Although the morphologic, biochemical and clinical characteristics of the anemia associated with chronic infection have been studied exten-sively (1), the pathogenesis of the anemia re-mains obscure. The profound alterations in iron and porphyrin metabolism which accompany this type of anemia have been interpreted as indi-cating a decreased rate of erythrocyte production as the result of a quantitative defect in the rate-of conversion of protoporphyrin to hemoglobin (1, 2). The usual evidences of increased blood destruction, such as increased urobilinogen ex-cretion and elevated serum bilirubin concentration, are lacking in the anemia of chronic infection (1). Studies of the erythrocyte survival time have yielded conflicting results. Mollison (3), using the Ashby differential agglutination technique, found a normal disappearance rate for erythrocytes transfused into six patients with chronic sepsis and anemia. Brown (4), employing the same technique, observed a decreased life span of transfused erythrocytes in four of five cases. In pulmonary tuberculosis Hollingsworth and Hol-lingsworth (5) reported recently that the life span of autotransfused Cr51-tagged erythrocytes is nor-mal. Since the anemia which is associated with rheu-matic fever and rheumatoid arthritis is morpho-logically and biochemically similar to that associ-ated with chronic sepsis (1), it seems appropri-ate to comment on several studies in these condi-tions. Reinhold (6), using the Ashby method, found the erythrocyte life span to be decreased in
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Bush et al. (1956) studied this question.
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