Mechanism of development of bronze baby syndrome in neonates treated with phototherapy.
Mechanism of development of bronze baby syndrome in neonates treated with phototherapy.
复制标题
光疗治疗新生儿青铜婴儿综合征的发生机制。
作者：
S. Onishi;S. Itoh;K. Isobe;H. Togari;H. Kitoh;Y. Nishimura
在接受类似治疗的患有和不患有青铜婴儿综合症的婴儿的光疗过程中，对未知色素和光胆红素 IX α（两种主要胆红素光产物）的血清浓度进行了比较。通过高压液相色谱法估计，与光疗期间对照高胆红素血症新生儿相比，青铜婴儿综合征婴儿的血清未知色素浓度显着升高。然而，青铜婴儿综合征婴儿与对照组的血清光胆红素IXα浓度没有差异。通过高压液相色谱从体外实验获得的胆红素光产物中分离出的未知色素逐渐分解为棕色产物，其吸收光谱与青铜婴儿综合症婴儿的血清相似。这一事实可能是由于胆红素光产物的肝脏排泄功能降低，尤其是已知色素，因为其主要排泄途径是胆道途径。体内积累的色素可在自由基反应后聚合并形成胆褐素样物质。结论是棕色颜料是由未知颜料形成的。
Comparisons of serum concentrations of unknown pigment and photobilirubin IX alpha , the two main bilirubin photoproducts, were made during phototherapy in infants with and without bronze baby syndrome who were treated similarly. The serum concentrations of unknown pigment estimated by high-pressure liquid chromatography in infants with the bronze baby syndrome were significantly increased in comparison with those in the control hyperbilirubinemic neonates during phototherapy. However, there was no difference in the serum concentrations of photobilirubin IX alpha between infants with bronze baby syndrome and the control groups. The unknown pigment separated from bilirubin photoproducts obtained from experiments in vitro by high-pressure liquid chromatography was gradually decomposed into brown products that showed the absorption spectrum similar to that of the serum of infants with bronze baby syndrome. This fact is probably due to reduction in hepatic excretory function of bilirubin photoproducts, especially in known pigment, because its main excretory pathway is the biliary route. The pigment accumulated in the body may be polymerized and forms bilifuscin-like substances following a free radical reaction. It is concluded that the brown pigment is formed via unknown pigment.