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为探讨新生儿肝炎综合征发病的遗传机制 ,应用火箭电泳法检测了 35例肝炎综合征新生儿、31例健康新生儿和 46例成人 (成人对照组 30例 ,患儿父母 1 6例 )血浆α1 ACT水平 ,对新生儿肝炎综合征患儿急性发病期、临床痊愈期以及健康新生儿血浆α1 ACT水平的变化进行了比较 :采用全自动生化分析仪检测了先天性α1 ACT缺陷患儿急性发病期血清的总胆红素 (TB)、直接胆红素 (DB)、谷丙转氨酶(ALT)。结果表明患儿急性发病期血浆α1 ACT水平显著高于临床痊愈期 ,也显著高于儿童对照组 ;35例患儿中 8例血浆α1 ACT缺陷 ,5例决定为先天性α1 ACT缺陷 ,且5例患儿在急性发病期血浆α1 ACT水平与其血清TB、DB、ALT水平成显著的负相关。因此 ,提示先天性α1 ACT缺陷可能是新生儿肝炎综合征发病的遗传机制之一。
In order to explore the genetic mechanism of neonatal hepatitis syndrome, rhesus electrophoresis was used to detect 35 cases of neonatal hepatitis syndrome, 31 healthy newborns and 46 adults (30 cases of adult control group, 16 cases of parents of children) plasma α1 ACT levels in children with acute and chronic hepatitis B were compared in acute onset, clinical recovery and plasma levels of α1-ACT in healthy newborns: Acute biochemical analysis of children with congenital α1-ACT deficiencies Total serum bilirubin (TB), direct bilirubin (DB), alanine aminotransferase (ALT). The results showed that the plasma level of α1 ACT was significantly higher in the acute stage of children than in the clinical recovery group, and also significantly higher than the children control group; 8 of 35 children with plasma alpha1 ACT deficiency, 5 cases of congenital alpha1 ACT deficiency, and 5 The plasma levels of α1 ACT in children with acute onset were significantly and negatively correlated with the levels of serum TB, DB and ALT. Therefore, suggesting that congenital α1 ACT deficiency may be one of the genetic mechanisms of neonatal hepatitis syndrome.