Okuda K, Ohkubo H, Musha H, Kotoda K, Abe H, Tanikawa K
Gut. 1976 Aug;17(8):588-94. doi: 10.1136/gut.17.8.588.
Five patients showing a normal to near-normal BSP test and a marked delay in ICG plasma clearance, and two families with clustering of the same abnormality, are described. Two had Gilbert's syndrome, one was convalescing from acute hepatitis, and the other two had no detectable liver abnormality. Measured indices of ICG metabolism indicated a marked reduction in the hepatic uptake, storage capacity, biliary transport maximum, and an increased reflux into plasma. Biochemical studies on the binding of ICG by plasma proteins failed to demonstrate any difference from normal controls. Thus, the primary defect seems to be in the transport of ICG by the hepatocyte. Although the relationship of the defect in ICG metabolism to other constitutional hyperbilirubinaemias is not clear, it is possible that the defect in these patients is a constitutional one involving some steps in the hepatic disposal of organic anions.
本文描述了5例BSP试验正常或接近正常但ICG血浆清除明显延迟的患者,以及两个存在相同异常聚集情况的家族。其中2例患有吉尔伯特综合征,1例正从急性肝炎中康复,另外2例未检测到肝脏异常。测量的ICG代谢指标显示肝脏摄取、储存能力、胆汁转运最大值显著降低,且反流回血浆的量增加。关于血浆蛋白与ICG结合的生化研究未发现与正常对照有任何差异。因此,主要缺陷似乎在于肝细胞对ICG的转运。虽然ICG代谢缺陷与其他体质性高胆红素血症的关系尚不清楚,但这些患者的缺陷可能是一种体质性缺陷,涉及肝脏处理有机阴离子的某些步骤。