Prevention of Iron Deficiency in Infants and Toddlers

Am Fam Physician. 2002 Oct 1;66(vii):1217-1225.

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Article Sections

  • Abstract
  • Mental, Motor, and Behavior Furnishings
  • Iron Deficiency Anemia After the Beginning Year of Life
  • Main Prevention
  • Secondary Prevention
  • References

The prevalence of nutritional iron deficiency anemia in infants and toddlers has declined dramatically since 1960. However, satisfaction with this achievement must be tempered because iron deficiency anemia in infants and toddlers is associated with long-lasting diminished mental, motor, and behavioral functioning. Additionally, the prevalence of iron deficiency anemia in one- to three-year-one-time children seems to exist increasing. The verbal relationship between iron deficiency anemia and the developmental effects is not well understood, just these effects do not occur until atomic number 26 deficiency becomes astringent and chronic enough to produce anemia. At that point, treatment with fe can reverse the anemia and restore iron sufficiency, still the poorer developmental functioning appears to persist. Therefore, intervention should focus on the primary prevention of iron deficiency. In the first year of life, measures to prevent iron deficiency include completely avoiding cow's milk, starting atomic number 26 supplementation at four to six months of age in breastfed infants, and using fe-fortified formula when not breastfeeding. Low-iron formula should not exist used. In the second year of life, iron deficiency tin can be prevented by use of a diversified diet that is rich in sources of iron and vitamin C, limiting cow's milk consumption to less than 24 oz per mean solar day, and providing a daily iron-fortified vitamin. All infants and toddlers who did not receive primary prevention should be screened for atomic number 26 deficiency. Screening is performed at nine to 12 months, six months after, and at 24 months of age. The hemoglobin/hematocrit level lone detects only patients with plenty atomic number 26 deficiency to be bloodless. Screening by erythrocyte protoporphyrin or ruby-red-cell distribution width identifies earlier stages of iron deficiency. A positive screening test is an indication for a therapeutic trial of iron, which remains the definitive method of establishing a diagnosis of iron deficiency.

A high prevalence of iron deficiency anemia in U.S. infants was first widely noted in the 1930s. 30 years later, when the prevalence charge per unit had non dropped,1 iron deficiency began to be seen every bit a significant public health trouble. Because nutritional factors were the cause in the vast bulk of these cases, iron deficiency anemia began to be referred to equally nutritional anemia.i It before long became standard to screen all infants between ix and 12 months of age for iron deficiency by screening for anemia. Anemia became the ordinarily employed marker for iron deficiency, and the hematocrit level became the screening test.

This universal screening strategy, in conjunction with an increase in the popularity of breastfeeding, iron-fortification of infant formulas and cereals, the start of the Special Supplemental Food Program for Women, Infants, and Children (WIC) in 1972, and teaching of physicians and the public, was extremely successful. By the mid-1980s, a dramatic reject in the prevalence of iron deficiency anemia was noticed across the socioeconomic spectrum throughout the United States.2 In 1971, 23 per centum of nine- to 36-calendar month-old children in an inner city clinic in New Haven, Conn., had a hemoglobin level beneath 9.8 g per dL (98 yard per L).i By 1984, the rate in the same clinic had dropped to ane pct.three A study of centre-class nine- to 23-month-sometime infants in a private practise in Minneapolis found that a 7.6 percent prevalence of anemia between 1969 and 1973 decreased to a prevalence of 2.8 percent between 1982 and 1986.four

This achievement in the reduction of iron deficiency anemia in children has been considered a major success story. By 1987, leaders in the field suggested that routine screening for iron deficiency was no longer indicated except in known high-risk populations and should exist replaced by selective screening based on the individual patient's risk for iron deficiency.5 It appeared that although the medical customs needed to remain vigilant and identify pockets of continued elevated prevalence, iron deficiency anemia was no longer the public health threat that it had been. Unfortunately, atomic number 26 deficiency anemia is still with us, and its developmental effects appear to be long-lasting.

Mental, Motor, and Beliefs Effects

  • Abstract
  • Mental, Motor, and Behavior Effects
  • Iron Deficiency Anemia After the First Yr of Life
  • Master Prevention
  • Secondary Prevention
  • References

The association between iron deficiency anemia and diminished mental, motor, and behavioral development in infants is not a recent discovery. A possible link was noted in the tardily 1970s,vi and subsequent studies of 12- to 23-month-quondam infants in the past two decades confirmed those findings.7–10 By the 1990s, the association between iron deficiency anemia and lower developmental exam scores was well-established but may not accept received the expected amount of attending in the The states because of the shrinking prevalence of iron deficiency anemia. In recent years, it has become articulate that these furnishings are long-lasting despite correction of the iron deficiency anemia.

Mental, motor, and beliefs effects develop only when fe deficiency is astringent enough to cause anemia.seven,8 In studies using Bayley Scales of Infant Development,7 infants with iron deficiency anemia receive lower scores on mental and motor tests, including gross and fine motor coordination,xi and demonstrate affective differences, such equally wariness, fright, and unhappiness.ix These findings have been confirmed by a variety of studies in dissimilar cultural settings.12 Further study of the beliefs component found activity differences, with the bloodless infants being less playful, tiring more than easily, and preferring to be held.x These mental and motor effects are not detectable on routine physical examination; it is non known if the beliefs changes are noticeable.

Treatment with iron, with subsequent complete resolution of the anemia and the atomic number 26 deficiency, does not correct all of the behavior furnishings.10 Furthermore, the lower mental and motor examination scores associated with iron deficiency anemia persist.7–9 In the longest trial to engagement, children reevaluated at 11 to fourteen years of age demonstrated functional impairment in schoolhouse despite complete correction of the iron deficiency anemia they had as infants.13

These children were more likely to have repeated a grade, to have reduced arithmetic achievement and written expression, and to show differences in motor function, spatial retention and selective recall. In addition, their behavior was more than likely to exist characterized equally problematic by parents and teachers.

Fe Deficiency Anemia After the First Yr of Life

  • Abstract
  • Mental, Motor, and Beliefs Effects
  • Fe Deficiency Anemia Afterward the Outset Year of Life
  • Primary Prevention
  • Secondary Prevention
  • References

Historically, the prevention of iron deficiency anemia has focused on the first 12 months of life. Information technology appears that toddlers deserve the aforementioned degree of attending because of the risk of developmental furnishings from iron deficiency anemia and because the prevalence of iron deficiency anemia between one and iii years of age may be greater than was formerly thought.

Ii large-calibration studies, the Third National Health and Diet Examination Survey (NHANES 3)14 and the Third Report on Nutrition Monitoring in the United States (1988–1991),15 reported the prevalence of iron deficiency anemia in 1- to two-yr-olds to exist 3 percent, and in 1- to three-year-olds to be 15 percent.

A more than recent study, conducted in an urban setting with an equal mix of lower and middle socioeconomic groups, noted that 10 per centum of ane- to three-year-olds had iron deficiency anemia.fifteen Severe cases of iron deficiency anemia (hemoglobin level less than 6 g per dL [60 g per L]) have been reported in this historic period range also.16 In a longitudinal report of toddlers, 12-calendar month-olds were noted to be receiving almost 100 percent of the recommended daily assart (RDA) for iron, but by xviii months of age, the intake of iron had declined to a level well below the recommended amount.17

These findings might have been anticipated because 1- to iii-twelvemonth-olds accept the everyman daily iron intake of whatsoever age group across the lifespan.15 At one year, breastfeeding or atomic number 26-fortified formula is often replaced with cow's milk, non–iron-fortified cereals enter the nutrition, and juices reduce the child'southward ambition for solid food.

Primary Prevention

  • Abstract
  • Mental, Motor, and Behavior Effects
  • Iron Deficiency Anemia After the First Twelvemonth of Life
  • Main Prevention
  • Secondary Prevention
  • References

The principal prevention of iron deficiency anemia in infants and toddlers hinges on good for you feeding practices. In infants, the introduction of cow's milk in the first year of life is the greatest dietary risk gene for the development of iron deficiency and iron deficiency anemia.18–20 Cow's milk is low in iron, and its iron is poorly absorbed.21 In addition, it decreases the absorption of iron from other dietary sources.21 Therefore, the strict abstention of moo-cow's milk in the first 12 months of life is essential in preventing iron deficiency anemia.

Breastfeeding is the ideal feeding practice for many well-documented reasons, including lowering the take chances of atomic number 26 deficiency anemia. Although breast milk is low in iron content, about 50 per centum of the iron is bioavailable to the baby.12 Yet, exclusive breastfeeding later iv to half dozen months puts infants at run a risk for iron deficiency. Therefore, some form of dietary iron supplement that provides i mg elemental atomic number 26 per kg per 24-hour interval is recommended for term infants starting at four22,23 to six12,20 months of age. Iron-fortified cereal can assistance meet this requirement24; however, many cereal-fed infants even so develop iron deficiency anemia.25

To preclude atomic number 26 deficiency, another option is a daily oral atomic number 26 supplement, using ferrous sulfate drops26 or infant vitamin drops with iron. Vitamin drops comprise 10 mg of elemental iron per dropper, which is the RDA for children six months to six years of age.26,27 Iron supplementation via drops or iron-fortified cereal should be continued throughout the flow of breastfeeding. Breastfed preterm and low-birth-weight infants require supplementation at a dosage of ii mg of oral elemental iron per kg per day, starting at 2 to four weeks of age.26 Infants weighing less than 1,500 m (3 lb, iv oz) demand higher dosages (3 mg per kg per 24-hour interval for i,000 one thousand [two lb, three oz] to 1,500 g and 4 mg per kg per day for less than i,000 g).12 All supplemental fe preparations, specially those for adults, should be stored out of the achieve of children to prevent fatal poisonings.

Infants started on formula at birth and those switched from breast milk to formula should receive iron-fortified formula.28 Term and preterm infants (weighing more than 1,000 g) who are fed fe-fortified formulas are able to maintain iron sufficiency without additional iron supplementation.26,29 Vitamins given to these infants should not incorporate iron.

Low-atomic number 26 formulas (less than 6.7 mg per L of iron) place infants at risk for atomic number 26 deficiency anemia while offering no reward over standard fe-fortified formulas with respect to gastrointestinal side effects.30 Controlled31 and double-blinded crossover32 trials show no deviation betwixt low- and standard-iron formulas in the frequency of fussiness, cramping, colic, regurgitation, flatus, or stool characteristics (except a darker color with standard fe-fortified formulas). Moreover, iron given at higher dosages to care for known atomic number 26 deficiency anemia in 12-month-former infants caused no more gastrointestinal side furnishings than placebo.33

In the second year of life, moo-cow's milk continues to crusade problems in maintaining iron stores, and its consumption should exist express to less than 24 oz per day,34 with some clinicians calling for a stricter limit of sixteen oz per day. Mothers who wish to continue to chest-feed afterward 12 months of age should be encouraged to do so, and iron supplementation should be maintained in some form. If chest-feeding is stopped earlier 24 months, a recent suggestion has been to substitute iron-fortified formula for moo-cow's milk because of the negative effects of moo-cow's milk on iron status.22 This may not exist practical for many parents.

Other preventive measures for toddlers include encouraging a diversified nutrition rich in sources of iron and vitamin C, continuing use of cereals fortified with fe instead of more advertised cereals, fugitive excessive juice intake, and giving an iron-containing vitamin.xv

Secondary Prevention

  • Abstract
  • Mental, Motor, and Behavior Effects
  • Atomic number 26 Deficiency Anemia After the First Year of Life
  • Primary Prevention
  • Secondary Prevention
  • References

SCREENING

Infants with i or more risk factors (Table 1) should be screened for iron deficiency. Of these risks, the introduction of moo-cow'southward milk in the first yr of life is the virtually strong dietary gene for the development of iron deficiency.xx Poverty also significantly increases the chance for fe deficiency anemia, leading to the recommendation for connected routine screening of all infants from lower socioeconomic backgrounds.24 Forgoing screening might be considered if it is certain an baby has received principal prevention.

Table 1

Take chances Factors for Iron Deficiency in the Starting time Yr of Life

Diet

Cow's milk ingestion

Depression-iron formula

Breastfeeding without atomic number 26 supplementation

Prenatal/perinatal

Anemia during pregnancy

Poorly controlled diabetes

Low nascency weight

Prematurity

Multiple gestation

Socioeconomic

Depression socioeconomic background

Recent immigration from a developing state

Other

Qualified for but not receiving WIC assistance

Rate of weight gain greater than average

Screening in the first year is performed between nine26 and 12 months of age.24 Special consideration is given to preterm and low-birth-weight infants, who are screened at six months of age and by three months for those who have not received oral iron supplements or iron-fortified formula.26

Later 12 months, any toddler who was at take chances as an infant but not screened needs to be tested at that time for fe deficiency. Other toddlers at risk (east.g., past history of iron deficiency anemia, cow's milk consumption of more than 24 oz per twenty-four hour period, diet low in iron and vitamin C, or recent clearing from a developing country) should be screened between 15 and 18 months and at 24 months.34 A positive screening test requires confirmation with a therapeutic trial of atomic number 26. A negative screen provides an opportunity to arbitrate with principal prevention.

The ideal screening test would be capable of identifying atomic number 26 deficiency in the absence of anemia. This would let for the treatment of atomic number 26 deficiency in the pre-anemic phase, preventing fe deficiency anemia and its associated mental, motor, and behavior effects. No such test is widely used at this time. The standard test has been the hemoglobin (or hematocrit) level, which leads to the diagnosis only if the iron deficiency is severe plenty to cause anemia. This approach has been chosen into question because the developmental consequences of atomic number 26 deficiency anemia suggest that identification of iron deficiency before anemia would be preferable.35

The serum ferritin level, transferrin saturation, and erythrocyte protoporphyrin level also can be used in the diagnosis of iron deficiency (Effigy 1).36 Of these, the erythrocyte protoporphyrin measurement has the advantages of lower cost and office-based availability. Clinical studies have demonstrated its effectiveness every bit a screening tool.37,38 While an elevated erythrocyte protoporphyrin level is not as specific for iron deficiency as other markers, the decline in the prevalence and severity of pb toxicity makes an elevated erythrocyte protoporphyrin level a probable positive screen for fe deficiency.

Stages of Fe Deficiency

FIGURE 1.

Stages of fe deficiency. (Hgb = hemoglobin; EP = erythrocyte protoporphyrin; RDW = carmine-prison cell distribution width; MCV = hateful corpuscular book)

Note: Cut-off values are for infants.

Adapted with permission from Dallman PR. Atomic number 26 deficiency: diagnosis and treatment. West J Med 1981; 134:498.

Practices with a large number of infant and toddler patients at hazard for iron deficiency or a high prevalence of iron deficiency anemia may find it helpful to invest in an office hematofluorimeter to measure erythrocyte protoporphyrin. Equally a screening test, information technology will miss some cases of iron deficiency fifty-fifty in the presence of anemia, making the combination of erythrocyte protoporphyrin and hemoglobin measurement a more effective screening strategy.

If erythrocyte protoporphyrin measurement is not an choice, obtaining a red-cell distribution width (RDW) with the hemoglobin measurement could be a consideration.14 An elevated RDW is believed to exist an early indicator of fe deficiency and might prompt a therapeutic trial of iron (Figure ii) to confirm the diagnosis.12 This is an attractive approach considering the consummate blood count (CBC) with red claret cell indexes alone could be used to screen for iron deficiency and fe deficiency anemia. Nevertheless, this use of RDW is non currently standard practice, and cut-off values for RDW are instrument-specific and must be known by the ordering clinician.

Therapeutic Trial of Iron to Diagnose Iron Deficiency

Effigy ii.

Therapeutic trial of iron to diagnose iron deficiency. (Hgb = hemoglobin)

*--20 percentage of ferrous sulfate is elemental fe.

NOTE: If hematocrit is used equally screening test, a iii-unit increase is diagnostic.

If obtaining a CBC or an erythrocyte protoporphyrin level is impractical, screening solely with hemoglobin should non be abased. It is better to discover a patient who has adult atomic number 26 deficiency anemia than to miss the diagnosis, equally severity and chronicity of the status may worsen the outcome. Another reason to go along hemoglobin as part of the screening strategy is that a baseline hemoglobin level is ultimately necessary in the confirmation of the diagnosis of atomic number 26 deficiency.39 When the erythrocyte protoporphyrin level is elevated or the hemoglobin is low (less than eleven g per dL [110 g per L]), a therapeutic trial of oral fe is the gold standard to establish the diagnosis of iron deficiency.forty Black infants ordinarily accept slightly lower hemoglobin levels, and a cutoff of 10.7 g per dL [107 one thousand per L] defines anemia in this population.26

A therapeutic trial of iron is the preferred approach to diagnosing iron deficiency because it is more reliable and less expensive than obtaining an iron panel.41,42 In children, it is important to remember that a recent infection tin can transiently depress the hemoglobin.43,44 Therefore, information technology is recommended to filibuster testing in an baby or toddler who had an infection within the previous two weeks.26 If the therapeutic trial of iron is negative, a work-up for the etiology of the anemia is indicated.

Other hematopoietic markers are being evaluated for their potential to simultaneously screen for and diagnose iron deficiency in infants and toddlers. The serum circulating transferrin receptor assay is a relatively new examination, and the virtually recent test of iron condition to be suggested is reticulocyte hemoglobin content.45 Neither modality is widely bachelor, and both need more than clinical study.

TREATMENT

After a positive screening test for iron deficiency and a diagnosis confirmed by a therapeutic trial of iron, the baby or toddler should consummate a course of iron therapy. Elemental fe, at a dosage of three mg per kg, is given orally (usually every bit ferrous sulfate syrup, which is 20 percent elemental iron) once daily before breakfast.21,26 Absorption is improved if it is ingested with a source of vitamin C, such as orangish juice. Total length of treatment is three months, including the ane-month therapeutic trial of atomic number 26.26

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The Author

evidence all writer info

LOUIS A. KAZAL, JR., M.D., is a Robert Wood Johnson health policy fellow at the Found of Medicine in Washington D.C., and is principal medical officeholder of the Navajo Health Foundation/Sage Memorial Hospital in Ganado, Ariz. A graduate of Jefferson Medical College, Philadelphia, he completed a residency in family practice at McKay-Dee Infirmary Middle, Ogden, affiliate of the University of Utah Schoolhouse of Medicine. Dr. Kazal holds a volunteer faculty appointment as clinical acquaintance professor in the Section of Family and Community Medicine at Baylor College of Medicine, Houston....

Accost correspondence to Louis A. Kazal, Jr., M.D., Dartmouth-Hitchcock Community Health Center, I Medical Center Dr., Lebanon, NH 03766. Reprints are not available from the author.

The writer indicates that he does non have any conflicts of interest. Sources of funding: none reported.

The author thanks Carmen James and Eva Hubbard Grabarek for help with the manuscript and Anthony F. Valdini, Yard.D., for editorial input.

REFERENCES

testify all references

1. Katzman R, Novack A, Pearson H. Nutritional anemia in an inner-urban center community. Human relationship to historic period and ethnic group. JAMA. 1972;222:670–three. ...

two. Yip R, Binkin NJ, Fleshood L, Trowbridge FL. Declining prevalence of anemia amongst depression-income children in the U.s.. JAMA. 1987;258:1619–23.

3. Vazquez-Seoane P, Windom R, Pearson HA. Disappearance of atomic number 26-deficiency anemia in a high-take chances infant population given supplemental iron. Due north Engl J Med. 1985;313:1239–40.

4. Yip R, Walsh KM, Goldfarb MG, Binkin NJ. Declining prevalence of anemia in babyhood in a middle-class setting: a pediatric success story?. Pediatrics. 1987;80:330–4.

v. Dallman PR. Has routine screening of infants for anemia go obsolete in the United States?. Pediatrics. 1987;80:439–41.

six. Oski FA. The nonhematologic manifestations of iron deficiency. Am J Dis Child. 1979;133:315–22.

vii. Lozoff B, Brittenham GM, Wolf AW, McClish DK, Kuhnert PM, Jimenez Eastward, et al. Fe deficiency anemia and iron therapy effects on infant developmental test performance. Pediatrics. 1987;79:981–95.

viii. Walter T, De Andraca I, Chadud P, Perales CG. Iron deficiency anemia: adverse effects on infant psychomotor development. Pediatrics. 1989;84:7–17.

9. Lozoff B, Wolf AW, Jimenez E. Iron-deficiency anemia and infant development: effects of extended oral atomic number 26 therapy. J Pediatr. 1996;129:382–9.

10. Lozoff B, Klein NK, Nelson EC, McClish DK, Manuel Grand, Chacon ME. Beliefs of infants with iron-deficiency anemia. Child Dev. 1998;69:24–36.

eleven. Oski FA, Honig Every bit. The furnishings of therapy on the developmental scores of iron-deficient infants. J Pediatr. 1978;92:21–v.

12. Oski FA. Iron deficiency in infancy and child-hood. N Engl J Med. 1993;329:190–3.

13. Lozoff B, Jimenez E, Hagen J, Mollen E, Wolf AW. Poorer behavioral and developmental outcome more ten years later treatment for iron deficiency in infancy. Pediatrics. 2000;105:E51.

14. Looker AC, Dallman PR, Carroll MD, Gunter EW, Johnson CL. Prevalence of iron deficiency in the The states. JAMA. 1997;277:973–6.

xv. Eden AN, Mir MA. Iron deficiency in 1- to 3-twelvemonth-old children. A pediatric failure?. Arch Pediatr Adolesc Med. 1997;151:986–8.

16. Kwiatkowski JL, West TB, Heidary N, Smith-Whitley K, Cohen AR. Astringent iron deficiency anemia in young children. J Pediatr. 1999;135:514–half dozen.

17. Picciano MF, Smiciklas-Wright H, Birch LL, Mitchell DC, Murray-Kolb L, McConahy KL. Nutritional guidance is needed during dietary transition in early on childhood. Pediatrics. 2000;106(1 pt 1):109–14.

18. Sadowitz PD, Oski FA. Iron condition and infant feeding practices in an urban convalescent center. Pediatrics. 1983;72:33–6.

nineteen. Tunnessen WW Jr, Oski FA. Consequences of starting whole cow milk at half-dozen months of age. J Pediatr. 1987;111(6 pt 1):813–half dozen.

xx. Pizarro F, Yip R, Dallman PR, Olivares M, Her-trampf E, Walter T. Iron condition with unlike infant feeding regimens: relevance to screening and prevention of atomic number 26 deficiency. J Pediatr. 1991;118:687–92.

21. Dallman PR, Siimes MA, Stekel A. Iron deficiency in infancy and childhood. Am J Clin Nutr. 1980;33:86–118.

22. Berth IW, Aukett MA. Atomic number 26 deficiency anaemia in infancy and early childhood. Arch Dis Child. 1997;76:549–54.

23. Calvo EB, Galindo AC, Aspres NB. Iron status in exclusively breast-fed infants. Pediatrics. 1992;90:375–9.

24. Screening for iron deficiency anemia—including iron prophylaxis. U.S. Preventive Services Task Strength. Guide to clinical preventive services. 2nd ed. Baltimore: Williams & Wilkins, 1996;231–46.

25. Walter T, Dallman PR, Pizarro F, Velozo 50, Pena G, Bartholmey SJ, et al. Effectiveness of iron-fortified infant cereal in prevention of iron deficiency anemia. Pediatrics. 1993;91:976–82.

26. Earl RO, Woteki CE, Found of Medicine Commission on the Prevention, Detection, and Direction of Atomic number 26 Deficiency Anemia Among U.S. Children and Women of Childbearing Age. Fe deficiency anemia: recommended guidelines for the prevention, detection, and management amongst U.S. children and women of childbearing historic period. Washington, D.C.: National Academy Press, 1993.

27. Filer LJ Jr. Fe needs during rapid growth and mental development. J Pediatr. 1990;117(two pt two):S143–half-dozen.

28. American Academy of Pediatrics Committee on Nutrition. Fe-fortified infant formulas. Pediatrics. 1989;84:1114–5.

29. Irigoyen Thousand, Davidson LL, Carriero D, Seaman C. Randomized, placebo-controlled trial of atomic number 26 supplementation in infants with low hemoglobin levels fed iron-fortified formula. Pediatrics. 1991;88:320–6.

30. American University of Pediatrics Commission on Nutrition. Iron fortification of infant formulas. Pediatrics. 1999;104(1 pt 1):119–23.

31. Oski FA. Atomic number 26-fortified formulas and gastrointestinal symptoms in infants: a controlled report. Pediatrics. 1980;66:168–70.

32. Nelson SE, Ziegler EE, Copeland AM, Edwards BB, Fomon SJ. Lack of adverse reactions to iron-fortified formula. Pediatrics. 1988;81:360–4.

33. Reeves JD, Yip R. Lack of adverse side effects of oral ferrous sulfate therapy in 1-twelvemonth-old infants. Pediatrics. 1985;75:352–5.

34. Centers for Disease Control and Prevention. Recommendations to prevent and command fe deficiency in the The states. Morb Mortal Wkly Rev MMWR. 1998;47(RR-3):1–29.

35. Kazal LA Jr. Failure of hematocrit to find iron deficiency in infants. J Fam Pract. 1996;42:237–40.

36. Dallman PR. Fe deficiency: diagnosis and treatment. West J Med. 1981;134:496–505.

37. Yip R, Schwartz S, Deinard AS. Screening for iron deficiency with the erythrocyte protoporphyrin examination. Pediatrics. 1983;72:214–9.

38. Siegel RM, LaGrone DH. The apply of zinc protoporphyrin in screening young children for iron deficiency. Clin Pediatr [Phila]. 1994;33:473–nine.

39. Dallman PR, Yip R. Changing characteristics of babyhood anemia. J Pediatr. 1989;114:161–iv.

xl. Reeves JD, Vichinsky East, Addiego J Jr, Lubin BH. Iron deficiency in health and disease. Adv Pediatr. 1983;30:281–320.

41. Dallman PR. Biochemical and hematologic indices of iron deficiency. In: Pollitt E, Leibel RL, eds. Iron deficiency: brain biochemistry and behavior. New York: Raven, 1982:63–77.

42. Driggers DA, Reeves JD, Lo EY, Dallman PR. Iron deficiency in one-year-old infants: comparing of results of a therapeutic trial in infants with anemia or depression-normal hemoglobin values. J Pediatr. 1981;98:753–eight.

43. Reeves JD, Yip R, Kiley VA, Dallman PR. Iron deficiency in infants: the influence of mild antecedent infection. J Pediatr. 1984;105:874–9.

44. Olivares Chiliad, Walter T, Osorio M, Chadud P, Schlesinger Fifty. Anemia of a balmy viral infection: the measles vaccine equally a model. Pediatrics. 1989;84:851–five.

45. Brugnara C, Zurakowski D, DiCanzio J, Boyd T, Platt O. Reticulocyte hemoglobin content to diagnose iron deficiency in children. JAMA. 1999;281:2225–30.

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