Duodenal mucosal ferritin in rheumatoid arthritis: implications for anaemia of chronic disease |
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Authors: | O'Toole PA; Sykes H; Phelan M; Thompson RN; Lombard MG |
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Institution: | Department of Medicine, University of Liverpool, UK; Rheumatology Department, Fazakerly Hospital, Aintree Hospitals NHS Trust, Liverpool, UK; Corresponding author at: Gastroenterology Research Group, Department of Medicine, University of Liverpool, PO Box 147, Liverpool L69 3BX, UK |
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Abstract: | Anaemia is a common feature of rheumatoid arthritis (RA) and other chronic
diseases. Among the alterations in iron metabolism contributing to this
effect is a decrease in intestinal iron absorption. The mechanism for this
is unknown, but might involve a 'mucosal block' process similar to that
proposed in iron overload, whereby increased expression of an enterocyte
storage protein binds absorbed iron and prevents its transfer to the
circulation. We examined the effect of disease-modifying therapy on
ferritin expression in duodenal mucosa in RA to determine whether it may
play a role in the 'mucosal block' process. Endoscopic small bowel biopsies
were obtained from 11 patients with active RA both before, and 6 months
after, a course of either gold or methotrexate (MTX). Mucosal ferritin
levels 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 fall
in duodenal mucosal ferritin correlated with indices of disease activity at
start of therapy, and the largest decreases were in those patients showing
the best response to treatment in terms of a fall in inflammatory markers.
Site-specific changes in mucosal ferritin may underlie the altered iron
absorption observed in active inflammatory disease by modifying the
enterocyte 'mucosal block'.
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