Abstract
Summary
Impaired reticuloendothelial outflow was studied in patients with rheumatoid arthritis and in swine given endotoxin. In both of these situations, ceruloplasmin and ceruloplasmin ferroxidase activity either remained the same or increased. Administration of ceruloplasmin did not prevent or overcome the endotoxin-induced block. Thus, the “RE iron block” of the anemia of chronic disease cannot be explained by inhibition of the ceruloplasmin dependent step in iron metabolism.
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