Iron deficiency anemia is the most common of all types of anemias encountered in clinical practice. Yet it is often mismanaged. Iron deficiency anemia needs to be differentiated from other types of hypochromic microcytic anemias, which include:
Anaemia of chronic disorder
Iron is the most abundant metal in human body, about 3.5 grams are present in an adult man; yet the body rigorously conserves it like a trace element.
About 2.3 g iron is present in hemoglobin, 1 g in body stores, 0.14 g in myoglobin and 0.066 g in enzymes.
Daily loss is about 1-2 mg. Average intake is 10-15 mg, out of which only 10% (1-2 mg) is absorbed. This absorption is enhanced in iron deficiency to around 20-25% of intake (3-5 mg).
Cells regulate iron acquisition through post-transcriptional control of apoferritin and transferrin receptor synthesis. mRNA of both proteins contain iron responsive elements (IRE) capable of binding iron regulatory proteins (IRP) 1 & 2.
Binding of these proteins has opposing effects on two mRNAs. Transferrin receptor synthesis is directly influenced by the rate of erythropoiesis and indirectly by amount of storage iron (ferritin).
For an individual to become iron deficient, a prolonged period (approximately 6 years), of negative iron balance is required.
Stages of Iron Deficiency
1. Pre-latent iron deficiency
Reduction in iron stores without reduction in plasma iron. Serum ferritin & bone marrow iron are reduced.
2. Latent iron deficiency
Exhaustion of iron stores without reduction in hemoglobin concentration. Plasma iron decreases, total iron binding capacity increases and transferrin saturation decreases.
3. Iron deficiency anemia
Hb concentration starts declining. Early stage is discovered by chance. Late stage (Hb 8.0 gm) is symptomatic.
Continued negative iron balance results in depletion of iron stores, which leads to reduction in plasma iron. This in turn causes reduction in hemoglobin synthesis along with increase in free erythrocyte protoporphyrin, hypochromia and microcytosis. This leads to anemia.
Negative iron balance results from:
Increases requirements (females) or slow and steady loss (occult blood loss)
Decreased in-take (poverty, habits)
Combination of the two (most common)
It takes about eight years to develop iron deficiency and another 2-3 years to become symptomatic. Patients with rapidly developing anemia seldom become iron deficient as iron is replaced by way of red cell transfusions administered to treat it.
Causes of Iron Deficiency
Increased loss (blood loss, 1 ml = 0.5 mg iron )
Infancy and Childhood
Prematurity (reduced transfer )
Low birth weight (reduced iron store)
Increased requirement (with growth)
Uncommon vascular anomalies
Dietary habits / Pica
Hook worms and Schistosomiasis
Ulcerative lesions of GIT
Chronic Aspirin ingestion (1-4 ml / day with 02 Tab)
Runners anaemia (50% of joggers and runners)
Nosocomial (ITC 42 ml / day)
Diagnosis of Iron Deficiency Anemia
Assessment of Iron stores
Bone marrow iron
Plasma Iron studies
Serum transferrin (TIBC)
Serum Transferrin receptors
Red Cell Parameters
Red cell free protoporphyrin
Red cell indices
More marked changes in red cell indices and morphology
The most important component of effective management for iron deficiency anemia is to find out the cause of chronic negative iron balance and to treat it. Age, sex, socio-economic factors and occupation is important in determining the cause.
Replacement therapy alone will not be able to induce sustained remission.
Investigations to Determine the Cause
Thorough physical examination
Urine for hemoglobin, haemosidrin, ova
Faeces for ova, parasites, occult blood
Radiological, Endoscopic examinations
Others, as already discussed
Oral administration is the best approach. Addition of other elements has no advantage. Enteric coating and sustained release reduces absorption. Modification of dietary habits greatly improves absorption as well.
Optimal response occurs with 200 mg elemental iron/day. For children 1.5-2 mg/kg/day elemental iron is enough. Peak reticulocyte (5-10%) count occurs between 5th-10th day. Hb at 03 weeks becomes nearly 60% to normal, and normal in 2 months. Indices become normal in 6 months.
Indications for Parental Therapy
Anatomical lesions of upper GIT
Functional lesions of upper GIT
Iron requirement in mg can be found by using the formula (15 – pt Hb in g/dl) x body weight in kg x 3
It is given either 2 mg I/M daily or total dose I/V.
Gain in patient acceptance is more important than the reduced absorption of iron.
Causes of Failure