Plasma iron 115 ± 50 115 ug/100 mL (uM) (21 ± 9) (21)

<60 (<11)

<40 (<7)

Transferrin saturation, % 35 ± 15 30



Sideroblasts, % 40-60 40-60



RBC protoporphyrin ug/100 mL RBC 30 30 (umol/L RBC) (0.53) (0.53)

100 (1.8)

200 (3.5)

Erythrocytes Normal Normal Normal

Microcytic/ hypochromic

FIGURE 53-5 Sequential changes (from left to right) in the development of iron deficiency in the adult. Rectangles enclose abnormal test results that identify the stage of Fe-deficiency. RE marrow Fe, reticuloendothelial hemosiderin; RBC, red blood cells.

FIGURE 53-5 Sequential changes (from left to right) in the development of iron deficiency in the adult. Rectangles enclose abnormal test results that identify the stage of Fe-deficiency. RE marrow Fe, reticuloendothelial hemosiderin; RBC, red blood cells.

Iron deficiency in infants and young children can lead to behavioral disturbances and can impair development, effects that may not be fully reversible. Iron deficiency in children also can lead to an increased risk of lead toxicity secondary to pica and an increased absorption of heavy metals. Premature and low-birth-weight infants are at greatest risk for developing iron deficiency, especially if they are not breast-fed and/or do not receive iron-fortified formula. After age 2-3, the requirement for iron declines until adolescence, when rapid growth combined with irregular dietary habits again increase the risk of iron deficiency. Adolescent girls are at greatest risk; the dietary iron intake of most girls ages 11-18 is insufficient to meet their requirements.

Treatment of Iron Deficiency general therapeutic principles The response of iron-deficiency anemia to iron therapy is influenced by several factors, including the severity of anemia, the ability of the patient to tolerate and absorb medicinal iron, and the presence of other complicating illnesses. Therapeutic effectiveness is best measured by the resulting increase in the rate of production of red cells. The magnitude of the marrow response to iron therapy is proportional to the severity of the anemia (level of erythropoietin stimulation) and the amount of iron delivered to marrow precursors.

The patient's ability to tolerate and absorb medicinal iron is a key factor in determining the rate of response to therapy. The small intestine regulates absorption, and with increasing doses of oral iron, limits iron uptake. This provides a natural ceiling on how much iron can be supplied by oral therapy. In the patient with a moderately severe iron-deficiency anemia, tolerable doses of oral iron will deliver, at most, 40-60 mg of iron/day to the erythroid marrow. This is an amount sufficient for production rates of two to three times normal.

Complicating illness also can interfere with the response of an iron-deficiency anemia to iron therapy. By decreasing the number of red cell precursors, intrinsic disease of the marrow can blunt the response. Inflammatory illnesses suppress the rate of red cell production, both by reducing iron absorption and reticuloendothelial release and by direct inhibition of erythropoietin and erythroid precursors. Continued blood loss can mask the response as measured by recovery of the Hb or hematocrit.

Clinically, the effectiveness of iron therapy is best evaluated by tracking the reticulocyte response and the rise in the Hb or the hematocrit. An increase in the reticulocyte count is not observed for at least 4-7 days after beginning therapy. An increase in the Hb level takes even longer. A decision as to the effectiveness of treatment should not be made until 3-4 weeks after the start of treatment, when an increase in the Hb concentration (2 g/dL is considered a positive response, assuming that no other change in the patient's clinical status can account for the improvement and that the patient has not been transfused.

If the response to oral iron is inadequate, the diagnosis must be reconsidered. A full laboratory evaluation should be conducted, and poor compliance by the patient or the presence of a concurrent inflammatory disease must be explored. A source of continued bleeding obviously should be sought. If no other explanation can be found, an evaluation of the patient's ability to absorb oral iron should be considered. There is no justification for merely continuing oral iron therapy beyond 3-4 weeks if a favorable response has not occurred.

therapy with oral iron Orally administered ferrous sulfate is the treatment of choice for iron deficiency. Ferrous salts are absorbed about three times as well as ferric salts, and the discrepancy increases at high dosages. Variations in the particular ferrous salt have relatively little effect on bioavailability.

Ferrous sulfate (feosol, others) is the hydrated salt, FeSO4 • 7H2O, which contains 20% iron. Ferrous fumarate (feostat, others) contains 33% iron and is moderately soluble in water, stable, and almost tasteless. Ferrous gluconate (fergon, others), which contains 12% iron, also is used in the therapy of iron-deficiency anemia. Polysaccharide-iron complex (niferex, others), a compound of ferrihydrite and carbohydrate, has comparable absorption. The effective dose of these preparations is based on iron content.

The average dose for the treatment of iron-deficiency anemia is about 200 mg of iron/day (2-3 mg/kg/day), given in three equal doses of 65 mg. Children weighing 15-30 kg can take half the average adult dose, while small children and infants can tolerate relatively large doses of iron (e.g., 5 mg/kg). The dose used is a compromise between the desired therapeutic action and the adverse effects. Prophylaxis and mild nutritional iron deficiency may be managed with modest doses. When the object is the prevention of iron deficiency in pregnant women, for example, doses of 15-30 mg of iron/day are adequate to meet the 3-6 mg daily requirement of the last 2 trimesters.

938 SECTION XI Drugs Acting on the Blood and the Blood-Forming Organs Table 53-4

Average Response to Oral Iron

Total Dose (mg Fe/day)

Estimated Absorption

Increase in Hemoglobin (g/L of blood/day)

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