摘要
目的:观察新生儿缺氧缺血性脑病发生过程中胆红素与血红素加氧酶1活性的变化,探讨两者在缺氧缺血性脑病发生发展中的作用。方法:选择1998-01/2003-12西安交通大学第一医院产科出生并收住新生儿病房的患儿200例。纳入标准:①窒息儿根据新生儿生后Apgar评分0-3分为重度窒息,4～7分为轻度窒息。②缺氧缺血性脑病患儿临床诊断符合新生儿缺氧缺血性脑病标准。③高胆红素血症的诊断标准符合足月儿胆红素>205μmol/L。④新生儿黄疸诊断标准血清胆红素>85μmol/L时,临床出现肉眼黄疸。依据缺氧缺血程度分为2组,窒息组和缺氧缺血性脑病组。窒息组分为轻度、重度2个亚组,缺氧缺血性脑病组分为轻度,中度,重度3个亚组,每个亚组40例,对照组选择同期出生的健康新生儿40例,与窒息组和缺氧缺血性脑病组患儿的胎龄和出生体质量差异无显著性。取患儿股静脉血4mL,采用生化分析仪测定窒息组和缺氧缺血性脑病组患儿的胆红素值,并在急性期(3d内)和恢复期(10d内)用464nm和530nm双波长分光光度法测定样品反应物中胆红素生成量代表血红素加氧酶1活性,以每秒每升血清生成胆红素量为单位(μkat/L)。同时测定正常对照组新生儿的胆红素值和血红素加氧酶1活性。对样本均数比较采用方差分析。结果:①胆红素水平:轻度窒息组明显高于重度窒息组和对照[(325.62±39.1),(243.64±37.6),(305.70±51.3)μmol/L,F=10.89,P<0.01]。轻度、重度缺氧缺血性脑病组胆红素水平接近[(89.4±8.1),(86.7±3.9)μmol/L]。②胆血红素加氧酶1活性:重度窒息组急性期血红素加氧酶1活性值明显高于轻度窒息组急性期和恢复期,重度窒息组恢复期和对照组(F=38.63,P<0.01);重度缺氧缺血性脑病组急性期血红素加氧酶1活性明显高于恢复期,也明显高于轻度和中度缺氧缺血性脑病组(急性期和恢复期)(F=8.93,P<0.01)。③黄疸发生率:轻度窒息组发生高胆红素血症22例,生理性黄疸12例,黄疸发生率85%;重度窒息组发生高胆红素血症6例,生理性黄疸3例,黄疸发生率23%。对照组发生高胆红素血症20例,生理性黄疸12例,黄疸发生率80%。缺氧缺血性脑病组无高胆红素血症发生,轻度缺氧缺血性脑病组发生生理性黄疸6例,黄疸发生率15%;重度缺氧缺血性脑病组发生生理性黄疸5例,黄疸发生率13%。结论:当不同程度缺氧缺血使新生儿脑损伤时,血红素加氧酶1活性增加致胆红素的抗氧化作用途径开放,胆红素水平降低。提示胆红素水平、血红素加氧酶1活性能反映缺氧缺血性脑病患儿的病情严重程度,对缺氧缺血性脑病的诊断及预测预后具有一定的参考价值。
AIM: To investigate the changes of bilirubin level and heme oxygenase-1(HO-1) activity in neonates with hypoxic ischemic encephalopathy(HIE),and probe into their role in the attack and development of HIE. METHODS: Totally 200 subjects were selected from the neonates who were born and hospitalized in the room for neonates of the Department of Obstetrics & Gynecology in the First Affiliated Hospital of Xi'an Jiaotong University from January 1998 to December 2003.Inclusion criteria:①Asphyxial neonates were regarded as severe asphyxia if the Apgar score after birth was 0 to 3 points,and as mild asphyxia if the Apgar score after birth was 4 to 7 points;②The HIE neonates were in accordance with the judging standard for HIE of neonates clinically;③Diagnosis of hyperbilirubinemia was accordant with the bilirubin more than 205 μmol/L in term infants;④When serum bilirubin was more than 85 μmol/L in neonatal jaundice,jaundice was found by naked eyes clinically.The attacked neonates were divided into 2 groups according to their degree of hypoxia and ischemia:asphyxia group and HIE group,and then the former group was subdivided into mild and severe asphyxia groups,and the latter group was subdivided into mild,moderate and severe HIE groups,with 40 cases in each subgroups.Another 40 healthy neonates born in the same period were selected as controls,and their gestational age and birth body mass were similar to the attacked ones.Serum bilirubin in 4 mL femoral vein from attacked neonates was detected in the asphyxia groups and HIE groups by biochemical analysis.The activity of HO-1 was measured by 464-nm and 530-nm spectrophotometry at acute phase(within 3 days) and recovery phase(within 10 days) respectively,using per minute,per liter as units of serum bilirubin(μkat/L).Meanwhile the level of serum bilirubin and activity of HO-1 were measured in the normal controls.The mean was compared by analysis of variance. RESULTS:①The level of serum bilirubin in the mild asphyxia group[(325.62±39.1) μmol/L] was significantly higher than that in the severe asphyxia group[(243.64±37.6) μmol/L] and the control group[(305.70 ±51.3)μmol/L](F=10.89,P < 0.01),and that was similar in the mild and severe HIE groups[(89.4±8.1) μmol/L,(86.7±3.9) μmol/L].②The activity of HO-1 in the severe asphyxia group at acute phase was significantly higher than that in the mild asphyxia group at acute and recovery phases,the severe asphyxia group at recovery phase and the control group(F=38.63,P < 0.01);That in the severe HIE group at acute phase was significantly higher than that in the severe HIE group at recovery phase,also the mild and moderate HIE groups at acute and recovery phases(F=8.93, P < 0.01).③In the mild asphyxia group,hyperbilirubinemia was found in 22 cases,and physiologic jaundice in 12 cases with the jaundice incidence of 85%;In the severe asphyxia group,hyperbilirubinemia was found in 6 cases,and physiologic jaundice in 3 cases with the jaundice incidence of 23%;In the control group,hyperbilirubinemia was found in 20 cases,and physiologic jaundice in 12 cases with the jaundice incidence of 80%;No hyperbilirubinemia was found in the HIE groups,however physiologic jaundice was found in 6 cases with the jaundice incidence of 15% in mild HIE group,and in 5 cases with the jaundice incidence of 13% in the severe HIE group. CONCLUSION: When neonatal brain is damaged by different degrees of hypoxic ischemia,the antioxidant pathway of bilirubin is opened attributing to the increase of HO-1 activity,and thus the level of bilirubin is lowered.The results indicate that the level of bilirubin and the activity of HO-1 can reflect the severity of HIE in neonates, providing certain referenced significance for the diagnosis of HIE and the prediction of its prognosis.
出处
《中国临床康复》
CAS
CSCD
北大核心
2005年第23期190-191,共2页
Chinese Journal of Clinical Rehabilitation
