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Hemochromatosis and Vitamin C
- James C. Barton, MD;
- Paul C. Adams, MD; and
- Lawrie W. Powell, MD, PhD
- Southern Iron Disorders Center; Birmingham, AL 35209 (Barton) London Health Sciences Center; London, Ontario N6A 5A5, Canada (Adams) Queensland Institute of Medical Research, University of Queensland; Brisbane 4029 QLD, Australia (Powell)
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IN RESPONSE
In persons who have thalassemia major with iron overload, vitamin C (ascorbic acid) can mobilize iron stored in reticuloendothelial cells, sometimes leading to acute cardiac toxicity (1). Withdrawal of vitamin C supplementation has been associated with improvement of left ventricular function, and vitamin C deficiency may protect against the cardiac effects of iron overload in patients with thalassemia major (1). In contrast, there is little published evidence that vitamin C mobilizes large quantities of iron or induces acute (or chronic) toxicity in hemochromatosis. Urinary iron excretion, a measure of iron mobilization, was not increased by oral vitamin C in untreated patients with hemochromatosis who received an infusion of desferrioxamine. Furthermore, these patients experienced no associated adverse effects (2). In our review of hemochromatosis management, we cited the unusual report of a 29-year-old man who for 1 year had taken 1 g of ascorbic acid tablets daily and artificial orange juice containing supplementary ascorbic acid. Eight days after presentation, he died of complications of cardiomyopathy. At autopsy, well-known complications of iron overload due to hemochromatosis, including severe iron deposition in his myocardium, pancreas, and liver, and micronodular cirrhosis, were discovered (3). Accordingly, the authors' conclusion that this patient's ingestion of large amounts of ascorbic acid could have induced or accelerated the development of cardiomyopathy was “speculative” (3).
Mean leukocyte ascorbic acid concentrations were significantly lower in untreated than in treated persons with hemochromatosis (4). This indicates that vitamin C deficiency is common in untreated persons with hemochromatosis and that iron overload is the main cause of the deficiency. Unlike iron overload in thalassemia, excess iron in hemochromatosis is deposited predominantly in parenchymal cells. Thus, differences in vitamin C metabolism, cellular iron deposition, and ferrokinetics could account for the apparently dissimilar clinical effects of vitamin C in mobilizing excess stored iron in patients with thalassemia major and hemochromatosis, respectively.
We do not advocate that persons with hemochromatosis take vitamin C routinely (3), even though many untreated patients have vitamin C deficiency (4). Our dietary recommendations indicated that “There is no rationale for discouraging patients with hemochromatosis from consuming fresh fruits and vegetables containing vitamin C, but it seems prudent to advise them to limit ingestion of vitamin C in supplements to 500 mg/d.” We believe that our suggestions are consistent with the existing clinical data on the interrelation of vitamin C, iron overload, and hemochromatosis.
James C. Barton, MD
Southern Iron Disorders Center; Birmingham, AL 35209
Paul C. Adams, MD
London Health Sciences Center; London, Ontario N6A 5A5, Canada
Lawrie W. Powell, MD, PhD
Queensland Institute of Medical Research, University of Queensland; Brisbane 4029 QLD, Australia
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
