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© 1990 British Society for Rheumatology


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IMPAIRED IRON UPTAKE AND TRANSFERRIN BINDING BY ERYTHROBLASTS IN THE ANAEMIA OF RHEUMATOID ARTHRITIS

G. VREUGDENHIL1,2, M. J. KROOS3, H. G. van EIJK3, B. LÖWENBERG4 and A. J. G. SWAAK2,5,

1Department of Internal Medicine, Zuiderziekenhuis Rotterdam, The Netherlands
2Department of Rheumatology, The Dr Daniel den Hoed Clinic Rotterdam, The Netherlands
3Department of Chemical Pathology, Erasmus University Rotterdam Rotterdam, The Netherlands
4Department of Haematology, The Dr Daniel den Hoed Clinic Rotterdam, The Netherlands
5Deparment of Autoimmune Diseases, Netherlands Red Cross Blood Transfusion Service Amsterdam, The Netherlands

Correspondence to: Correspondence to Dr A. Swaak, Department of Rheumatology, Groene Hilledijk 301, 3075 EA -Rotterdam, The Netherlands

Serum and bone marrow from 18 patients with rheumatoid arthritis (RA) and five healthy controls were studied in order to establish a possible role of impaired iron uptake and transferrin binding by erythroblasts in the pathophysiology of anaemia of chronic disease (ACD) in RA. Iron incorporation into erythroblasts was reduced in patients with ACD using a method based on incubation of erythroblasts with radiolabelled 59Fe-125I-transferrin. It correlated negatively with C-reac-tive protein (CRP). In iron deficient RA patients it tended to be reduced as well. These patients had the same level of RA disease activity as in ACD. Transferrin binding by erythroblasts was significantly impaired in ACD compared to controls, although it tended to be reduced in all RA groups.

These findings suggest that impaired iron uptake by erythroblasts, probably due to decreased transferrin binding to erythroblasts, might be a pathophysiological factor in ACD in RA

KEY WORDS: Iron incorporation, Transferrin binding, Erythroblasts, Anaemia of chronic disease, C-reactive protein


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