葡萄糖-6-磷酸脱氢酶缺乏症早产儿的血清胆红素动态监测结果分析

Analysis of dynamic monitoring of serum bilirubin in premature infants with glucose 6 phosphate dehydrogenase deficiency

目的探讨葡萄糖-6-磷酸脱氢酶(G6PD)缺乏症早产儿的血清胆红素动态变化特点,以指导G6PD缺乏病早产儿的临床诊断及治疗。方法选择2012年1月至2013年12月于广西百色妇幼保健院收治的40例G6PD缺乏症早产儿为研究对象,纳入G6PD缺乏组(n=40)。选择同期在本院出生的42例未合并G6PD缺乏症早产儿作为正常对照组(n=42)。采用经皮胆红素测量仪在出生后24,48,72,96,120,144,168h对两组早产儿进行血清胆红素动态监测,并比较两组早产儿高胆红素血症发生率和血清胆红素水平。结果两组高胆红素血症发生率比较(45.0%vs 14.3%),差异有统计学意义(χ2=9.336 0,P<0.01)。两组早产儿生后24h血清胆红素水平比较,差异无统计学意义(t=0.471 6,P>0.05)。G6PD缺乏组早产儿生后48,72,96,120,144,168h血清胆红素水平,均高于正常对照组,且差异有统计学意义(t=3.767 5,2.618 3,2.511 3,2.542 3,3.031 1,2.869 9;P<0.01)。结论 G6PD缺乏症早产儿易发生高胆红素血症,其血清胆红素水平于生后48h开始显著进高。

Objective To investigate the characteristics of bilirubin dynamic changes in premature infants with glucose 6 phosphate dehydrogenase（G6PD）deficiency.Methods From January 2013 to December 2013,a total of 40 premature infants with G6 PD deficiency were included into the study as G6 PD deficiency in the same hospital group（n=40）.Meanwhile 42 premature infants without G6 PD deficiency who were admitted into the same hospital were chosen as normal control group（n=42）.Serum bilirubin were monitored using percutaneous bilirubin measurement instrument at 24,48,72,96,120,144,168 h after birth,and the levels of serum bilirubin and the incidence rate of hyper bilirubinemia were compared between two groups.Results The incidence rate of hyperbilirubinemia in the G6 PD deficiency group was significantly higher than that of normal control group（45.0%vs 14.3%）,and the difference was significant（χ2=9.336 0,P〈0.01）.There was no significant difference between two groups in the serum bilirubin level at 24 hafter birth（t=0.471 6,P〉0.05）.The serum bilirubin levels of G6 PD deficiency group were significantly higher than those of normal control group at 48,72,96,120,144,168 hafter birth,and the differences between two groups had statistical significance（t=3.767 5,2.618 3,2.511 3,2.542 3,3.031 1,2.869 9;P〈0.01）.Conclusion The serum bilirubin levels of premature infants with G6 PD deficiency was prone to high bilirubinemia sickness.