Powell L W, McKeering L V, Halliday J W
Gut. 1975 Nov;16(11):909-12. doi: 10.1136/gut.16.11.909.
Purified tissue ferritins isolated from Bantu subjects with gross haemosiderosis, from a patient with idiopathic haemochromatosis (HC) treated by phlebotomy, and from rats with experimental iron overload were studied in order to determine the significance of the abnormality previously demonstrated in tissue isoferritins in patients with IHC. The isoferrin profile of the tissues from the Bantu subjects and the iron-loaded rats showed a similar abnormality to that previously found in patients with untreated IHC--that is, an abnormally uniform distribution of iron-containing isoferritins with an increase in the more basic isoferritins and an apparent absence of the more acidic ones. In contrast, tissues from the patient with treated IHC, who was iron depleted at the time of death, showed the normal organ-specific isoferritin distribution. These findings strongly suggest that the abnormal distribution of tissue isoferritins in IHC is an acquired phenomenon and unlikely to be related to an underlying genetic defect in ferritin or iron metabolism.
对从患有严重血色素沉着症的班图人、接受放血治疗的特发性血色素沉着症（HC）患者以及实验性铁过载大鼠中分离出的纯化组织铁蛋白进行了研究，以确定先前在特发性血色素沉着症患者的组织异铁蛋白中所显示异常的意义。班图人和铁过载大鼠组织的异铁蛋白谱显示出与先前在未经治疗的特发性血色素沉着症患者中发现的类似异常，即含铁异铁蛋白的分布异常均匀，碱性较强的异铁蛋白增加，而酸性较强的异铁蛋白明显缺失。相比之下，接受过治疗的特发性血色素沉着症患者在死亡时铁已耗竭，其组织显示出正常的器官特异性异铁蛋白分布。这些发现有力地表明，特发性血色素沉着症中组织异铁蛋白的异常分布是一种后天现象，不太可能与铁蛋白或铁代谢的潜在遗传缺陷有关。
