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34 - Iron overload due to excessive supplementation

Published online by Cambridge University Press:  01 June 2011

James C. Barton
Affiliation:
University of Alabama, Birmingham
Corwin Q. Edwards
Affiliation:
University of Utah Medical Center
Pradyumna D. Phatak
Affiliation:
University of Rochester Medical Center, New York
Robert S. Britton
Affiliation:
St Louis University, Missouri
Bruce R. Bacon
Affiliation:
St Louis University, Missouri
James C. Barton
Affiliation:
University of Alabama, Birmingham
Corwin Q. Edwards
Affiliation:
University of Utah School of Medicine, Salt Lake City
Pradyumna D. Phatak
Affiliation:
University of Rochester Medical Center, New York
Robert S. Britton
Affiliation:
St Louis University, Missouri
Bruce R. Bacon
Affiliation:
St Louis University, Missouri
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Summary

Iron overload occurs in some adults who have ingested iron supplements for prolonged intervals, and in some persons who have received excessive parenteral iron supplementation with iron–carbohydrate complexes.

Iron overload due to excessive oral iron supplements

One report included patients who reported that their only or predominant source of non-dietary iron was daily iron supplements that they had ingested for more than 5 years. Patients who received either much parenteral iron or repeated erythrocyte transfusions were excluded. Most previously reported patients with iron overload due to iron supplements have been whites, although an African-American case has been described. Some patients were advised or elected to take iron because they had anemia. Other patients had types of anemia that may have enhanced iron absorption. Iron measures, liver histology, and other features suggested that “hereditary hemochromatosis” caused or contributed to iron overload in some cases reported before the discovery of the gene HFE. In some cases, neither “hemochromatosis” nor a heritable type of anemia was apparent.

Patient characteristics

Four patients ingested approximately 153, 547, 1341, and 4898 g of inorganic iron as supplements, respectively, over many years each. Many patients developed endocrinopathy, arthropathy, hyperpigmentation, increased serum levels of hepatic transaminases, or cirrhosis without explanation other than iron overload, although some patients appeared to have no illness. Among four patients, one had HFE C282Y homozygosity and beta-thalassemia minor. Another had spherocytosis and no HFE coding region mutation.

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Publisher: Cambridge University Press
Print publication year: 2010

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