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AMA Arch Intern Med. 1954;94(1):22-33. doi:10.1001/archinte.1954.00250010028003.
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SINCE the liver is the body's chief repository of stored iron, it was inevitable that clinical investigation of the organ in its diseased state eventually included disturbances in that function of storage. Widespread use of needle biopsy has led to the realization that siderosis of the liver not infrequently follows acute viral hepatitis and certain nutritional disturbances.1 In turn, that observation has stimulated the investigation of changes in serum iron resulting from hepatic disease, particularly viral hepatitis. Reports of such studies are common in European literature but are few in this country, a real oversight when one considers the conclusion drawn by one investigator that "acute hepatitis is the only disease in human beings which is consistently associated with a marked hypersideremia." 2 The conclusion indicates a remarkable degree of specificity which, unfortunately, cannot often be assigned to a laboratory procedure. Certainly, it warrants investigation of serum iron determination as a test of hepatic function in the differential diagnosis of jaundice—still a


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