Chemical reactions of vitamin C with intravenous-iron formulations

Wang, Suxin; Geraci, Gina; Kuhlmann, Martin K.; Levin, Nathan W.; Handelman, Garry J.

doi:10.1093/ndt/gfm557

Cited by 18 publications

(16 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Ascorbic acid enhances iron mobilization to transferrin in serum from IS, but not from other IVI's (Sturm et al 2005;Wang et al 2008) and the order of chemical stability is not predictive for biostability in presence of ascorbic acid. As reported previously, transferrin-chelatable iron from IS increased in presence of ascorbic acid, but unexpectedly declined with FCM.…”

Section: Discussionmentioning

confidence: 93%

Iron sucrose and ferric carboxymaltose: no correlation between physicochemical stability and biological activity

et al. 2014

View full text Add to dashboard Cite

Intravenous iron preparations, like iron sucrose (IS) and ferric carboxymaltose (FCM) differ in their physicochemical stability. Thus differences in storage and utilization can be expected and were investigated in a non-clinical study in liver parenchyma HepG2-cells and THP-1 macrophages as models for toxicological and pharmacological target cells. HepG2-cells incorporated significant amounts of IS, elevated the labile iron pool (LIP) and ferritin and stimulated iron release. HepG2-cells had lower basal cellular iron and ferritin content than THP-1 macrophages, which showed only marginal accumulation of IS and FCM. However, FCM increased the LIP up to twofold and significantly elevated ferritin within 24 h in HepG2-cells. IS and FCM were non-toxic for HepG2-cells and THP-1 macrophages were more sensitive to FCM compared to IS at all concentrations tested. In a cell-free environment redox-active iron was higher with IS than FCM. Biostability testing via assessment of direct transfer to serum transferrin did not reflect the chemical stability of the complexes (i.e., FCM > IS). Effect of vitamin C on mobilisation to transferrin was an increase with IS and interestingly a decrease with FCM. In conclusion, FCM has low bioavailability for liver parenchyma cells, therefore liver iron deposition is unlikely. Ascorbic acid reduces transferrin-chelatable iron from ferric carboxymaltose, thus effects on hepcidin expression should be investigated in clinical studies.

show abstract

Section: Discussionmentioning

confidence: 93%

Iron sucrose and ferric carboxymaltose: no correlation between physicochemical stability and biological activity

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Thus, more labile iron is spontaneously released from IS than from ID in plasma [42,48]. Additionally, ascorbate can reduce and mobilize iron bound in IS but not in ID [18,49,50]. At last, less direct iron donation to transferrin [42] and less NTBI uptake by human hepatoma cells [51] have been found following ID administration, compared to IS.…”

Section: Discussionmentioning

confidence: 99%

Acute Oxidative Stress following Intravenous Iron Injection in Patients on Chronic Hemodialysis: A Comparison of Iron-Sucrose and Iron-Dextran

2010

View full text Add to dashboard Cite

Background/Aims: Intravascular iron release from parenteral iron formulations can catalyze various harmful oxidative reactions. These topics have mainly been investigated in vivo with iron-sucrose (IS). The aim of our study was to compare IS and iron-dextran (ID) regarding iron release and induction of oxidative stress. Methods: Twenty hemodialysis patients were enrolled. Plasma iron and oxidative stress parameters were measured before and 10 min after intravenous (IV) injection of 100 mg IS and ID, respectively. Results: Intravascular iron increased significantly more after IS. The mean ± SD changes in plasma iron were 314 ± 172% after IS versus 90 ± 44% after ID (p < 0.001). Comparable changes in non-transferrin bound iron were 86 ± 42 versus 45 ± 45%, respectively (p < 0.05). Plasma ascorbic free radical did not change following ID (–1.8 ± 11.2%) but increased by 29 ± 31.3% after IS (p < 0.01). Further, protein carbonyls increased following IS (p < 0.05) but not after ID. Conclusion: Increased oxidative stress was found only after IV injection with IS.

show abstract

“…• Dialysis patients are often vitamin C deficient [56,57], and this contributes to their anemia. Supplemental vitamin C helps the absorption of dietary iron and utilization of storage iron [58,59].…”

Section: Anemia Of Renal Diseasementioning

confidence: 99%

Iron and anemia in human biology: a review of mechanisms

2008

View full text Add to dashboard Cite

The biology of iron in relation to anemia is best understood by a review of the iron cycle, since the majority of iron for erythropoiesis is provided by iron recovered from senescent erythrocytes. In iron-deficiency anemia, storage iron declines until iron delivery to the bone marrow is insufficient for erythropoiesis. This can be monitored with clinical indicators, beginning with low plasma ferritin, followed by decreased plasma iron and transferrin saturation, and culminating in red blood cells with low-Hb content. When adequate dietary iron is provided, these markers show return to normal, indicating a response to the dietary supplement. Anemia of inflammation (also known as anemia of chronic disease, or ACD) follows a different course, because in this form of anemia storage iron is often abundant but not available for erythropoiesis. The diagnosis of ACD is more difficult than the diagnosis of iron-deficiency anemia, and often the first identified symptom is the failure to show a response to a dietary iron supplement. Confirmation of ACD is best obtained from elevated markers of inflammation. The treatment of ACD, which typically employs erythropoietin (EPO) supplements and intravenous iron (i.v.-iron), is empirical and often falls shorts of therapeutic goals. Dialysis patients show a complex pattern of anemia, which results from inadequate EPO production by the kidney, inflammation, changes in nutrition, and blood losses during treatment. EPO and i.v.-iron are the mainstays of treatment. Patients with heart failure can be anemic, with incidence as high as 50%. The causes are multifactorial; inflammation now appears to be the primary cause of this form of anemia, with contributions from increased plasma volume, effects of drug therapy, and other complications of heart disease. Discerning the mechanisms of anemia for the heart failure patient may aid rational therapy in each case.

show abstract

Chemical reactions of vitamin C with intravenous-iron formulations

Cited by 18 publications

References 35 publications

Iron sucrose and ferric carboxymaltose: no correlation between physicochemical stability and biological activity

Iron sucrose and ferric carboxymaltose: no correlation between physicochemical stability and biological activity

Acute Oxidative Stress following Intravenous Iron Injection in Patients on Chronic Hemodialysis: A Comparison of Iron-Sucrose and Iron-Dextran

Iron and anemia in human biology: a review of mechanisms

Contact Info

Product

Resources

About