By EMIL #{149}J. FREIIIEICH, AARON )sILLLER, CH iitI I s P. EMERSON ANI) JOSEPH F’. Ross I NFECTION ANI) INFLA()N have been shown to inipair the ability of the 1)Omie mnarrow to respomid to in(reased deniands for re(l cell production. Following acute or chronic blood loss, inflalnmuation slows the rate of hemoglobin productiomi;tm iii pernicious amiemia patiemits umidergoing adequate vitaniimi B-12 therapy, infection slows the rate of recovery;2 in patients with hemolytic anemias, inflammnation can depress hemiioglobin product ion amid rc’stilt in hypophastic crises.3 ‘ inflammnatioii does depress hemnogbobimi produl(tion, the niechamiism by which this occurs is not known. Inflammation also produces marked chamiges imi iron miietabolism. A decrease imiserumn iromi comicentration is a comistant findimig.5 The miiechamiism of the hypoferremia and its role imi the bomie miiarrow depression is not clearly umiderstood.
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Freireich et al. (1957) studied this question.
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