新生儿G-6-PD缺乏症高未结合胆红素血症的心肌损害

目的 探讨新生儿G-6—PD缺乏症的高未结合胆红素血症对心肌损害。方法 30例G—6-PD缺乏症新生儿分别于入院时(治疗前)和治疗后(显性黄疸消退后)抽血测定心肌酶、肝功能、肾功能等,部分病人同时作心电图检查,并与15例正常新生儿进行比较。结果 30例G—6—PD缺乏症患儿心肌酶及同功酶活性均有不同程度增高,尤以CK—MB活性明显升高,两组比较差异有非常显著意义(P<0.01)。CK—MB升高与黄疸程度呈正相关(r=0.487、P<0.01)。治疗前后,高未结合胆红素心肌酶比较、差异有非常显著意义(P<0.01)。结论 新生儿高未结合肥红素血症可出现心肌损害,与黄道出现程度有关。

Myocardial impairment caused by unconjugated hyperbilirubinemia in neonates with glucose-6-phosphate dehydrogenase deficiency

Objective To investigate relationship between unconjugated hyperbilirubinemia and myocardialimpairment in neonates with glucose-6-phosphate dehydrogenase (G-6PD) deficiency Relationship. MethodsThirty neonates with G-6-PD deficiency were studied as G-6-PD group. Their levels of serum myocardialenzymes and unconjugated bilirubin were tested before treatment and after the jaundice had gone down,compared with those of 15 normal neonates as control group. Results The level of unconjugated bilirubinincreased markedly in G-6-PD group before treatment. Their levels of LDH, AST, CK and CK-MB also werehigher than those in control group, especially levels of CK and CK-MB (p<0.01). The positive correlation wasfound between the level of unconjugated hyperbilirubinemia and the level of myocardial enzyme(r=0.48, p<0.01).The serum LDH, AST, CK and CK-MB were clearly higher before treatment than those after the jaundice hadgone down, respectively (p<0.01). Conclusions The myocardial impairment was obvious in neonates with G-6-PD deficiency. There was a close relationship between the level of unconjugated bilirubin and the degree ofmyocardial damage.