Deferoxamine

Brand Names: Deferoxamine

Clinical Names: Tris-hydroxamate Deferoxamine, DFO

Summary

generic name: Deferoxamine

synonym: Tris-hydroxamate deferoxamine (DFO)

type of drug: Iron chelating agent.

used to treat: iron overload; primarily used with individuals who have accumulated excessive levels of iron as a result of repeated transfusions for special anemia conditions not related to nutritional deficiencies; can also rid the body of excess aluminum.

overview of interactions:
• nutrient affecting drug performance: Iron

• nutrient affecting drug performance: Vitamin C




Interactions

nutrient affecting drug performance: Iron

• mechanism: Since deferoxamine is administered to individuals with dangerously high levels of iron it would be counter-productive to supplement with iron.

• nutritional concerns: An individual on deferoxamine should consult the prescribing physician before using any supplements containing iron.

nutrient affecting drug performance: Vitamin C

• mechanism: Vitamin C supplementation, even at low levels (200 mg per day), has consistently enhanced the ability of deferoxamine to rid the body of excess iron even though vitamin C may slightly increase iron absorption. In twelve studies at different dose levels of deferoxamine, ascorbate therapy was associated with increased iron excretion ranging from 24% to 245%.
(Hussain MA, et al. Lancet 1977 May 7;1(8019):977-979.)

Please read the disclaimer concerning the intent and limitations of the information provided here.
Do not rely solely on the information in this article.

The information presented in Interactions is for informational and educational purposes only. It is based on scientific studies (human, animal, or in vitro), clinical experience, case reports, and/or traditional usage with sources as cited in each topic. The results reported may not necessarily occur in all individuals and different individuals with the same medical conditions with the same symptoms will often require differing treatments. For many of the conditions discussed, treatment with conventional medical therapies, including prescription drugs or over-the-counter medications, is also available. Consult your physician, an appropriately trained healthcare practitioner, and/or pharmacist for any health concern or medical problem before using any herbal products or nutritional supplements or before making any changes in prescribed medications and/or before attempting to independently treat a medical condition using supplements, herbs, remedies, or other forms of self-care.


References

Hoffbrand AV, Wonke B. Iron chelation therapy. J Intern Med Suppl 1997;740:37-41.

Hoffbrand AV. Prospects for oral iron chelation therapy. J Lab Clin Med 1994 Apr;123(4):492-494. (Review)

Hussain MA, Green N, Flynn DM, Hoffbrand AV. Effect of dose, time, and ascorbate on iron excretion after subcutaneous desferrioxamine. Lancet 1977 May 7;1(8019):977-979.
Abstract: The effect of 12 and 24 h continuous subcutaneous infusion of desferrioxamine (D.F.) on urinary iron excretion was compared in 13 patients with beta-thalassaemia major and 1 with congenital sideroblastic anaemia, all of whom were receiving regular blood-transfusions. 750 mg D.F. given over a 12 h period, gave a mean total (30 h) iron excretion of 17-5 mg, which was not statistically different from the mean iron excretion of 21-5 mg when the same dose was delivered over 24 h. 1500 mg D.F. gave a mean urinary iron excretion of 28-1 mg with a 12 h infusion, which was significantly less than the mean iron excretion of 39-6 mg with 24 h infusion. The 1500 mg dose gave a significant increase in iron excretion compared with the 750 mg dose when given by either 12 h or 24 h infusion. 7 of 8 patients, given D.F. over a 12 h period, had increased iron excretion when the dose was increased from 750 to 2000 mg. When the dose was increased to 4000 mg, however, the effect on iron excretion was variable. On the other hand, ascorbic-acid therapy was invariably associated with increased iron excretion after subcutaneous D.F. In twelve studies at different dose levels of D.F., ascorbate therapy was associated with increased iron excretion ranging from 24 to 245%. It is concluded that in most patients with transfusional iron overload subcutaneous D.F over a 12 h period, at a dose ranging from 2 to 4 g daily with ascorbic-acid saturation, is at present the most satisfactory method of removing excess iron.

Sakagami H, Satoh K, Fukuchi K, Gomi K, Takeda M. Effect on an iron-chelator on ascorbate-induced cytotoxicity. Free Radic Biol Med 1997;23(2):260-270.
Abstract: We investigated the effect of deferoxamine mesylate (DFO), an iron chelator, to test whether ascorbate-induced cytotoxicity is due to iron-catalyzed oxidation. Exposing human promyelocytic leukemic HL-60 cells to either sodium ascorbate or ascorbic acid for 1 h resulted in the progressive production of apoptotic cells characterized by cell shrinkage, as well as nuclear and internucleosomal DNA fragmentation. The addition of micromolar to millimolar concentrations of DFO during the 1-h exposure did not inhibit, but rather enhanced the ascorbate-induced apoptosis in both regular and serum-free RPMI1640 medium. However, a higher concentration of serum significantly inhibited the ascorbate-induced cytotoxicity. In contrast, the cytotoxic activity of ascorbate against T98G human glioblastoma cells was enhanced or reduced by micromolar and millimolar concentrations of DFO, respectively. Ascorbate significantly increased the oxidation potential in the culture medium, and the pro-oxidant action of ascorbate was further augmented by the presence of the cells. DFO did not significantly affect the ascorbyl radical intensity and only slightly reduced the ascorbate-elevated oxidation potential. These data demonstrated that ascorbate can induce cytotoxicity even in iron-deficient medium.