Iron Compounds

Not all iron ingested in food is equally absorbable. Trivalent Fe3+ is virtually not taken up from the neutral milieu of the small bowel, where the divalent Fe2+ is markedly better absorbed. Uptake is particularly efficient in the form of heme (present in hemo- and myoglobin). Within the mucosal cells of the gut, iron is oxidized and either deposited as ferritin (see below) or passed on to the transport protein, transferrin, a Pi-gly-coprotein. The amount absorbed does not exceed that needed to balance losses due to epithelial shedding from skin and mucosae or hemorrhage (so-called "mucosal block"). In men, this amount is approx. 1 mg/d; in women, it is ap-prox. 2 mg/d (menstrual blood loss), corresponding to about 10% of the dietary intake. The transferrin-iron complex undergoes endocytotic uptake mainly into erythroblasts to be utilized for hemoglobin synthesis.

About 70% of the total body store of iron (~5 g) is contained within erythro-cytes. When these are degraded by macrophages of the reticuloendothelial (mononuclear phagocyte) system, iron is liberated from hemoglobin. Fe3+ can be stored as ferritin (= protein apoferri-tin + Fe3+) or returned to erythropoiesis sites via transferrin.

A frequent cause of iron deficiency is chronic blood loss due to gastric/intestinal ulcers or tumors. One liter of blood contains 500 mg of iron. Despite a significant increase in absorption rate (up to 50%), absorption is unable to keep up with losses and the body store of iron falls. Iron deficiency results in impaired synthesis of hemoglobin and anemia (p. 138).

The treatment of choice (after the cause of bleeding has been found and eliminated) consists of the oral administration of Fe2+ compounds, e.g., ferrous sulfate (daily dose 100 mg of iron equivalent to 300 mg of FeSO4, divided into multiple doses). Replenishing of iron stores may take several months. Oral administration, however, is advan tageous in that it is impossible to overload the body with iron through an intact mucosa because of its demand-regulated absorption (mucosal block).

Adverse effects. The frequent gastrointestinal complaints (epigastric pain, diarrhea, constipation) necessitate intake of iron preparations with or after meals, although absorption is higher from the empty stomach.

Interactions. Antacids inhibit iron absorption. Combination with ascorbic acid (Vitamin C), for protecting Fe2+ from oxidation to Fe3+, is theoretically sound, but practically is not needed.

Parenteral administration of Fe3+ salts is indicated only when adequate oral replacement is not possible. There is a risk of overdosage with iron deposition in tissues (hemosiderosis). The binding capacity of transferrin is limited and free Fe3+ is toxic. Therefore, Fe3+ complexes are employed that can donate Fe3+ directly to transferrin or can be phagocytosed by macrophages, enabling iron to be incorporated into ferritin stores. Possible adverse effects are, with i.m. injection: persistent pain at the injection site and skin discoloration; with i.v. injection: flushing, hypotension, anaphylactic shock.

Ferritin Transferrin Apoferrin

Uptake into macrophages spleen, liver, bone marrow

A. Iron: possible routes of administration and fate in the organism

Uptake into macrophages spleen, liver, bone marrow

A. Iron: possible routes of administration and fate in the organism

Constipation Prescription

Constipation Prescription

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