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

Total blood volume (TBV) and red cell volume (RCV) determinations have become an established diagnostic procedure in a variety of conditions; they are being used increasingly to estimate the requirement of blood transfusion. A common laboratory practice is to determine indirectly the RCV and/or the TBV by measuring the plasma volume (PV) and the venous hematocrit (VH). This procedure is technically simple and has been made popular by a number of semiautomatic electronic devices. In the healthy population we find results of the direct and the indirect measure of the RCV to be not statistically different, although they may differ by as much as ± 10% in individual cases. Larger discrepancies between the results of the two methods have been reported in patients by numerous investigators. In the present study the RCV based on the PV was found to be significantly larger in many patients than the RCV measured directly by tagging of red cells. Emphasis is here placed on the severity of this discrepancy in the general bed‐patient population. The differences in the RCV cannot be explained alone by the variability of the hematocrit in the large and small vessels, but must involve an early loss of the albumin and/or the tag from the vascular bed. These findings cast doubt on the validity of the measure of the PV, and consequently of the estimated RCV, in a considerable number of patients. It will be shown that the discrepancies noted can be reduced significantly by basing the measure of the plasma volume on the highest T‐1824 density or on the highest 131I (RISA) activity obtained three to ten minutes postinfusion of the tag.

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1. Fresh and stored red cells, transfused in healthy subjects, disappear from the circulation during the first 24 hours at a rate in excess of that prevailing in subsequent 24 hour periods. When fresh red cells are transfused the excess first day loss is approximately 3 per cent. 2. Comparative survival studies using the nonagglutinable red cell method of Ashby have indicated that this excess immediate loss is not due to elution of Cr51, but to actual loss of red cells. 3. When red cells are stored improperly or for an extended period of time, the excess loss occurs very rapidly, and at one hour is approximately 50 per cent of the total loss at 24 hours. The limitations to the use of the dilution data of transfused stored cells to establish the 100 per cent value for the measure of the survival of the transfused red cells are implicit. 4. When the first 24 hour loss of transfused red cells is approximately 30 per cent or more, paradoxically the rate of loss in subsequent days is less than when fresh, undamaged red cells are transfused. This observation raises the question of interpretation of the measure of the red cell survival expressed as T ½.

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