Sinniah R
J Clin Pathol. 1969 Sep;22(5):567-72. doi: 10.1136/jcp.22.5.567.
In the present study, cirrhosis of the liver was found in one of six cases of transfusional siderosis. The relationship between iron overload and cirrhosis is discussed and the suggestion is made that factors other than iron deposition may have been responsible for the hepatic fibrosis. Three patients with a greater degree of iron overload, and for a longer period, did not develop fibrosis or cirrhosis. The possibility remains that iron absorbed from the gut and stored in excess without having passed through the haemoglobin molecule or the reticuloendothelial system may be toxic, as cases have been reported in which cirrhosis of the liver was attributed to prolonged iron medication. The cirrhosis in idiopathic haemochromatosis may be due to lack of an unknown hepatic cell enzyme, as in galactosaemia, and the increased iron absorption may be a concomitant finding. Transfusional or secondary haemochromatosis is not a definite entity, and the liver cirrhosis is probably due to causes other than the excess deposition of haemosiderin.
在本研究中,六例输血性血色病患者中有一例出现肝硬化。本文讨论了铁过载与肝硬化之间的关系,并提出除铁沉积外,其他因素可能是肝纤维化的原因。三名铁过载程度更高、时间更长的患者未发生纤维化或肝硬化。肠道吸收的铁未经血红蛋白分子或网状内皮系统而过量储存可能具有毒性,因为已有报道称肝 硬化可归因于长期铁剂治疗。特发性血色素沉着症中的肝硬化可能是由于缺乏一种未知的肝细胞酶,如半乳糖血症,而铁吸收增加可能是一个伴随发现。输血性或继发性血色素沉着症并非一个明确的实体,肝硬化可能是由含铁血黄素过量沉积以外的原因引起的。