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DƯỢC LÍ Goodman & Gilman's The Pharmacological Basis of Therapeutics 12th, 2010

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1080

SECTION IV

INFLAMMATION. IMMUNOMODULATION, AND HEMATOPOIESIS

Table 37–4

Daily Iron Intake and Absorption

IRON REQUIREMENT AVAILABLE IRON (mg/kg) SAFETY FACTOR

SUBJECT (mg/kg) POOR DIET–GOOD DIET AVAILABLE/REQUIREMENT

Infant 67 33–66 0.5–1

Child 22 48–96 2–4

Adolescent (male) 21 30–60 1.5–3

Adolescent (female) 20 30–60 1.5–3

Adult (male) 13 26–52 2–4

Adult (female) 21 18–36 1–2

Mid-to-late pregnancy 80 18–36 0.22–0.45

risk, whereas iron balance in adult men and nonmenstruating

women is reasonably secure. The difference between dietary supply

and requirements is reflected in the size of iron stores, which are

low or absent when iron balance is precarious and high when iron

balance is favorable (Table 37–2). Thus in infants after the third

month of life and in pregnant women after the first trimester, stores

of iron are negligible. Menstruating women have approximately

one-third the stored iron found in adult men, indicative of the extent

to which the additional average daily loss of ~0.5 mg of iron

affects iron balance.

Iron Deficiency. Iron deficiency is the most common

nutritional disorder (McLean et al., 2009). The prevalence

of iron-deficiency anemia in the U.S. is on the

order of 1-4% and depends on the economic status of

the population. In developing countries, up to 20-40%

Absorption of

nonheme iron (%)

20 0 mg

15

10

5

0

Low Medium High

Availability of nonheme iron

250 mg

500 mg

1000 mg

Figure 37–4. Effect of iron status on the absorption of nonheme

iron in food. The percentages of iron absorbed from diets of low,

medium, and high bioavailability in individuals with iron stores

of 0, 250, 500, and 1000 mg are portrayed. (After Monsen et al.,

1978; reproduced with permission by the American Journal of

Clinical Nutrition. © Am J Clin Nutr. American Society for

Clinical Nutrition.)

of infants and pregnant women may be affected. Better

iron balance has resulted from the practice of fortifying

flour, the use of iron-fortified formulas for infants,

and the prescription of medicinal iron supplements during

pregnancy.

Iron-deficiency anemia results from dietary

intake of iron that is inadequate to meet normal

requirements (nutritional iron deficiency), blood loss,

or interference with iron absorption (Clark, 2009).

This can have a genetic basis, as in iron-refractory iron

deficiency anemia in which patients have iron deficiency

that is unresponsive to oral iron, but partially

responsive to parenteral iron (Finberg, 2009). Poor

oral absorption also can be acquired, as in conditions

associated with impaired oral absorption of vitamin

B 12

(Fernandez-Banares et al., 2009), or following

partial gastrectomy. More severe iron deficiency is

usually the result of blood loss, either from the GI

tract, or in women, from the uterus. Finally, treatment

of patients with erythropoietin can result in a functional

iron deficiency.

Iron deficiency in infants and young children can

lead to behavioral disturbances and can impair development,

which 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-birthweight 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 the age of 2-3 years, the

requirement for iron declines until adolescence when

rapid growth combined with irregular dietary habits

again increases 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.

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