PubMed Health⌕ Search

PubMed · 11688076

Iron deficiency and the developing world.

Abstract

The dietary intake of iron in underdeveloped countries is based mainly on non-hem iron which is absorbed to a lesser degree that hem iron and is subjected to many interferences from inhibitors generally present in the diets, such as phenols, phytates, fibers, etc. Food fortification with iron is considered to be the best and cheapest long-term approach for correcting the deficiency. The iron source selected for this purpose has to be soluble, and of high bioavailability, even in a diet rich in inhibitors. Ferrochel may prove to be this type of compound.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A P MacPhail. 2001. Iron deficiency and the developing world.. https://pubmed.ncbi.nlm.nih.gov/11688076/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Hepcidin antimicrobial peptide transgenic mice exhibit features of the anemia of inflammation.

The anemia of inflammation is an acquired disorder affecting patients with a variety of medical conditions, and it is characterized by changes in iron homeostasis and erythropoiesis. Mounting evidence suggests that hepcidin antimicrobial peptide plays a primary role in the pathogenesis of the anemia of inflammation. To evaluate which features of this anemia can be attributed to hepcidin, we have generated mice carrying a tetracycline-regulated hepcidin transgene. Expression of the hepcidin transgene resulted in down-regulation of endogenous hepcidin mRNA. The transgenic mice developed a mild-to-moderate anemia associated with iron deficiency and iron-restricted erythropoiesis. Similar to the anemia of inflammation, iron accumulated in tissue macrophages, whereas a relative paucity of iron was found in the liver. Circulating erythrocytes in transgenic animals had normal survival rates, but transgenic animals had an impaired response to erythropoietin. Thus, hepcidin transgenic mice recapitulate each of the key features of anemia of inflammation in human patients and serve as a useful model of this prevalent disorder.

Anemia, Iron-Deficiency↗

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

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.

Anemia, Iron-Deficiency↗