THE ANEMIA OF INFECTION. IV. THE LACK OF RELATIONSHIP BETWEEN THE DIVERSION OF IRON FROM THE PLASMA AND THE ORIGIN OF THE ANEMIA 1

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Abstract
IV. Patients with anemia of chronic infection were subjected to continuous intravenous infusions of Fe for periods as long as 72 hrs. It was found that considerably more Fe was required to maintain a normal plasma Fe level than would be expected from the results of a single intraven. injn. of Fe. The higher the plasma iron value desired, the more inefficient was the infusion. Furthermore, the infusion of Fe failed to increase Hb formation. The observations suggest that there is a braking mechanism which prevents the plasma Fe from rising above a certain level. Furthermore, since even very intensive iron therapy is ineffective in relieving the anemia of infection, it follows that Fe is not the limiting factor in the production of the anemia even though diversion of Fe from the plasma does occur. V. In order to determine the fate of the Fe when it is given in the presence of inflammation, radioactive Fe was injected intravenously in normal rats and dogs and in animals with acute inflammation produced by the injn. of turpentine or various bacterial cultures. A number of rats with inflammation showed retarded hemo-poiesis and increased deposition of Fe59 in the liver and spleen as compared to the control animals. There was good inverse correlation between the Fe59 in the liver and in the blood in both the normal rats and in the animals with inflammation. Analyses of the inflamed tissues for Fe59 indicated that no significant quantity of Fe was diverted to the inflamed area. Insignificant percentages of large doses of intravenously injected Fe were found in the exudate of a sterile abscess and in the excreta of a dog that had received turpentine intramusc. These observations indicate that the major diversion of plasma Fe in infection is to the ordinary storage tissues, mainly the liver. The diversion is related to the hypoferremia. These studies indicate that the lack of Fe is not the fundamental factor in the pathogenesis of the anemia of infection. Since there seems to be no deficiency of erythrocyte protoporphyrin or of Cu, by elimination the protein moiety of Hb is suspected as being involved in the pathogenesis of this anemia.