Effect of Dose, Time, and Ascorbate on Iron Excretion After Subcutaneous Desferrioxamine

Hussain, M A; Green, N.; Flynn, Denis; Hoffbrand, A. V.

doi:10.1016/s0140-6736(77)92279-6

Cited by 77 publications

(32 citation statements)

References 13 publications

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“…The major issues remaining to be to be resolved are whether (1) long-term treatment of patients with L1 leads to a reduction in the basal LPI levels, and (2) L1 in vivo chelation capacity can be further improved by ascorbate supplemented to iron-overloaded patients, as demonstrated earlier by Holfbrand and coworkers for desferrioxamine. 38 Finally, the observed correlation between NTBI forms and LPI (Table 1) provides experimental support for the assumption that components of NTBI have a chemically labile character that can be revealed by physiologic concentrations of ascorbate. Since such a correlation might be masked by the presence of plasma antioxidants, LPI may be more prominent in cases where antioxidant levels decrease, such as in thalassemia 7 and in compromised infants.…”

Section: Discussionmentioning

confidence: 58%

Labile plasma iron in iron overload: redox activity and susceptibility to chelation

Espósito

Breuer

Sirankapracha

et al. 2003

Blood

413

327

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Plasma non-transferrin-bound-iron (NTBI) is believed to be responsible for catalyzing the formation of reactive radicals in the circulation of iron overloaded subjects, resulting in accumulation of oxidation products. We assessed the redox active component of NTBI in the plasma of healthy and ␤-thalassemic patients. The labile plasma iron (LPI) was determined with the fluorogenic dihydrorhodamine 123 by monitoring the generation of reactive radicals prompted by ascorbate but blocked by iron chelators. The assay was LPI specific since it was generated by physiologic concentrations of ascorbate, involved no sample manipulation, and was blocked by iron chelators that bind iron selectively. LPI, essentially absent from sera of healthy individuals, was present in those of ␤-thalassemia patients at levels (1-16 M) that correlated significantly with those of NTBI measured as mobilizer-dependent chelatable iron or desferrioxamine chelatable iron. Oral treatment of patients with deferiprone (L1) raised plasma NTBI due to iron mobilization but did not lead to LPI appearance, indicating that L1-chelated iron in plasma was not redox active. Moreover, oral L1 treatment eliminated LPI in patients. The approach enabled the assessment of LPI susceptibility to in vivo or in vitro chelation and the potential of LPI to cause tissue damage, as found in iron overload conditions. (Blood. 2003;102: 2670-2677)

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Section: Discussionmentioning

confidence: 58%

Labile plasma iron in iron overload: redox activity and susceptibility to chelation

Espósito

Breuer

Sirankapracha

et al. 2003

Blood

413

327

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“…In patients with SH or IH, DF-induced UIE, measured after a prolonged period of oral supplementation with vitamin C, is significantly higher than before the vita min C treatment [1][2][3]. However, it has been observed that vitamin C may have a toxic effect in these conditions, possibly related to the increase in membrane lipids peroxidation, which may be prevented by Table I -p < 0.05 -concomitant administration of an iron chelating agent [5].…”

Section: Discussionmentioning

confidence: 99%

“…Roth in idiopathic (IH) and secondary hemochromatosis (SH) a significant in crease in desferrioxamine (DF)-induced urinary iron excretion (UIE) was observed after prolonged oral supplementation with vitamin C [1][2][3][4]. The effect of ascorbic acid is probably related to the release of iron from ferritin by its reduction to the ferrous state, this potentiating effect of DF-induced iron excretion overwhelming concomitant increase in intestinal iron absorption [1,2].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Ascorbic Acid on Desferrioxamine-Induced Urinary Iron Excretion in Idiopathic Hemochromatosis

Conte¹,

Brunelli²,

Ferrario³

et al. 1984

Acta Haematol

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The effect on urinary iron excretion (UIE) of vitamin C administered orally 2 h after the start of an 8-hour desferrioxamine (DF) i.v. infusion was studied in 12 patients with untreated idiopathic hemochromatosis (IH). Mean ± SEM basal UIE of 324.6 ± 84.6 μg/24h increased after a 1-gram i.v. DF infusion to 8,778.5 ± 1,191.4 μg/ 24 h; when vitamin C 1 or 2 g were added to DF i.v. infusion, there were further increases to 11,241.5 ± 1,486.1 (p < 0.01) and 13,531.2 ± 1,697.2 μg/24h (p < 0.05 versus the last value), respectively. Basal UIE did not significantly increase after oral vitamin C administration alone. No side effects were observed.

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“…Desferrioxamine subcutaneous infusion has been shown to produce negative iron balance in transfusion-dependent thal [5][6][7][8][9], but, to the best of our knowledge, there is no study concerning the effect of this treatment in thal patients with chronic persistent (CPH) or active (CAH) hepatitis.…”

Section: Introductionmentioning

confidence: 99%

Iron Chelation in Transfusion-Dependent Thalassemia with Chronic Hepatitis

Virgiliis¹,

Cossu²,

Sanna³

et al. 1982

Acta Haematol

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In this study maximum urinary iron elimination with continuous desferrioxamine subcutaneous infusion was obtained in thalassemia major patients with chronic persistent or active hepatitis with lower doses (60 mg/kg) than those necessary in patients without hepatitis (80 mg/kg). Since dose-response curves were highly variable the treatment schedule should be tailored to the individual needs of each patient. Both groups may achieve iron balance but chronic hepatitis patients have more frequently a net urinary iron excretion. In patients with chronic hepatitis no correlation was found between serum ferritin levels or serum ferritin/aspartate aminotransferase ratios and transfusional iron overload while serum ferritin/aspartate aminotransferase ratios were seen to be correlated with liver iron stores.

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Effect of Dose, Time, and Ascorbate on Iron Excretion After Subcutaneous Desferrioxamine

Cited by 77 publications

References 13 publications

Labile plasma iron in iron overload: redox activity and susceptibility to chelation

Labile plasma iron in iron overload: redox activity and susceptibility to chelation

Effect of Ascorbic Acid on Desferrioxamine-Induced Urinary Iron Excretion in Idiopathic Hemochromatosis

Iron Chelation in Transfusion-Dependent Thalassemia with Chronic Hepatitis

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