Nature of anaemia in rheumatoid arthritis. VII. Storage of iron in rheumatoid disease.

Nature of anaemia in rheumatoid arthritis. XI. Changes in iron metabolism induced by the 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).…”

A case of sjögren's syndrome with severe anemia due to myelitis

“…Approximately 25-40% of patients with Sjrgren's syndrome develop mild anemia [10,11] which might be explained by sequestration of iron in joint membranes [8], impaired erythropoietin secretion [12], drug effects, especially via induction of gastrointestinal blood loss, hemolysis [9], and chronic renal failure. More recently immune suppression of hemopoetic cells [3,6] and pure red cell aplasia [4] have been described in rheumatic diseases which were attributed to serum components, especially IgM, rheumatoid factor [6], or IgG [4].…”

Lymph node iron in rheumatoid arthritis. Histology, ultrastructure, and chemical concentration.

“…The hypoferraemia coupled with evidence of increased iron storage (Lawson, Owen, and Mowat, 1967) suggests that the RES may be reluctant to release storage iron (Weinstein, 1959;Owen and Lawson, 1966). Efforts to demonstrate increased concentrations of iron in liver, spleen, and lymph nodes in patients not treated with iron have up until now been unsuccessful (Gardner and Roy, 1961).…”