素分析研究

目的探讨新生儿非结合性高胆红素血症遗传学特征及病因相关因素。方法 (1)选择2015年12月-2017年12月入院治疗的新生儿非结合性高胆红素血症患者55例,设为观察组;选择同期分娩的正常新生儿55例,设为观察组。对观察组采用突变特异性扩增系统(ARMS)法检测新生儿G6PD基因突变情况及类型,分析新生儿非结合性高胆红素血症的遗传学特征;(2)进行单因素及多因素Logistic回归分析,分析新生儿非结核性高胆红素血症病因相关因素。结果对入组的110例新生儿非结核性高胆红素均完成遗传学检查,PCR结果表明:对于G1338A突变者能扩增出361bp特异性电泳带;对于G1376T突变者则可以扩增出345bp特异性电泳带。对于阴性对照组中经右601bp部位存在对照泳带。观察组55例新生儿中1388突变51例,1376突变4例;单因素结果表明:新生儿非结合性高胆红素血症发生率与性别、体重、宫内窘迫、遗传代谢病及ABO溶血发生率无统计学意义(P0.05);新生儿非结合性高胆红素血症发生率与早产、感染、头皮血肿、围产窒息关系密切(P0.05);多因素Logistic回归分析结果表明:新生儿非结合性高胆红素血症发生率与早产、感染、头皮血肿、围产窒息关系密切(P0.05)。结论新生儿非结合性高胆红素血症患儿常伴有G1388A、G1376T位基因突变的主要类型,并且病因相关因素较多,临床上应根据病因相关因素制定有效的措施进行干预,降低疾病发生率。     

试管婴儿(IVF-ET)新生儿期情况分析

目的前瞻性对体外授精-胚胎移植(IVF-ET)技术受孕出生的新生儿进行评估,探讨实施IVF-ET技术出生新生儿的安全性.方法从自2000年10月～2004年12月在本院接受IVF-ET治疗后受孕181例孕妇进行前瞻性追踪观察,将其分娩的新生儿254个作为观察组,本院产科自然妊娠分娩的新生儿1205个作为对照组,对两组单胎和总体新生儿胎龄、出生体重、Apgar评分、高胆红素血症、新生儿窒息、新生儿死亡及新生儿畸形发病率的进行观察比较.结果单胎新生儿的出生体重、Apgar评分、新生儿死亡率及新生儿畸形率与对照组无差异性(P＞0.05);单胎新生儿窒息率观察组低于对照组,两组比较有显著差异性(P＜0.05).两组总体比较新生儿畸形、新生儿窒息率、新生儿死亡率无差异性(P＞0.05),而新生儿低体重出生率、高胆红素血症、住院治疗时间,观察组明显高于对照组,两组比较有极显著差异性(P＜0.01);而Apgar评分观察组低于对照组两者比较有差异性(P＜0.05).结论 IVF-ET技术不增加新生儿畸形和围产期死亡率;多胎是IVF-ET技术主要并发症,是早产和低体重出生儿、高胆红素血症、新生儿窒息等新生儿不良结局的主要原因.     

剖宫产与新生儿高胆红素血症的关系探讨

目的　探讨剖宫产分娩与新生儿高胆红素血症的关系。方法　对我院 2 0 0 0年 1月至 2 0 0 1年 9月期间在产科病房出生的新生儿进行微量血清胆红素测定 ,比较剖宫产娩出的新生儿与非剖宫产娩出的新生儿发生高胆红素血症的情况。结果　剖宫产组新生儿高胆红素血症的发生率为 39 6 % (4 70 / 1188) ,非剖宫产组新生儿高胆红素血症的发生率为 2 2 8%(2 4 5 / 10 74 ) ,两者差异有统计学意义 ,χ2 =73 2 ,P <0 0 5。剖宫产组中母亲有妊娠合并症者新生儿高胆发生率为 4 0 1%(10 0 / 2 4 9) ,母亲无妊娠合并症者新生儿高胆发生率为 39 4 % (370 / 939) ,两者差异无统计学意义 ,χ2 =0 0 4 7,P >0 0 5。结论　剖宫产可能是引起新生儿高胆红素血症的原因之一。     

葡萄糖6磷酸脱氢酶新生儿早期诊断的临床应用

目的通过脐带血检验早期诊断新生儿G6PD缺陷,探讨G6PD缺陷程度与患儿高胆红素血症发生率的相关性.方法对1302例足月健康新生儿脐带血进行G6PD定量检验后跟踪调查其高胆红素血症发生率.结果(1)106例G6PD缺陷的患儿发生高胆红素血症25例(23.58%);1196例G6PD正常的新生儿发生高胆红素血症31例(2.59%).两组病例高胆红素血症的发生率有极显著差别(χ2=104.25 P＜0.01).(2)49例G6PD显著缺陷的患儿发生高胆红素血症19例(38.78%);57例G6PD轻度缺陷的患儿发生高胆红素血症6例(10.53%).两组病例高胆红素血症发生率有极显著差别(χ2=11.67 P＜0.01).结论G6PD缺陷是本地区新生儿发生高胆红素血症的主要病因之一,G6PD活性越低,患儿发生高胆红素血症的可能性越大.     

极低出生体重儿临床相关因素及与预后的关系

目的探讨极低出生体重儿的围产期及临床特点,分析其与预后的关系.方法分析110例极低出生体重儿(含12例超低出生体重儿)的一般情况、产科及母孕期情况、新生儿临床特点.结果胎龄小于32w者占79%,小于胎龄儿占17.3%,41%为多胎;32%有胎膜早破史,18%母亲有妊高征;36%有窒息复苏史;产科异常是胎儿早产的主要原因.呼吸暂停、低体温、高胆红素血症及低血糖是常见的并发症;多胎、围产期异常及小于胎龄儿是极低出生体重儿主要死亡原因,生于院内或转运者死亡率明显低于院外出生者(P<0.01).结论加强对高危孕妇及新生儿的监护,普及新生儿窒息复苏知识,将有助于改善极低出生体重儿的预后.     

新生儿高胆红素血症G6PD缺乏症筛查及临床意义

目的探讨葡萄糖6磷酸脱氢酶（G6PD）缺乏与新生儿高胆红素发生率及发病时间的关系,为高胆的临床诊断及治疗提供科学依据。方法对2008年1月至2009年12月在韶关市妇幼保健院分娩的活产新生儿采用荧光斑点法对其进行G6PD筛查,对G6PD缺乏的患儿,按姓别分组调查其高胆发生率及发病时间。结果 G6PD缺乏的患儿高胆发生率显著高于对照组新生儿;男性高胆发生率显著高于女性;G6PD缺乏的患儿的发病时间主要在生后一用周内。结论 G6PD缺乏为新生儿高胆的重要病因,发病率男性高于女性,发病高峰在出生2～4天,对G6PD缺乏的高胆患儿进行早期干预,能有效减轻G6PD缺乏新生儿溶血的程度和避免发生核黄疸。     

新生儿高间接胆红素血症致病因素的Logistic回归分析

目的探讨新生儿早期高间接胆红素血症（高胆）与多种围产因素的关联性,找出相关的危险因素,为高胆的早期防治提供理论依据。方法对160例高胆患儿（病例组）与160例正常新生儿（对照组）的围产资料进行Logistic回归分析。结果多因素分析提示：胎膜早破、羊水粪染、胎儿窘迫或窒息、生后头3d体重下降〉10％、出生体重偏低、母妊娠期严重合并症（妊娠期高血压／妊娠期糖尿病／严重贫血等）、早产、头皮血肿、母产前使用催产素或镇静剂、剖宫产、高龄初产是新生儿高胆红素血症的主要危险因素,而产次、脐带绕颈、双胎或多胎等因素未显示出对高胆红素血症的明确影响。结论积极处理孕期疾病,严格掌握剖宫产指征,减少人为催产比例,加强高危妊娠、高危分娩的监测,积极喂养并及时处理新生儿并发症,可有效减少高胆红素血症的发生。     

妊娠糖尿病孕妇之新生儿出生体重与其血糖的分析及护理

目的探讨GDM孕妇所分娩的新生儿出生体重与其血糖的关系。方法选择2006年7月至2007年12月在我院出生的GDM孕妇所分娩的新生儿作为研究对象,根据新生儿出生体重分为正常体重组（2.5～〈4.0kg=和异常体重组（〈2.5kg、≥4.0kg=,新生儿出生后密切观察是否出现低血糖症状,均于出生后1h内测其指尖血糖,分析不同体重新生儿血糖数值及低血糖发生率。结果新生儿指尖血糖〈2.22mmol/L者共8例,经处理后血糖均恢复正常。新生儿异常体重组低血糖发生率高于正常体重组,P值〈0.05。结论GDM孕妇之新生儿出生体重〈2.5kg和≥4.0kg者低血糖发生率高于正常体重新生儿。认为在GDM孕妇之新生儿低血糖观察护理中低体重儿及巨大胎儿为重中之重。     

新生儿高胆红素血症治疗研究的若干进展

近年来国内、国外对新生儿高胆红素血症（高胆）的冶疗进行了广泛的研究，特别是在高胆光疗的研究中，取得了不少实质性的进展。一、光疗治疗新生儿高胆红素血症从四十年代起人们就开始用蓝光照射治疗新生儿高胆红素血症，随着光疗的广泛应用和研究的不断深入，对光疗的认识也逐渐加深，但直到近几年人们才进行了光疗治疗新生儿高胆的大群体调查和细致的分组观察研究[1]。1、光疗对高胆红素血症疗效评价：光疗治疗新生儿高胆血症有效，但是否对不同体重儿、不同状况新生儿高胆都有明确的疗效？是否有远期副作用？这些还不甚明了。近年来国际…     

喂养方式与新生儿高胆红素血症的关系

将229例足月健康新生儿(Apgar评分8～10分)按照喂养的方式分为母婴同室和混合喂养两组,观察在两种喂养方式下高胆红素血症的发病率和血清胆红素的水平。结果表明,两组新生儿的高胆红素血症发病率没有显著性差异,母婴同室的高胆红素血症发病率并没有高于混合喂养组,但母婴同室组的血清胆红素水平却明显低于混合组(P<0.02)。尤其在不明原因黄疸的新生儿中,两种喂养方式下的血清胆红素水平有非常显著的差异(P<0.001)。喂养方式在ABO血型不合、G-6-PD缺陷、母HBsAg阳性等因素组的新生儿高胆红素血症的发病率和血清胆红素水平中影响不大。母婴同室可降低新生儿血清胆红素水平,提高新生儿的机体状态。     

母血、脐血INS、GLUC、COR RIA及其意义

目的：测定胎龄儿（AGA）母血、脐血胰岛素（INS）、胰高血糖素（GLUC）、皮质醇（COR）水平,探讨AGA体重与孕妇体重指数（BMI）及母血脐血INS、GLUC、COR相关性及意义。方法：随机选取无明显产科并发症的母亲及新生儿,共26对,新生儿分为体重偏低组（A组）及体重偏高组（B组）,采用放射免疫分析测定INS、GLUC、COR含量。结果：新生儿体重与孕妇BMI有明显关系,B组孕妇BMI显著高于A组（P〈0．05）;新生儿GLUC与COR水平与孕妇比较也具重要的统计学意义（P〈0．05,P〈0．01）;B组新生儿COR含量远高于A组水平（P〈0．01）,而GLUC则相反（P〈0．05）。结论：胎儿发育与孕妇BMI及母血、脐血INS、GLUC及COR水平有关,提示母亲营养状况与上述三种代谢激素的分泌水平直接影响胎儿发育。     

脐带绕颈181例临床分析

目的探讨脐带绕颈的发生原因、诊断方法、产程处理及对围产儿的影响。方法选择脐带绕颈181例进行回顾性分析。结果脐带过短无1例发生脐带绕颈;脐带绕颈>3周者,脐带过长组明显多于脐带正常组(P<0.01),脐带绕颈的胎儿宫内窘迫率为25.41%,窒息率为11.60%,两组比较均P<0.01。脐带绕颈组自然分娩率明显低于对照组(P<0.01),阴道手术产与剖宫产均高于对照组(P<0.01)。结论脐带绕颈与脐带长度有一定的关系,脐带过长是导致脐带绕颈的基本原因。脐带绕颈会明显增加胎儿窘迫、新生儿窒息的发生率。     

正常新生儿出生时的生长抑素和神经紧张素水平

采用放射免疫技术，测定了14例正常足月新生儿及其母亲血中生长抑素和神经紧张素浓度，发现脐动脉生长抑素和神经紧张素浓度明显高于脐静脉浓度（P均＜0．01），二者均明显高于分娩后即刻母亲静脉血中相应的激素浓度（P均＜0．01）；脐动脉pH与脐动脉生长抑素和神经紧张素浓度存在一种负相关关系（P均＜0．01）。提示脐血中高浓度的生长抑素和神经紧张素极可能是胎儿源性的，且可能与分娩引起的胎儿应激有关。     

Neonatal hyperbilirubinemia and a common mutation of the bilirubin uridine diphosphate-glucuronosyltransferase gene in Japanese

Neonatal hyperbilirubinemia, which is prevalent among Asian peoples, has been considered as a physiological phenomenon, and its metabolic basis has not been clearly explained. Gilbert syndrome is a common inherited disease of unconjugated hyperbilirubinemia due to decreased bilirubin uridine diphosphate-glucuronosyltransferase (B-UGT), and its role in neonatal jaundice has recently been considered. We have previously reported that the Gly71Arg mutation of the B-UGT gene associated with Gilbert syndrome is prevalent in Japanese, Korean, and Chinese populations and was more frequently detected in neonates with severe hyperbilirubinemia than in control subjects. We have studied 159 Japanese full-term neonates, evaluating the relationship between the B-UGT genotype and the severity of jaundice, as assessed with a transcutaneous bilirubinometer. The gene frequency of the Gly71Arg mutation in these neonates was 0.19, and neonates carrying the Gly71Arg mutation had significantly increased bilirubin levels on days 2–4, manifested in a gene dose-dependent manner. The frequency of the Gly71Arg mutation was 0.47 in the neonates who required phototherapy (i.e., those with more severe hyperbilirubinemia), significantly higher than 0.16 in the neonates who did not require the therapy. The gene frequency of the TA repeat promoter polymorphism, the (TA)₇ mutation, was 0.07, and neonates carrying this mutation did not have an increase in bilirubin. These results suggested that the Gly71Arg mutation contributes to the high incidence of neonatal hyperbilirubinemia in Japanese. Received: June 16, 1998 / Accepted: August 5, 1998     

Effect of immune status on dengue 2 virus replication in cultured leukocytes from infants and children.

Cord blood leukocytes from neonates with maternal dengue antibody supported dengue 2 virus replication in vitro; those from neonates without maternal antibody did not. Cord bloods of infants born to dengue-immune mothers contained a potent enhancing factor which gradually decayed with age and which was absent from neonates born to nonimmune mothers. Permissiveness of cultures of washed peripheral blood leukocytes from infants with maternal antibody declined steadily with increasing age in parallel with the decay of maternal antibody, and the leukocytes were no longer permissive after 10 to 12 months. The demonstration of a dengue maternal infection-enhancing factor in human cord blood from dengue-immune mothers supports the hypothesis that severe primary dengue hemorrhagic fever with shock seen in Bangkok infants is related to maternal immune status.     

新生儿高胆红素血症患者血小板功能测定

报告了30例新生儿高咀红素血症患儿和17例正常新生儿的血小板粘附率、聚集率、血小板，第3因子有效性测定结果．经统计学分析新生儿高胆红素血症时血小板粘附率升高．取集率下降．血小板第3因子活性减低与年龄有关而与黄疸无关．光疗时血小板粘附率．聚集串无影响．但能提高血小板第3因子的活性．并提示新生儿高胆红素血症时应慎用抗凝药．     

Prevalence of uridine glucuronosyl transferase 1A1 (UGT1A1) mutations in Malay neonates with severe jaundice

A number of genetic risk factors have been implicated in the development of neonatal severe hyperbilirubinaemia. This includes mutations in the uridine glucoronosyl transferase 1A1 (UGT1A1) gene which is responsible for unconjugated hyperbilirubinemia in Gilbert's Syndrome. We studied the prevalence of UGT1A1 gene mutations in a group of Malay neonates to determine whether they are risk factors to severe neonatal jaundice. One hundred and twenty-five Malay neonates with severe hyperbilirubinemia were studied. Ninety-eight infants without severe hyperbilirubinaemia were randomly selected from healthy Malay term infants (controls). DNA from EDTA cord blood samples were examined for UGT1A1 mutations nt211G > A and nt247T > C using established Taqman SNP genotyping assays and the UGT1A1*28 variant was detected by the Agilent 2100 bioanalyzer. All samples were also screened for common Malay G6PD variants using established techniques. The frequency of UGT1A1 211G > A mutation is significantly higher in the severely hyperbilirubinemic group (13%) than the control group (4%; p = 0.015) and all the positive cases were heterozygous for the mutation. There was no significant difference in the frequency of UGT1A1*28 mutation between the severely hyperbilirubinemic (3.5%) and the control group (0.01%; p = 0.09). None of the neonates in both groups carried the nt247 T > C mutation. The prevalence of G6PD mutation was significantly higher in the severely jaundiced group than control (9% vs 4%; p = 0.04). In conclusion, nt 211 G > A alleles constitute at least 12% of UGT1A1 mutations underlying unconjugated hyperbilirubinemia and appears to be a significant independent risk factor associated with severe neonatal hyperbilirubinemia in the Malay newborns.     

长时程脑电监测对评估HIE预后的价值

目的:探讨脑电图(EEG)长时程监测对新生儿缺氧缺血性脑病(HIE)预后的临床价值。方法:对在我院高危儿室住院的52例HIE的患儿进行12～24 h的EEG监测,将其脑电信息储存,采用(日)福山幸夫"新生儿异常EEG"诊断标准进行回放分析。并随访35例患儿,对预后进行评估。结果:52例患儿中,35例表现为不同程度的背景脑电活动降低,异常率占67%,且临床为中、重型HIE患儿的EEG异常率(100%),明显高于轻型HIE患儿的异常率(39%)(P<0.01)。EEG表现为中、高度背景脑电活动降低者,留有后遗症的几率(8/24,33%)高于轻型EEG背景活动降低者的几率(2/28,7%)(P<0.05)。在出生>1周后的新生儿。EEG仍表现为中、高度背景脑电活动降低的患儿,留有癫癎、脑瘫的几率(11例均有后遗症)明显高于出生后1周内背景脑电活动降低患儿的几率(4/13,31%) (P<0.01)。结论:EEG表现为轻度背景脑电活动降低者,预后良好,中度背景脑电活动降低者预后不良,高度背景脑电活动降低者预后极差。因此长时程脑电监测对新生儿HIE诊断及预后的评估具有重要意义。     

Prediction of the development of atopic symptoms in early childhood by cord IgE-binding factors (soluble Fc epsilon R2)

The relationship of cord serum sFc epsilon R2 levels to the development of atopic symptoms in early childhood was studied. Cord sFc epsilon R2 was 444.2 +/- 235.1 pg/ml (n = 77), which was not significantly different from maternal serum sFc epsilon R2 (541.7 +/- 346.9 pg/ml, n = 42). However, there was no correlation between cord and maternal serum sFc epsilon R2, suggesting that most, if not all, of cord serum sFc epsilon R2 was produced by the fetus itself. Cord serum sFc epsilon R2 in infants who developed atopic symptoms later was significantly higher than that in infants who were free of atopic symptoms (P less than 0.01 at 7 and 13 months of age). The incidence of the development of atopic symptoms increased with the increase of cord serum sFc epsilon R2. These results suggest that sFc epsilon R2 is related to the development of atopic disorders and that the measurement of cord serum sFc epsilon R2 may be of value in predicting the development of atopic disorders in early childhood.