Duodenal mucosal ferritin in rheumatoid arthritis: implications for anaemia of chronic disease

Anaemia is a common feature of rheumatoid arthritis (RA) and other chronicdiseases. Among the alterations in iron metabolism contributing to thiseffect is a decrease in intestinal iron absorption. The mechanism for thisis unknown, but might involve a 'mucosal block' process similar to thatproposed in iron overload, whereby increased expression of an enterocytestorage protein binds absorbed iron and prevents its transfer to thecirculation. We examined the effect of disease-modifying therapy onferritin expression in duodenal mucosa in RA to determine whether it mayplay a role in the 'mucosal block' process. Endoscopic small bowel biopsieswere obtained from 11 patients with active RA both before, and 6 monthsafter, a course of either gold or methotrexate (MTX). Mucosal ferritinlevels in small bowel and stomach were measured by radio-immune assay.Duodenal mucosal ferritin decreased significantly following treatment (p<0.05). There were no changes in gastric mucosal ferritin. The fallin duodenal mucosal ferritin correlated with indices of disease activity atstart of therapy, and the largest decreases were in those patients showingthe best response to treatment in terms of a fall in inflammatory markers.Site-specific changes in mucosal ferritin may underlie the altered ironabsorption observed in active inflammatory disease by modifying theenterocyte 'mucosal block'.