Iron metabolism in rheumatoid arthritis

Abstract

Patients with rheumatoid arthritis were found to have a rapid plasma clearance of iron, a low serum iron, and a diminished absorption of iron from the gastrointestinal tract. These abnormalities appear to be manifestations of an abnormal iron metabolism which is probably present in all patients with rheumatoid arthritis. Anemia represents the end result of the more severe degrees of the abnormality. Chronic blood loss, hemolysis, increased blood volume, and bone marrow depression represent secondary complications superimposed on the underIying abnormality.Esseva trovate que patientes con arthritis rheumatoidee ha un rapide clearance de ferro in le plasma. Lor concentration de ferro sera1 es basse. IIles ha un reducite absorption de ferro ab le vias gastro-intestinal. Iste anormalitates pare esser manifestationes de un anormal metabolismo de ferro le qua1 es probabilemente presente in omne patientes con arthritis rheumatoidee. Anemia representa le resultato terminal del grados plus sever de iste anormalitate. Chronic perdita de sanguine, hemolyse, augmento del volumine de sanguine, e depression del medulla ossee representa complicationes secundari que se superimpone a1 subjacente anormalitate.NEMIA IS RECOGNIZED as a common manifestatim of rheumatoid A arthritis. Short, Bauer, and Reynolds* found approximately 23 per cent of a large series of patients anemic on the basis of red cell count. The mechanism of production of this anemia has been a subject of investigation, and there is considerable difference in opinions expressed by various investigators.The present paper reports the results of the study of iron metabolism in 29 patients with rheumatoid aithritis. METHODSHemoglobin determination was done by the Oxyhemoglobin method standardized by the iron determination and the 0, capacity.2 The microhematocrit technique was used,3 and Ted blood cell count and white blood cell count were done by an electronic cell counter.4 Sedimentation rate was done using the Cutler method.5 Osmotic fragility of the red blood cells was carried out according to the method of Parpart.6 The rheumatoid factor was meisured by latex particle fixation.7 The electrophoresis of serum protein was carried out by paper electrophoresis.* Platelet count was done with the phase method.9Serum iron determinations were done according to the method outlined by Schales.10 Unsaturated isron binding capacity was done by the method of Ventura.11 Direct and indirect Coombs tests were performed at 37" C. using commercial antiserum.12 Blood volume determinations were done by Cr51 tagging of red blood cells13 or with Evans blue dye dihtion technique.14 Total circulating hemoglobin was calculated on the basis of the patient's venous hemoglobin and the blood volume with a correction factor of .93.14 From the

Iron in the synovial membrane in rheumatoid arthritis and other joint diseases.

“…The aetiology of the anaemia remains uncertain. A common feature is hypoferraemia which is coupled with a rapid plasma clearance of iron (Raymond, Bowie, and Dugan, 1965). These workers have confirmed the work of Freireich, Ross, Bayles, Emerson, and Finch (1957b), which showed that the utilization of exogenous iron from erythrocyte production was unimpaired and that the total daily production of erythrocyte haemoglobin was normal.…”

Concentration of iron in synovial membrane, synovial fluid, and serum in rheumatoid arthritis and other joint diseases.

“…However, it is not thought likely that the circulating transferrin-bound iron would be transferred directly to synovial cells in the quantities demonstrated here. The level of serum iron in rheumatoid arthritis is consistently low (Brendstrup, 1953;Raymond, Bowie, and Dugan, 1965), and there was no relationship shown here between the serum iron and the synovial tissue iron. Synovial fluid iron also shows no correlation with synovial tissue iron and we consider it is more likely that the red cells extruded into the synovial fluid and the synovial membrane provide the iron which is seen in these extensive deposits (for further discussion-see Muirden and Senator, 1968).…”

Ferritin in Synovial Cells in Patients with Rheumatoid Arthritis

“…Iron is normally absorbed from the gut (Roy, Alexander, and Duthie, 1955), and chronic blood loss from the gastrointestinal tract cannot explain the majority of cases of anaemia. The recent studies of Raymond, Bowie, and Dugan (1965) have emphasized that there is an increased plasma clearance of iron and it has been suggested that the reticulo-endothelial cells and perhaps hepatic parenchymal cells may be unusually avid for iron. A parallel could exist here with the anaemia of infection and inflammation, where it has been reported that there is defective re-utilization of iron probably related to a defect in release of iron from storage sites, principally the liver and spleen (Haurani, Burke, and Martinez, 1965).…”