Bioavailability of carbonyl iron: A randomized, double‐blind study

Devasthali, Shirish D.; Gordeuk, Victor R.; Brittenham, Gary M.; Bravo, Joanne R.; Hughes, Margaret; Keating, Louise J.

doi:10.1111/j.1600-0609.1991.tb01538.x

Cited by 42 publications

(11 citation statements)

References 15 publications

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“…When carbonyl iron is consumed without a meal in pharmacologic (100 mg) doses, it is reported to have a relative bioavailability in humans of about 70% that of ferrous sulfate. 43 It seems probable that the low levels of elemental iron (40 mg/kg) added to wheat flour would have little impact on iron nutrition, but the much higher levels added to commercial infant cereals (200-550 mgkg) together with vitamin C could contribute substantially to the prevention of iron deficiency anemia.…”

Section: Compounds Poorly Soluble In Dilute Acidsmentioning

confidence: 99%

Preventing Iron Deficiency Through Food Fortification

2009

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Section: Compounds Poorly Soluble In Dilute Acidsmentioning

confidence: 99%

Preventing Iron Deficiency Through Food Fortification

2009

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“…If side-effects limit compliance, the medication can be administered with food, or the dose can be reduced. One 500-mg ferrous sulphate dose nightly at bedtime may be an effective therapy in adults [19]. …”

Section: Oral Iron Therapymentioning

confidence: 99%

Iron therapy for renal anemia: how much needed, how much harmful?

Hörl

2007

Pediatr Nephrol

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Iron deficiency is the most common cause of hyporesponsiveness to erythropoiesis-stimulating agents (ESAs) in end-stage renal disease (ESRD) patients. Iron deficiency can easily be corrected by intravenous iron administration, which is more effective than oral iron supplementation, at least in adult patients with chronic kidney disease (CKD). Iron status can be monitored by different parameters such as ferritin, transferrin saturation, percentage of hypochromic red blood cells, and/or the reticulocyte hemoglobin content, but an increased erythropoietic response to iron supplementation is the most widely accepted reference standard of iron-deficient erythropoiesis. Parenteral iron therapy is not without acute and chronic adverse events. While provocative animal and in vitro studies suggest induction of inflammation, oxidative stress, and kidney damage by available parenteral iron preparations, several recent clinical studies showed the opposite effects as long as intravenous iron was adequately dosed. Thus, within the recommended international guidelines, parenteral iron administration is safe. Intravenous iron therapy should be withheld during acute infection but not during inflammation. The integration of ESA and intravenous iron therapy into anemia management allowed attainment of target hemoglobin values in the majority of pediatric and adult CKD and ESRD patients.

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“…treated rats revealed no morphological changes (data not shown). Devasthali et al (1991) reported that ferrous sulphate, as a dietary iron supplement, causes gastrointestinal side effects. Present findings indicate a significant decrease in body weight of iron-treated rats compared to controls.…”

Section: Figure 4 A: Western Blot For Brush Border Sucrase In Purifiedmentioning

confidence: 98%

Effect of Chronic Iron Ingestion on the Development of Brush Border Enzymes in Rat Intestine

Vir

Kaur

Mahmood

2007

Toxicology Mechanisms and Methods

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Iron is an essential element for biological systems. There is increasing evidence that excess iron supplementation results in the deposition of iron in the duodenum and enhances mucosal injury and cell proliferation in the colon and cecum. In the present study we examined whether chronic exposure to high levels of iron fortification affects the functional integrity of the small intestine, especially the activities of various brush border enzymes. Wistar rats were fed iron 29 mg/kg body weight (or 6.58 mg/kg Fe) daily in the form of FeSO(4).7H(2)O for 39 days. The activities of brush border alkaline phosphatase (AP) (p < 0.001), sucrase (p < 0.01), maltase (p < 0.05), lactase (p < 0.05), and trehalase (p < 0.001) were reduced in purified membranes in iron-fed animals compared to controls. However, the activities of leucine amino peptidase (LAP) and gamma-glutamyl transpeptidase (gamma-GTP) were unaffected under these conditions. Analysis of alkaline phosphatase activity across the crypt-villus unit revealed a significant decrease (p < 0.05) all across the crypt-villus length, while sucrase activity was reduced (p < 0.01) only in the midvillus axis in iron-exposed animals. Kinetic studies showed a decrease in V(max) of AP from 1.11 to 0.83 units/mg protein and for sucrase from 0.77 to 0.43 units/mg protein in iron-fed rats, with no change in the apparent K(m) of the enzymes (AP, 8 mM; sucrase, 10 mM). Western blot analysis corroborated these findings. These results indicate that chronic iron exposure alters the activities of brush border enzymes, resulting in intestinal dysfunctions.

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Bioavailability of carbonyl iron: A randomized, double‐blind study

Cited by 42 publications

References 15 publications

Preventing Iron Deficiency Through Food Fortification

Preventing Iron Deficiency Through Food Fortification

Iron therapy for renal anemia: how much needed, how much harmful?

Effect of Chronic Iron Ingestion on the Development of Brush Border Enzymes in Rat Intestine

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