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ARS Home » Northeast Area » Beltsville, Maryland (BHNRC) » Beltsville Human Nutrition Research Center » Diet, Genomics and Immunology Laboratory » Research » Publications at this Location » Publication #78593


item Fields, Meira
item Lewis, Charles

Submitted to: Clinical Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/27/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary: Iron deficiency is the most common nutritional deficiency reported in the U.S. and ferritin levels are used routinely to diagnose and detect iron status in humans. The question that we asked was whether plasma ferritin can be used to diagnose anemia in copper deficiency and whether it is a reliable index of iron status. We fed rats copper-deficient and copper-adequate diets containing three levels of iron; low, adequate and fortified. Only in copper deficiency the anemia was more severe as the levels of dietary iron were increased. Plasma ferritin, however, did not reflect these abnormalities. Data show; (a) copper and iron influence each other, (b) when the diet is low in copper, the additional intake of iron is harmful and (c), plasma ferritin cannot be used to diagnose anemia and is not a reliable index of available iron stores in copper deficiency. Information derived from this study has important practical significance regarding the use of ferritin in clinical practice. Those who directly will benefit from this study are clinicians and health professionals who need to diagnose cases presenting as abnormalities of copper and iron metabolism. They should be aware of limitations and need in identifying other alternate functional tests to differentiate iron-deficiency anemia from anemia associated with copper deficiency.

Technical Abstract: The present investigation was carried out to determine whether ferritin, a conventional key laboratory index used in the assessment of iron status may help in the diagnosis of copper-deficiency anemia. Weanling male rats were fed a copper-deficient and adequate diets containing three levels of dietary iron. Regardless of copper, the consumption of low levels of dietary iron (19 ug Fe/g diet) resulted in anemia. Unlike copper-adequate rats, however, there was a significant negative response of hemoglobin and hematocrit to increases in dietary iron in copper-deficient rats. The most severe anemia was noted in copper-deficient rats fed the added iron (88 ug Fe/g). The anemia of copper deficiency, however, was not due to depletion of iron, but to augmented and unavailable iron stores. The highest levels of hepatic iron were associated with the most severe anemia. Plasma ferritin did not reflect these abnormalities. In contrast, in copper-adequate rats, levels of hepatic iron and plasma ferritin correlated with the degree of anemia. Data show that ferritin is not a reliable index of iron stores and therefore cannot be used alone to diagnose anemia of copper deficiency.