Tissue Iron and the Reticulo-Endothelial System in Rheumatoid Arthritis

Nature of anaemia in rheumatoid arthritis. 8. Iron content of synovial tissue in patients with rheumatoid arthritis and in normal individuals.

“…The mean iron content of synovial tissue from patients with rheumatoid arthritis was 17 -2 + 9.99 mg./100 g. and from controls it was 2-8+ 3 06 mg./100 g. This difference is significant (X2=15X5; P<0 001). The results are compared in Table III with those obtained in other organs by the same method (Gardner and Roy, 1961). The mean iron content of the synovial tissue of the knee joints of eight patients with rheumatoid arthritis was 15 *2 mg./100 g., which is also significantly greater than that of the control synovial tissue, all of which was obtained from knee joints.…”

“…of patients with rheumatoid arthritis, although iron was detected by a chemical method in every case. Gardner and Roy (1961) estimated the iron content of a variety of tissues obtained post mortem and found no increase of iron in the tissues of patients with rheumatoid arthritis when compared with controls. However, there was an impression of hyperplasia of the reticulo-endothelial system in the patients with rheumatoid arthritis.…”

Nature of anaemia in rheumatoid arthritis. XI. Changes in iron metabolism induced by the administration of corticotrophin.

“…Since there is proliferation of synovial tissue in patients with rheumatoid arthritis, it follows that relatively large quantities of iron must be deposited in this tissue. No evidence of large iron stores in other sites has been found in these patients (Gardner and Roy, 1961). This retention of iron by synovial tissue would appear to take place during episodes of active inflammation, since plasma iron values return to normal when activity of the disease is suppressed by administration of corticotrophin.…”

“…Several previous reports in this series have described abnormalities in the metabolism of iron in this disease (Roy, Alexander, and Duthie, 1955;Richmond, Gardner, Roy, and Duthie, 1956;Richmond, Roy, Gardner, Alexander, and Duthie, 1958;Gardner and Roy, 1961;Owen and Lawson, 1966;Lawson, Owen, and Mowat, 1967), and the present state of knowledge has been reviewed by Mowat and Hothersall (1968). The plasma iron is low in the presence of active disease (Bruzzone and Massimello, 1940;Nilsson, 1948), and the level is well correlated to the activity of the disease (Engstedt and Strandberg, 1966).…”

Anemia associated with rheumatoid disease

“…The rapid serum iron clearance varies directly with the rheumatoid disease activity (1 1,12), and increased avidity for iron by an active reticuloendothelial system is implied (8,9). Excessive reticuloendothelial iron deposits certainly occur in some patients with rheumatoid disease (13,14), but if failure to make this iron available for erythropoiesis is the primary cause of the anemia, an iron deficient blood film should develop; however, this is uncommon in rheumatoid disease (15). These last abnormalities of iron handling are widely accepted to be important in the pathogenesis of "anemia of chronic disease" with which rheumatoid anemia is classified (16), but neither the etiology nor the mechanism of the abnormalities have been clarified.…”