The selective deposition of hemosiderin in the liver parenchyma during pernicious anemia does not constitute evidence that there is a hemolytic cause for the disease located in the portal region. The repeated introduction of small amounts of free hemoglobin into the general circulation, by the subcutaneous route, leads, as we have shown, to an identical siderosis. Larger amounts of hemoglobin cause a renal pigmentation equalling or exceeding the hepatic, a fact that is in keeping with what is known of the physiology of hemoglobin excretion and of the findings in human beings afteroutspoken hemolysis.

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