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 59Fe-ferric citrate during a standard meal together with a non-absorbable marker, 51Cr-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.
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