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特发性血色素沉着症中肠道黏膜对铁的摄取及铁潴留:黏膜异常的证据

Intestinal mucosal uptake of iron and iron retention in idiopathic haemochromatosis as evidence for a mucosal abnormality.

作者信息

Powell L W, Campbell C B, Wilson E

出版信息

Gut. 1970 Sep;11(9):727-31. doi: 10.1136/gut.11.9.727.

Abstract

The process of iron absorption has been studied in 23 patients with idiopathic haemochromatosis, in eight with iron-deficiency anaemia, and in 20 control subjects. The initial uptake of iron by the intestinal mucosa was estimated by administering (59)Fe-ferric citrate during a standard meal together with a non-absorbable marker, (51)Cr-chromic chloride. Body iron absorption (iron retained at 14 days) was measured by whole body counting with discriminant analysis to separate the two isotopes. Thus, the fraction of the initial mucosal uptake finally retained in the body was calculated (the mucosal transport index of iron). In control subjects the mean values for mucosal uptake of iron and body iron absorption were 12.0 - SD 4.9% and 3.6 - SD 2.4%, with a mean mucosal transport index of 0.31 - SD 0.21. Mucosal iron uptake and body absorption were both considerably increased in the patients with iron-deficiency anaemia (33.5 - 15.6 and 29.8 - 17.0% respectively) and in the eight patients with idiopathic haemochromatosis treated by venesection therapy until the excess iron stores were removed (27.2 - 12.0 and 26.6 - 14.6% respectively). The mucosal transport index in all these subjects approached 1.0. Eight patients with haemochromatosis were studied before venesection therapy. The mucosal uptake of iron was within the normal range in all (mean 14.0 - 2.8%) but body iron absorption was increased in five (mean 9.1 - 4.8%). The mean mucosal transport index of iron was significantly increased in this group (0.62 - 0.28; p < 0.01). The findings suggest that the increased iron absorption in subjects with idiopathic haemochromatosis results from an abnormality of the intestinal mucosa and not from altered intraluminal factors. However, whether the aberrant mucosal cell function is a primary defect in the cell or an acquired change, dependent on humoral or corporeal factors, is unknown.

摘要

对23例特发性血色素沉着症患者、8例缺铁性贫血患者及20名对照者的铁吸收过程进行了研究。通过在标准餐时给予(59)铁 - 柠檬酸铁及不可吸收标记物(51)铬 - 氯化铬来估计肠道黏膜对铁的初始摄取。通过全身计数及判别分析测量机体铁吸收(14天时保留的铁)以区分这两种同位素。由此计算出最终保留在体内的初始黏膜摄取铁的比例(铁的黏膜转运指数)。在对照者中,铁的黏膜摄取及机体铁吸收的平均值分别为12.0 - 标准差4.9%和3.6 - 标准差2.4%,平均黏膜转运指数为0.31 - 标准差0.21。缺铁性贫血患者以及8例经放血疗法治疗直至过量铁储存被清除的特发性血色素沉着症患者的黏膜铁摄取和机体铁吸收均显著增加(分别为33.5 - 15.6和29.8 - 17.0%)。所有这些患者的黏膜转运指数均接近1.0。对8例血色素沉着症患者在放血疗法前进行了研究。所有患者的铁黏膜摄取均在正常范围内(平均14.0 - 2.8%),但5例患者的机体铁吸收增加(平均9.1 - 4.8%)。该组铁的平均黏膜转运指数显著增加(0.62 - 0.28;p < 0.01)。研究结果表明,特发性血色素沉着症患者铁吸收增加是由肠道黏膜异常所致,而非腔内因素改变所致。然而,异常的黏膜细胞功能是细胞的原发性缺陷还是依赖于体液或实体因素的后天性改变尚不清楚。

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