Iron deficiency

Dosage for treating Iron Deficiency

Oral iron supplementation

1 - 2 mg/kg/day is the preventative dose for iron deficiency

3 - 6 mg/kg/day is the recommended dose for treatment of iron deficiency and IDA. Higher doses should be considered in those children with severe anaemia (Hb <80 g/L).

Iron supplements should be continued for a minimum of 3 months after anaemia has been corrected to replenish stores. Hb and ferritin should be checked at this time point.

(R1)

A 40kg child should receive between 120 - 240mg of elemental Iron daily to treat IDA.

120mg of el. Iron is 46 drops of Maltofer, or 10 tabs of HemeBoost.

Iron bisglycinate with Folinic acid

In conclusion, ferrous bisglycinate with folinic acid as a multivitamin nutraceutical format is comparable to standard ferrous fumarate for the clinical management of iron deficiency during pregnancy, with comparatively better absorption, tolerability, and efficacy and with a lower elemental iron dosage. (R2)

Effects of Iron deficiency on ETC

1. Most Fe-S proteins decreased in concentration due to iron deficiency, except for the Rieske cluster of Complex III (Fe-Sbc-1).
2. In Complex II, Fe-S cluster S-1 was decreased by 38% and cluster S-3 by 59%.
3. Complex I Fe-S clusters were substantially decreased.
4. The Fe-S cluster of electron-transferring flavoprotein dehydrogenase was 55% lower.
5. Succinate and NADH dehydrogenase activities, as well as maximal rates of reversed electron transport, were about 80% lower.
6. Oxidase activities decreased by about 70%.
7. Decreases in cytochrome content were insufficient to explain the loss of oxidase activity and did not affect dehydrogenases or reversed electron transport.
8. Despite reductions in maximal rates of ATP formation, the efficiency of phosphorylative coupling remained unaffected.
9. The loss of Fe-S clusters led to decreased dehydrogenase activities.
10. Iron depletion from the complexes was not a random process.

(R5)

TIBC become elevated before serum iron reduces

Five nonanemic patients with normal erythrocytic indexes were found to have normal serum iron, elevated total iron-binding capacity, normal percentage of saturation of transferrin, and depleted bone marrow iron stores.

These findings suggest that during the development of iron deficiency, an elevation of total iron-binding capacity occurs before the decrease of the serum iron. This may represent a compensatory mechanism to mobilize all traces of tissue iron to maintain normal erythropoiesis. (R6)