Department of Pediatric Hematology and Oncology, University Medical Center Eppendorf, Hamburg, Germany.
Pediatr Blood Cancer. 2010 May;54(5):758-60. doi: 10.1002/pbc.22390.
We report a Caucasian neonate with chronic non-spherocytic hemolytic anemia due to a class I G6PD deficiency. A novel mutation missense mutation in exon eight of the G6PD gene was detected (c.827C>T p.Pro276Leu). Bilirubin peaked on day 5 at 24 mg/dl with a conjugated bilirubin of 17 mg/dl. Jaundice resolved within 4 weeks. A detailed work-up failed to reveal other specific factors contributing to cholestasis. Severe hemolytic disease of the newborn may cause cholestasis even in the absence of associated primary hepato-biliary disease.
我们报告了一例因 I 类 G6PD 缺乏症导致慢性非球形细胞溶血性贫血的高加索新生儿。在 G6PD 基因的外显子 8 中检测到一种新的错义突变(c.827C>T p.Pro276Leu)。胆红素在第 5 天达到峰值,为 24mg/dl,结合胆红素为 17mg/dl。黄疸在 4 周内消退。详细的检查未能发现其他导致胆汁淤积的特定因素。即使没有相关的原发性肝胆疾病,严重的新生儿溶血病也可能导致胆汁淤积。