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).
Published: Ann Intern Med. 1999;131(6):476.