Questions? Call 888-624-8373

PAPERBACK
list:$31.50
Web:$28.35
add to cart

PDF BOOK
your price: $24.50
add to cart

Rights & Permissions

topleft topright

Iron Deficiency Anemia: Recommended Guidelines for the Prevention, Detection, and Management Among U.S. Children and Women of Childbearing Age (1993)
Institute of Medicine (IOM)

Page
41
bottomleft bottomright

The following HTML text is provided to enhance online readability. Many aspects of typography translate only awkwardly to HTML. Please use the page image as the authoritative form to ensure accuracy.


B

Iron Deficiency Anemia: A Synthesis of Current Scientific Knowledge and U.S. Recommendations for Prevention and Treatment

Peter R. Dallman

Iron deficiency anemia is a relatively common nutritional problem in the United States, particularly among infants, adolescents, and women of childbearing age. Its prevention deserves a high priority because iron deficiency anemia has serious consequences, yet its prevalence can be substantially reduced at modest cost. There has been great progress in preventing iron deficiency anemia among infants and children, but the prevalence among pregnant women of childbearing age remains high. The purpose of this appendix is to provide a brief review of the characteristics of iron deficiency anemia and to review recent guidelines for its prevention in primary health care settings.

This appendix provided background information for the Committee on the Prevention, Detection, and Management of Iron Deficiency Anemia Among U.S. Children and Women of Childbearing Age of the Food and Nutrition Board, Institute of Medicine. It also incorporated revisions and additions suggested after review of the paper by the committee, but does not indicate universal concurrence with its content. The committee then developed summary guidelines for children, nonpregnant women of childbearing age, and pregnant women that are contained in the main report.

Review of Knowledge

Metabolism and Physiology
Iron in the Body

The total amount of iron in the body of an adult woman averages 2.3 g (Bothwell et al., 1979), about the weight of a dime. Figure B-1 shows the distribution of this iron, which is similar in women of reproductive age and in children. An average of about 85 percent of total body iron can be classified as essential because it serves well-defined physiologic functions. Essential iron

Page
41

Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 41
--> B Iron Deficiency Anemia: A Synthesis of Current Scientific Knowledge and U.S. Recommendations for Prevention and Treatment Peter R. Dallman Iron deficiency anemia is a relatively common nutritional problem in the United States, particularly among infants, adolescents, and women of childbearing age. Its prevention deserves a high priority because iron deficiency anemia has serious consequences, yet its prevalence can be substantially reduced at modest cost. There has been great progress in preventing iron deficiency anemia among infants and children, but the prevalence among pregnant women of childbearing age remains high. The purpose of this appendix is to provide a brief review of the characteristics of iron deficiency anemia and to review recent guidelines for its prevention in primary health care settings. This appendix provided background information for the Committee on the Prevention, Detection, and Management of Iron Deficiency Anemia Among U.S. Children and Women of Childbearing Age of the Food and Nutrition Board, Institute of Medicine. It also incorporated revisions and additions suggested after review of the paper by the committee, but does not indicate universal concurrence with its content. The committee then developed summary guidelines for children, nonpregnant women of childbearing age, and pregnant women that are contained in the main report. Review of Knowledge Metabolism and Physiology Iron in the Body The total amount of iron in the body of an adult woman averages 2.3 g (Bothwell et al., 1979), about the weight of a dime. Figure B-1 shows the distribution of this iron, which is similar in women of reproductive age and in children. An average of about 85 percent of total body iron can be classified as essential because it serves well-defined physiologic functions. Essential iron

OCR for page 42
--> Figure B-1 Distribution of iron in women of childbearing potential (total body iron, 2.3 g—the weight of a dime). Source: Values are from Table 1, p. 2, in Bothwell and Charlton (1981). compounds include hemoglobin, which accounts for about three-quarters of total body iron and functions in the transport of oxygen from the lungs to tissues. Because hemoglobin circulates in the blood and accounts for a large proportion of essential body iron, its concentration often best reflects iron status. Other essential iron compounds include myoglobin, the red iron protein of muscle, and the mitochondrial iron proteins, which are essential for the oxidative production of cellular energy in the form of adenosine triphosphate. Iron deficiency is not associated with physiologic impairment until the production of essential iron compounds is diminished (Dallman, 1986). A second category of iron compounds is referred to as storage iron. Storage iron compounds include ferritin and hemosiderin, which are present primarily in the liver, spleen, and bone marrow. They serve as a reserve that ensures an adequate supply of iron for the production of essential iron compounds, and they maintain body iron homeostasis by regulating the amount of iron absorbed from the diet. Storage iron is less abundant in women and children than in men: about 14 percent of total body iron, on average (Figure B-l), and about 25 percent respectively. The serum ferritin concentration provides an estimate of storage iron reserves. Iron Homeostasis Body Iron Regulation Body iron is regulated primarily by modifying the percentage of food iron that is absorbed. Among healthy, nonpregnant women, body iron remains relatively stable, because the amount of iron absorbed each

OCR for page 43
--> Figure B-2 Iron balance in women of childbearing potential. Source: Based on Bothwell et al. (1979). day is roughly equivalent to the amount of iron lost (Figure B-2) and is less than 0.05 percent of total body iron (Bothwell et al., 1979). Iron homeostasis is normally maintained because iron absorption is inversely proportional to the mount of storage iron. When storage iron decreases, as it does during pregnancy or rapid growth, iron absorption increases (Figure B-3). This homeostatic adaptation is greatest with diets containing high levels of available iron (Cook, 1990). Low iron stores per se indicate that an individual is vulnerable to developing iron deficiency anemia, but as long as the production of essential iron remains intact, there are no known physiologic handicaps from having low iron reserves (Dallman, 1986). Iron Loss and Absorption Differences between Women and Men Women have greater iron losses and absorb a greater percentage of iron from food than do men. During their childbearing years, women typically have less storage iron than men primarily because of menstrual blood loss (Bothwell et al., 1979). They compensate by absorbing, on average, about twice as much iron from the diet as men, 12 versus 6 percent (Table B-1). Average menstrual blood loss is about 30 ml/month (Hallberg et al., 1966), but 10 percent of women regularly lose more than 80 ml/month (Figure B-4) and are likely to become anemic because their iron loss is usually greater than that which can be compensated for by increased absorption of iron from the

OCR for page 44
--> Figure B-3 Non-heme iron absorption from three different types of diets as the percent absorption of non-heme iron by individuals with no body iron stores and with 250-, 500-, and 1,000-mg iron stores. As iron stores decrease, the percentage of iron absorbed increases, helping to maintain homeostasis. This compensatory mechanism is less effective with diets of low iron bioavailability (common in developing countries) than with diets with medium and high levels of iron bioavailability, which are more typical in the United States. A daily diet of low iron bioavailability is one containing fewer than 30 g of meat, poultry, or fish (lean, raw weight) or less than 25 mg of ascorbic acid. The comparable figures for a diet of medium iron bioavailability are 30 to 90 g of meat, poultry, or fish or 25 to 75 mg of ascorbic acid, whereas a diet of high iron bioavailability is one containing more than 90 g of meat, poultry, or fish or more than 75 mg of ascorbic acid. Alternatively, it is one containing 30 to 90 g of meat, poultry, or fish plus 25 to 75 mg of ascorbic acid. SOURCE: Data from Monsen and coworkers (197g), in Bothwell et al. (1979). diet. Unfortunately, such women are typically unaware of their high levels of blood loss. Consequently, the most practical way to identify them is by screening for anemia as part of a periodic health maintenance checkup (LSRO, 1991). Menstrual blood loss varies with some methods of contraception (Figure B-5), roughly decreasing to half with oral contraceptives (the pill) and doubling with intrauterine devices (IUDs) (Bothwell and Charlton, 1981), Thus, inquiring about the method of contraception helps to predict the risk of iron deficiency; the risk is greatest in women who use an IUD. Iron Needs During Pregnancy Pregnancy imposes increased iron needs for the growth of the fetus and for expansion of maternal blood volume (Hallberg, 1988; IOM, 1990a) (Figure B-6). Even women who are not iron deficient at the beginning of pregnancy (on the basis of the hemoglobin concentration) are at risk of developing an iron-responsive depression in hemoglobin concentration in the third trimester unless they receive supplemental iron (Table B-2). Among women who are already iron deficient when they become pregnant, the severity of the deficiency will usually increase as pregnancy progresses unless they take an iron supplement.

OCR for page 45
--> TABLE B-1 Iron Balance in Women Compared with That in Men Iron Parameter Women Men Total body iron, g 2.3 3.5 Storage iron, g 0.3 1.0 Food iron, mg/day 11 15 Iron absorption, percent 12 6 Iron absorption, mg/day 1.3 0.9 Iron loss, mg/day 1.3 0.9   SOURCE: Based primarily on data in Bothwell et al. (1979). Figure B-4 Frequency distribution of menstrual blood loss. Although the mean menstrual blood loss is about 30 ml/month, about 10 percent of women lose more than 80 ml/month. SOURCE: Data from Hallberg et al. (1966), adapted from Bothwell et al. (1979).

OCR for page 46
--> Figure B-5 Menstrual blood loss by method of contraception as mean ± standard deviation menstrual blood loss in three groups of women. The control group comprised normal women, the pill group comprised normal women taking the combination variety of oral contraceptives, and the IUD group comprised women using intrauterine devices (IUDs). Source: Figure from Bothwell and Charlton (1981). Figure B-6 Schematic representation of the need for absorbed iron during pregnancy. Iron requirements increase markedly during the second and third trimesters. Source: From Bothwell et al. (1979).

OCR for page 47
--> TABLE B-2 Effects of Iron Supplementation on Mean Hemoglobin Concentration in Late Pregnancy Dose of Elemental Irona Number of Subjects Hemoglobin, g/dl, at 35-36 weeks of Gestation Reference Supplemented Controls Supplemented Controls Differenceb 30 mg/day as ferrous 49 46 12.4 11.4 1.0 Chanarin and Rothman, 1971 fumaratec             100 mg, twice daily, with meals, sustained release 24 26 12.4 11.4 1.0 Svanberg et al., 1976 100 mg, twice daily, sustained release 16 16 12.7 11.0 1.7 Puolakka et al., 1980 65 mg (+ 350 µg of folate) 21 24 12.7 11.0 1.6 Taylor et al., 1982 200 mg/day 22 23 12.6 11.3 1.3 Romslo et al., 1983 105 mg, sustained release, at breakfast 21 23 12.6 12.2 0.4 Wallenburg and van Eijk, 1984 65 mg as part of multivitamin-mineral supplement after meals 16 13 12.4 11.4 1.0 Dawson and McGanity, 1987 a Ferrous sulfate, unless otherwise stated. b All differences were statistically significant except for Wallenburg and van Eijk (1984). c Doses of 60 and 120 mg did not result in higher hemoglobin values. SOURCE: From IOM (1990b).

OCR for page 48
--> Iron Needs of Infants Among infants, iron needs are primarily for growth. A high hemoglobin concentration at birth and abundant neonatal iron stores protect most term infants against iron deficiency until 4 months of age (Dallman, 1988). Indeed, total body iron scarcely changes during this period because of the physiologic decline in hemoglobin concentration; iron stores also diminish by 4 months of age (Figure B-7). Term infants are at the greatest risk of developing iron deficiency between 4 and 12 months of age and subsequently, when the iron needs for rapid growth must be supplied by the diet. At 1 year of age, for example, iron absorption is about four times greater than excretion, the difference being used for growth (Figure B-8). The risk of developing iron deficiency anemia during this period depends largely on the diet (Penrod et al., 1990; Pizarro et al., 1991; Tunnessen and Oski, 1987). Although iron deficiency anemia is rare in infants receiving iron-fortified formula, it is common in those fed unfortified formula or cow's milk (Figure B-9). Cow's milk not only has an extremely low concentration of iron but it also results in increased fecal blood loss (Ziegler et al., 1990) (Figure B-10). Furthermore, the higher calcium content of cow's milk compared with that of breast milk contributes to poor iron absorption (Hallberg et al., 1992). Exclusively breastfed infants may also develop iron deficiency, but only after about 6 months of age (Calvo et al., 1992; Duncan et al., 1985; Pizarro et al., 1991; Siimes et al., 1984), if they are not given an iron supplement (Figure B-9). Figure B-7 Changes in body iron during infancy. There is little change in total body iron between birth and 4 months of age. In contrast, total body iron increases markedly during later infancy. The high iron needs from 4 to 12 months of age help to explain why the risk of iron deficiency is greatest during this period. Source: Dallman (1988).

OCR for page 49
--> Figure B-8 Iron metabolism in the 1-year-old infant. Iron absorption must exceed iron loss to allow growth; however, daily iron absorption and loss, even in infancy, are normally a minute percentage of total body iron. MB + ENZ = myoglobin and enzyme iron. Source: Reproduced with minor modifications from Dallman (1988), with permission from Hanley & Belfus. In the United States, there has recently been a marked decline in the prevalence of iron deficiency anemia among infants and young children (Yip et al., 1987a,b). This improvement is attributable to concurrent changes in infant feeding practices that would be expected to improve iron nutrition, including less use of cow's milk in the first year of life, more use of iron-fortified formulas, and less use of low-iron formulas (Fomon, 1987). Iron absorption studies suggest (Fomon et al., 1989) and clinical trials indicate (Walter et al., 1993) that iron-fortified infant cereals also play a significant role in preventing iron deficiency anemia. Low-birth-weight infants may become iron deficient after 2 months of age and possibly earlier unless they are given an iron supplement (Lundström et al., 1977; Siimes et al., 1984) (Figure B-11). Their iron needs are greater because of their lower neonatal stores, a more rapid relative growth rate, and often, blood loss resulting from the increased number of laboratory studies that their early care may require. For low-birth-weight infants fed human milk, supplemental iron is recommended to start at about 2 weeks of age at a dose of 2 to 3 mg of elemental iron per kg/day (AAP, CON, 1985). Infants fed iron-fortified formula usually obtain sufficient amounts of iron to make an additional supplement unnecessary.

OCR for page 50
--> Figure B-9 Iron deficiency anemia among 9-month-old children who have been fed different diets. Source: From Pizzaro et al. (1991). Figure B-10 The fecal hemoglobin concentrations of infants fed formula (•) and infants fed cow's milk (o) after 168 days of age. Early feeding of cow's milk to infants results in increased fecal blood loss. Bars indicate standard errors. Source: Adapted from Ziegler et al. (1990).

OCR for page 51
--> Figure B-11 Iron deficiency anemia among low-birth-weight infants. Low-birth -weight infants weighing 1,000 to 2,000 g are likely to develop iron deficiency anemia after 2 months of age if not given iron supplements (o). The supplemented infants (•) received a total of 2 mg of iron/kg/day as ferrous sulfate starting at 2 weeks of age. Source: From Lundström et al. (1977). Childhood and Adolescence After infancy, iron deficiency becomes less common (Yip et al., 1987a,b) as the rate of growth decreases and the diet becomes more diversified. During adolescence, however, the prevalence of iron deficiency rises again (LSRO, 1984) because iron needs increase with the adolescent growth spun (Dallman, 1992) (Figure B-12). Presumably, iron deficiency is even more common among pregnant adolescents, in whom the iron needs for pregnancy follow closely after the increased needs for growth. However, no iron deficiency prevalence data for pregnant adolescents in the general population are available.

OCR for page 88
--> trimester and less than 10.5 g/dl in the second trimester. The routine use of ferrous iron at a dose of about 30 rag/day was recommended for nonanemic women starting at 12 weeks of gestation.1 Anemia before conception or during pregnancy should be treated with 60 to 120 mg of ferrous iron per day, no more than about 60 mg per dose. A vitamin-mineral supplement containing 15 mg of zinc and 2 mg of copper was recommended to be taken at a different time of the day.2 The hemoglobin should be checked for improvement after about 1 month, and the dose should be lowered to 30 mg/day if the anemia has resolved. The possibility of side effects was mentioned, including the likelihood that nausea, cramps, constipation, or diarrhea, should they develop, often persist for no longer than 3 to 5 days. Liquid and chewable preparations were offered as alternatives for women who have trouble swallowing pills or capsules. The relevant information provided about iron supplements is summarized in Table B-13. Life Research Office: Guidelines For The Assessment And Management Of Iron Deficiency In Women Of Childbearing Age This report (LSRO, 1991) focused primarily on the problem of iron deficiency in nonpregnant women. The recommendations for pregnant women were essentially the same as those of the Institute of Medicine (IOM, 1990a, 1992). The prevalence of iron deficiency in the total population was considered to be sufficiently low to preclude recommending an increase in current levels of iron fortification in standardized food. The prevalence of iron deficiency in nonpregnant women of childbearing age was too low to justify supplementing all women. Women with iron deficiency anemia should therefore be detected by laboratory screening, and intervention with iron supplements should be recommended for women with iron deficiency anemia. Nonpregnant women should be screened for anemia (hemoglobin concentration, <12.0 g/dl, or hematocrit, <36 percent, with corrections for altitude and smoking [Table B-11]). For mild anemia (a hemoglobin concentration of between 10.0 and 12.0 g/all), a therapeutic dose of iron, 60 mg twice a day, should be given for 6 weeks. Check for a change in hemoglobin concentration and continue for a total of 6 months, and then lower the dose to 30 mg/day and monitor iron status. For severe anemia (a hemoglobin concentration of <10.0 g/dl), investigate further for the cause of anemia (note that such low values are very rare). To make an etiologic diagnosis of anemia, serum ferritin concentra 1   Note that recent developments argue for earlier initiation of iron or iron and folate: Studies indicate an association of anemia (Kim et al., 1992) or iron deficiency anemia (Scholl et al., 1992) early in pregnancy with low-birth-weight (IOM, 1992) and the CDC recommendations that all women of childbearing potential consume 0.4 nag of folate per day (CDC, 1992; IOM, 1992). 2   The necessity for this recommendation might be reevaluated in light of evidence for decreased compliance when medication is recommended at intervals more frequent than once a day (IOM, 1992).

OCR for page 89
--> TABLE B-13 Information About Iron Supplements Types of iron preparations Well-absorbed iron compounds include ferrous sulfate, exsiccated ferrous sulfate, ferrous gluconate, and ferrous fumarate. Slow-release iron compounds are available if there are side effects, but these are more expensive and are not as well absorbed. Liquid and chewable preparations are available for those who have trouble swallowing tablets. Iron compounds can be given alone, in combination with folate, or as part of a multivitamin-mineral combination, according to the clinical circumstances. Drug Facts and Comparisons (Kastrup, 1992) is a useful, frequently updated reference for contents and costs of currently marketed iron products. It is available in many pharmacies and medical libraries. Iron doses can be expressed in terms of elemental iron, as here, or in terms of the iron compound: 30 mg of elemental iron is equivalent to: 150 mg of ferrous sulfate about 95 mg of exsiccated ferrous sulfate 90 mg of ferrous fumarate 250 mg of ferrous gluconate 60 mg of elemental iron is equivalent to: 300 mg of ferrous sulfate about 190 mg of exsiccated ferrous sulfate 180 mg of ferrous fumarate 500 mg of ferrous gluconate What to tell the patient to improve compliance and safety Taking iron to prevent or treat iron deficiency anemia helps to reduce fatigue and increase your ability to adapt to delivery. Let me give you the name of a liquid or chewable preparation if you have difficulty swallowing tablets. Iron-containing supplements are best taken between meals or at bedtime with water or juice, not tea, coffee, or milk (once-a-day regimens favor compliance). You may notice a darkening in the color of your stools, which normally results from taking iron tablets. Higher doses of iron sometimes cause stomach discomfort, constipation, or less often, diarrhea, but these problems often persist for no longer than the first 3 to 5 days after you start taking iron. If problems persist, we can lower the dose or recommend a different (slow-release) preparation that can be taken with meals. Use safety caps (let me show you how), and keep supplements out of the reach of children because iron is a very common cause of poisoning (Litovitz et al., 1992). SOURCE: IOM (1992).

OCR for page 90
--> tion determination is the preferred test. A value of less than 12 µg/liter by itself indicates iron deficiency. A value of less than 15 µg/liter in an anemic individual indicates iron deficiency anemia. Therapeutic doses of iron for anemia should be given under medical supervision. The total daily dose can be between 60 and 180 mg/day but should not be more than about 60 mg per dose. Take iron alone with water or fruit juice, not with milk, tea, or coffee. A maintenance dose of iron is 30 mg/day (range, 15 to 60 mg) when taken as prescribed (see discussion of RDAs below). Advise on diet. For follow-up, on a 6-week revisit, modify the dose according to the change in the hemoglobin concentration and compliance. Consider other causes of anemia if there has been no response. Pregnant women should routinely take a maintenance dose of iron in the second and third trimesters even if they are not anemic. If anemic, they should receive a therapeutic dose of iron as described below. New CDC criteria for anemia during pregnancy should be used (Table B-11) (CDC, 1989). Recommended Dietary Allowances, 10th Edition For nonpregnant women, 15 mg of iron per day was considered to provide a sufficient margin of safety for essentially all adult women in the United States except for those with the most extreme menstrual losses, given usual dietary patterns (NRC, 1989). This is a reduction from 18 mg/day in the 1980 RDAs. For pregnant women, a daily increment of 15 mg/day (or a total of 30 mg/day) is recommended; this value is averaged over the entire pregnancy (NRC, 1989). Since the increased requirements of iron during pregnancy cannot be met by the iron content of the habitual diet of most Americans or the iron stores of at least some women, daily iron supplements are usually recommended. Editorial Discussions There is a widely held view in Britain (Hibbard, 1988) and elsewhere (Hemminki and Starfield, 1978) that no medication (including iron supplements) should be given to pregnant women in the absence of proven need. The view of Hemminki and coworkers (1989) was based on an earlier meta-analysis indicating no proven benefits of using vitamin or mineral supplements (Hemminki and Starfield, 1978). Hibbard (1988) proposed screening pregnant women and treating those in low-risk categories with iron only if they have a low serum ferritin concentration or anemia, but Horn (1988), in the same issue of the British Medical Journal as the article by Hibbard (1988), recommended

OCR for page 91
--> routine iron supplementation as practical and cost-effective. Hibbard (1988) also recommended routine iron administration if concomitant folic acid treatment was used. Thus, the recent recommendation to use folate before conception and early in pregnancy would also include the use of iron if iron and folate combinations are prescribed, as is commonly the case. International Recommendations Directed Primarily to Developing Countries These recommendations are intended primarily for pregnant women in developing countries, where surveys have shown a prevalence of iron deficiency anemia often in excess of 50 percent (DeMaeyer et al., 1985). The recommendations have involved the routine use of relatively high doses of iron and folate. Poor distribution of tablets and poor compliance have been recognized as major problems. Various strategies for fortifying food with iron have been studied, but there has been little progress in implementing them on a broad scale. Fao/Who (1988) Requirements for absorbed iron were calculated for various age, sex, and pregnancy categories. Recommendations for dietary iron intakes are based on the estimated bioavailability of iron from the customary diet. The assumed percentage of iron absorbed primarily from cereal and legume diets, which have poor iron bioavailability, are 5 percent; that absorbed from diets with intermediate bioavailability, 10 percent; and that absorbed from diets with high bioavailability (meat and ascorbic acid-rich diets, as is usual in the United States), 15 percent. World Health Organization The document Preventing and Controlling Iron Deficiency Anemia Through Primary Health Care (DeMaeyer, 1989) noted the need for supplementation in situations such as pregnancy, in which rapid improvement in iron status is important. It recognized the problem of compliance, especially when there may be side effects and no perception of ill health. It also stressed the need for communication and the importance of motivation skills for health workers. For pregnant women, the recommendation was to take tablets containing 60 mg of iron and 250 lag of folate twice a day. A diet rich in heme iron and ascorbic acid was advocated. The desirability of iron fortification of a staple food and the control of infection were discussed. International Nutritional Anemia Consultative Group Tablets containing 60 mg of iron and 250 µg of folate twice a day without food were recommended for pregnant women. If there were side effects, the tablets were to be taken after meals or at a lower dose for 1 week before resuming a full dose. Diet modification and fortification were mentioned (INACG, 1989).

OCR for page 92
--> References AAP, CON (American Academy of Pediatrics, Committee on Nutrition). 1969. Iron balance and requirements in infancy. Pediatrics 43:134-142. AAP, CON (American Academy of Pediatrics, Committee on Nutrition). 1976. Iron supplementation for infants. Pediatrics 58:765-768. AAP, CON (American Academy of Pediatrics, Committee on Nutrition). 1985. Nutritional needs of low-birth-weight infants. Pediatrics 75:976-986. AAP, CON (American Academy of Pediatrics, Committee on Nutrition). 1989. Iron-fortified infant formulas. Pediatrics 84:1114-1115. AAP, CON (American Academy of Pediatrics, Committee on Nutrition). 1992. The use of whole cows milk in infancy. Pediatrics 89:1105-1109. AAP, CON (American Academy of Pediatrics, Committee on Nutrition). 1993. Pediatric Nutrition Handbook. Elk Grove, Ill: AAP. ACOG (American College of Obstetricians and Gynecologists). 1989. Committee on Professional Standards. Standards for Obstetric-Gynecological Services, 7th ed. Washington, D.C.: ACOG. AMA (American Medical Association). 1992. Guidelines for Adolescent Preventive Services. Report of the Department of Adolescent Health. Chicago: AMA. Annest, J.L., J.L. Pirckle, D. Makue, J.W. Neese, D.D. Bayse, and M.G. Kovar. 1983. Chronological trend in blood lead levels between 1976 and 1980. N. Engl. J. Med. 308:1373-1377. Babior, B.M., W.A. Peters, P.M. Briden, and C.L. Cetrulo. 1985. Pregnant women's absorption of iron from prenatal supplements. J. Reprod. Med. 30:355-357. Beutler, E. 1988. The common anemias. J. Am. Med. Assoc. 259:2433-2437. Bonnar, J., A. Goldberg, and J.A. Smith. 1969. Do pregnant women take their iron? Lancet 1:457-458. Bothwell, T.H., and R.W. Charlton. 1981. Iron Deficiency in Women. Washington, D.C.: International Nutrition Anemia Consultative Group. Bothwell, T.H., and P. Macphail. 1992. Prevention of iron deficiency by food fortification. Pp. 183-192 in Nutritional Anemias, S.J. Fomon and S. Zlotkin, eds. Nestlé Nutrition Workshop Series, Vol. 30. New York: Raven Press. Bothwell, T.H., R.W. Charlton, J.D. Cook, and C.A. Finch. 1979. Iron Metabolism in Man. Blackwell: Oxford. Bothwell, T.H., R.D. Baynes, B.J. MacFarlane, and A.P. MacPhail. 1989. Nutritional iron requirements and food iron absorption. J. Int. Med. 226:357-365. Calvo, E.B., A.C. Golindo, and N.B. Aspres. 1992. Iron status in exclusively breastfed infants. Pediatrics 90:375-379. Canadian Paediatric Society, Nutrition Committee. 1991. Meeting the iron needs of infants and young children: An update. Can. Med. Assoc. J. 144:1451-1453. Carriaga, M.T., B.S. Skikne, B. Finley, B. Cutler, and J.D. Cook. 1991. Serum transferrin receptor for the detection of iron deficiency in pregnancy. Am. J. Clin. Nutr. 54:1077-1081. CDC (Centers for Disease Control). 1989. CDC criteria for anemia in children and childbearing-aged women. Morbid. Mortal. Weekly Rep. 38:400-404. CDC (Centers for Disease Control). 1992. Recommendations for the use of folic acid to reduce the number of cases of spina bifida and other neural tube defects. Morbid. Mortal. Weekly Rep. 41 (No. RR-14 ): 1-7.

OCR for page 93
--> Chanarin, I., and D. Rothman. 1971. Further observations on the relation between iron and folate status in pregnancy. Br. Med. J. 2:81-84. Charlton, R.W., and T.H. Bothwell. 1983. Iron absorption. Annu. Rev. Meal. 34:55-68. Clapp, J.F., B.L. Seaward, R.H. Sleamaker, and J. Hiser. 1988. Maternal physiologic adaptations to early pregnancy. Am. J. Obstet Gynecol. 159:1456-1460. Clark, M., R. Royal, and R. Seeler. 1988. Interaction of iron deficiency and lead and the hematologic findings in children with severe lead poisoning. Pediatrics 81:247-254. Cook, J.D. 1990. Adaptation in iron metabolism. Am. J. Clin. Nutr. 51:301-308. Cook, J.D., and T.H. Bothwell. 1984. Availability of iron from infant food. Pp. 119-143 in Nutrition in Infancy and Childhood, A. Stekel, ed. New York: Raven Press. Cook, J.D., C.A. Finch, and N.J. Smith. 1976. Evaluation of the iron status of a population. Blood 48:449-455. Cook, J.D., S.S. Watson, K.M. Simpson, D.A. Lipschitz, and B.S. Skigne. 1984. The effect of high ascorbic acid supplementation on body iron stores. Blood 64:721-726. Cook, J.D., S.A. Dassenko, and S.R. Lynch. 1991. Assessment of the role of nonheine-iron availability in iron balance. Am. J. Clin. Nutr. 54:717-722. Cook, J.D., B.S. Skikme, and R.D. Baynes. 1993. Serum transferrin receptor. Annu. Rev. Med. 44:63-74. Cramer, J.A., R.H. Mattson, M.L. Prevey, R.D. Scheyer, and V.L. Ouellette. 1989. How often is medication taken as prescribed? A novel assessment technique. J. Am. Med. Assoc. 261:3273-3277. Cramer, J.A., R.D. Scheyer, and R.H. Mattson. 1990. Compliance declines between clinic visits. Arch. Intern. Med. 150:1509-1510. Crosby, W.H. 1986. Yin, yang, and iron. Nutrition Today July/Aug:14-16. Cross, C.E., B. Halliwell, E.T. Borish, W.A. Pryor, R.L. Saul, J.M. McDord, and D. Harman. 1987. Oxygen radicals and human disease. Ann. Intern. Med. 107:526-545. Czeizel, A.E., and I. Dudas. 1992. Prevention of the first occurrence of neural-robe defects by periconceptual vitamin supplementation. N. Engl. J. Med. 327:1832-1835. Dallman, P.R. 1986. Biochemical basis for manifestations of iron deficiency. Annu. Rev. Nutr. 6:13-40. Dallman, P.R. 1987. Iron deficiency and the immune response. Am. J. Clin. Nutr. 46:329-334. Dallman, P.R. 1988. Nutritional anemia of infancy: Iron, folic acid, and vitamin B12. Pp. 216-235 in Nutrition During Infancy, R.C. Tsang and B.L. Nichols, eds. Philadelphia: Hanley and Belfus. Dallman, P.R. 1992. Changing iron needs from birth through adolescence. Pp. 29-36 in Nutritional Anemias, S.J. Fomon and S. Zlotkin, eds. New York: Raven Press. Dallman, P.R., and J.D. Reeves. 1984. Laboratory diagnosis of iron deficiency. Pp. 11-44 in Nutrition in Infancy and Childhood, A. Stekel, ed. New York: Raven Press. Dallman, P.R., and M.A. Siimes. 1979. Percentile curves for hemoglobin and red cell volume in infancy and childhood. J. Pediatr. 94:26-31. Dallman, P.R., G.D. Bart, C.M. Allen, and H.R. Shinefield. 1978. Hemoglobin concentration in white, black, and Oriental children: is there a need for separate criteria in screening for anemia? Am. J. Clin. Nutr. 31:377-380.

OCR for page 94
--> Dawson, E.B., and W.J. McGanity. 1987. Protection of maternal iron stores in pregnancy. J. Reprod. Med. 32:478-487. DeMaeyer, E.M. 1989. Preventing and Controlling Iron Deficiency Anaemia Through Primary Health Care. Geneva: World Health Organization. DeMaeyer, E.M., M. Adiels-Tegman, and E. Rayston. 1985. The prevalence of anemia in the world. World Health Statist. Q. 38:302-316. DHHS/USDA (U.S. Department of Health and Human Services and U.S. Department of Agriculture). 1991. Nutrition and Your Health: Dietary Guidelines for Americans, 3rd ed. Washington, D.C.: U.S. Government Printing Office. Duncan, B., R.B. Schifman, J.J. Corrigan, and C. Schaefer. 1985. Iron and the exclusively breastfed infant from birth to six months. J. Pediatr. Gastroenterol. Nutr. 4:421-425. Ekenved, G., B. Arvidsson, and L. Sölvell. 1976. Influence of food on the absorption from different types of iron tablets. Scand. J. Haematol. 28(Suppl.):79-88. Expert Scientific Working Group. 1985. Summary of a report on assessment of the iron nutritional status of the United States population. Am. J. Clin. Nutr. 42:1318-1330. FAO/WHO (Food and Agriculture Organization of the United Nations/World Health Organization). 1988. 1988 Report of a Joint FAO/WHO Expert Consultation. Pp. 33-50 in Requirements of Vitamin A, Iron, Folate and Vitamin B12. Rome: Food and Agriculture Organization of the United Nations. Ferguson, B.J., B.S. Skigne, K.M. Simpson, R.D. Baynes, and J.D. Cook. 1992. Serum transferrin receptor distinguishes the anemia of chronic from iron deficiency anemia. J. Lab. Clin. Meal. 119:385-390. Fomon, S.J. 1987. Reflections on infant feeding in the 1970s and 1980s. Am. J. Clin. Nutr. 46:171-182. Fomon, S.J., E.E. Ziegler, R.R. Rogers, S.E. Nelson, B.B. Edwards, D.G. Guy, J.C. Erve, and M. Janghorbani. 1989. Iron absorption from infant foods. Pediatr. Res. 26:250-254. Galan, P., F. Cherouvrier, P. Preziosi, and S. Hercberg. 1991. Effects of the increased consumption of dairy products upon iron absorption. Eur. J. Clin. Nutr. 45:553-559. Gain, S.M., S.A. Ridella, A.S. Tetzold, and F. Falkner. 1981. Maternal hematological levels and pregnancy outcomes. Semin. Perinatol. 5:155-162. Groner, J.A., N.A. Holtzman, E. Charney, and D.E. Mellits. 1986. A randomized trial of oral iron on tests of short-term memory and attention span in young pregnant women. J. Adolescent Health Care 7:44-48. Hahn, P.F., E.L. Carothers, W.J. Darby, M. Martin, C.W. Sheppard, R.O. Cannon, A.S. Beam, P.M. Denson, J.C. Peterson, and G.S. McClellan. 1951. Iron metabolism in human pregnancy as studied with the radioactive isotope, Fe59 . Am. J. Obstet. Gynecol. 61:477-486. Hallberg, L. 1981. Bioavailability of dietary iron in man. Annu. Rev. Nutr. 1:123-147. Hallberg, L. 1992. Iron requirements. Comments on methods and some crucial concepts in iron nutrition. Biol. Trace Elements Res. 35:25-45. Hallberg, L. 1988. Iron balance in pregnancy. Pp 115-126 in Vitamins and Minerals in Pregnancy and Lactation, H. Berger, ed. Nestlé Nutrition Workshop Series, Vol. 16. New York: Raven Press. Hallberg, L., and L. Rossander. 1982. Absorption of iron from Western-type lunch and dinner meals. Am. J. Clin. Nutr. 35:502-509.

OCR for page 95
--> Hallberg, L., A.M. Högdahl, L. Nilsson, and G. Rybo. 1966. Menstrual blood loss—a population study. Variation at different ages and attempts to define normality. Acta Obstet. Gynecol. Scand. 45:320-351. Hallberg, L., L. Ryttinger, and L. Sölvell. 1967. Side effects of oral iron therapy: A double-blind study of different iron compounds in tablet form . Acta Med. Scand. Suppl. 459:3-10. Hallberg, L., M. Brune, M. Erlandsson, A.-S. Sandberg, and L. Rossander-Hultén. 1991. Calcium: Effect of different amounts on non-heme- and heine-iron absorption in humans. Am. J. Clin. Nutr. 53:112-119. Hallberg, L., L. Rossander-Hulten, M. Brune, and A. Gleerup. 1992. Bioavailability of iron in human milk and cow's milk in relation to their calcium contents. Pediatr. Res. 31:524-527. Hallberg, L., L. Hulten, G. Lindstedt, P.-A. Lunberg, M. Anders, J. Purens, B. Svanberg, and B. Swolin. In press. High prevalence of iron deficiency in Swedish adolescents. Pediatr. Res. Hambidge, K.M., N.F. Krebs, L. Sibley, and J. English. 1987. Acute effects of iron therapy on zinc status during pregnancy. Obstet. Gynecol. 70:593-596. Haynes, R.B. 1979. Strategies for improving compliance: A methodologic analysis and review. Pp 69-82 in Compliance in Health Care, R.B. Haynes, D.W. Taylor, and D.L. Sackett, eds. Baltimore: Johns Hopkins University Press. Haynes, R.B., D.W. Taylor, and D.L. Sackett, eds. 1979. Compliance in Health Care. Baltimore: Johns Hopkins University Press. Hemminki, E., and B. Starfield. 1978. Routine administration of iron and vitamins during pregnancy: Review of controlled clinical trials. Br. J. Obstet. Gynaecol. 85:404-410. Hibbard, B.M. 1988. Controversies in therapeutics. Iron and folate supplements during pregnancy: Supplementation is valuable only in selected patients. Br. Med. J. 297:1324-1326. Horn, E. 1988. Controversies in therapeutics. Iron and folate supplements during pregnancy: Supplementing everyone treats those at risk and is cost effective. Br. Med. J. 297:1325-1327. Hurrell, R.F. 1992. Prospects for improving the iron fortification of foods. Pp. 193-201 in Nutritional Anemias, S.J. Fomon and S. Zlotkin, eds. Nestlé Nutrition Workshop Series, Vol. 30. New York: Raven Press. Idjradinata, P., and E. Pollitt. 1993. Reversal of developmental delays in iron deficient anaemic infants treated with iron. Lancet 341:1-4. INACG (International Nutritional Anemia Consultative Group). 1989. Guidelines for the Control of Maternal Nutritional Anemia. International Life Sciences Institute-Nutrition Foundation. Washington, D.C.: INACG. IOM (Institute of Medicine). 1990a. Nutrition During Pregnancy. Report of the Committee on Nutritional Status During Pregnancy and Lactation, Food and Nutrition Board. Washington, D.C.: National Academy Press. IOM (Institute of Medicine). 1990b. Iron nutrition during pregnancy. Pp. 272-298 in Nutrition During Pregnancy. Report of the Committee on Nutritional Status During Pregnancy and Lactation, Food and Nutrition Board. Washington, D.C.: National Academy Press. IOM (Institute of Medicine). 1992. Nutrition During Pregnancy and Lactation: An Implementation Guide. Report of the Subcommittee for a Clinical Application Guide, Committee on Nutritional Status During Pregnancy and Lactation, Food and Nutrition Board. Washington, D.C.: National Academy Press.

OCR for page 96
--> Johnson-Spear, M.A., and R. Yip. In press. Hemoglobin difference between black and white women with comparable iron status: Justification for race-specific criteria? Am. J. Clin. Nutr. Kastrup, E.K., ed. 1992. Drug Facts and Comparisons. St. Louis: Facts and Comparisons. Kim, I., D.W. Hungerford, R. Yip, S.A. Kuester, C. Zyrkowski, and F.L. Trowbridge. 1992. Pregnancy nutrition surveillance system—United States, 1979-1990. CDC Surveillance Summaries. Morbid. Mortal. Weekly Rep. 41(No. SS-7):26-42. Laplan, J.P., J.L. Annest, P.M. Layde, and G.L. Rubin. 1986. Nutrient intake and supplementation in the United States (NHANES II). Am. J. Public Health 76:287-289. Litovitz, T.L., K.C. Holm, K.M. Bailey, and B.F. Schmitz. 1992. 1991 Annual report of the American Association of Poison Control Centers National Data Collection System. Am. J. Emerg. Med. 10:452-505. Looker, A.C., C. L. Johnson, M.A. McDowell, and E.A. Yetley. 1989. Iron status: Prevalence of impairment in three Hispanic groups in the United States. Am. J. Clin. Nutr. 49:553-558. Lozoff, B., E. Jimenez, and A.B. Wolf. 1991. Long-term developmental outcome of infants with iron deficiency. N. Engl. J. Med. 325:687-694. LSRO (Life Sciences Research Office). 1984. Assessment of the Iron Nutritional Status of the U.S. Population Based on Data Collected in the Second National Health and Nutrition Examination Survey, 1976-1980. Bethesda, Md.: Federation of American Societies for Experimental Biology. LSRO (Life Sciences Research Office). 1989. Nutrition Monitoring in the United States—An Update Report on Nutrition Monitoring. DHHS Publication No. (PHS) 89-1255. Public Health Service. Washington, D.C.: U.S. Government Printing Office. LSRO (Life Sciences Research Office). 1991. Guidelines for the Assessment and Management of Iron Deficiency in Women of Childbearing Age, S.A. Anderson, ed. Bethesda, Md.: Federation of American Societies for Experimental Biology. Lundström, U., M.A. Siimes, and P.R. Dallman. 1977. At what age does iron supplementation become necessary in low-birth-weight infants? J. Pediatr. 91:878-883. Monsen, E.R., L. Hallberg, M. Layrisse, D.M. Hegsted, J.D. Cook, W. Mertz, and C.A. Finch. 1978. Estimation of available dietary iron. Am. J. Clin. Nutr. 31:134-141. Murphy, J.F., J. O'Riordan, R.G. Newcombe, and E.C. Coles. 1986. Relation of hemoglobin levels in first and second trimesters to outcome of pregnancy. Lancet 1:992-994. NRC (National Research Council). 1989. Recommended Dietary Allowances, 10th ed. Report of the Subcommittee on the Tenth Edition of the RDAs, Food and Nutrition Board, Commission of Life Sciences. Washington, D.C.: National Academy Press. Penrod, J.C., K. Anderson, and P.B. Acosta. 1990. Impact on iron status of introducing cow's milk in the second six months of life. J. Pediatr. Gastroenterol. Nutr. 10:462-467. Perry, G.S., T. Byers, R. Yip, and S. Margen. 1992. Iron nutrition does not account for hemoglobin differences between blacks and whites. J. Nutr. 122:1417-1424.

OCR for page 97
--> Pizarro, F., R. Yip, P.R. Dallman, M. Olivares, E. Hertrampf, and R. Walter. 1991. Iron status with different infant feeding regimens: Relevance to screening and prevention of iron deficiency. J. Pediatr. 118:687-692. Pollitt, E., P. Hathirat, N.J. Kotchabhakdi, L. Missell, and A. Valyasevi. 1989. Iron deficiency and educational achievement in Thailand. Am. J. Clin. Nutr. 50:687-697. Porter, A.M.W. 1969. Drug defaulting in a general practice. Br. Med. J. 1:218-222. Puolakka, J., O. Jãnne, A. Pakarinen, and R. Vihko. 1980. Serum ferritin as a measure of stores during and after normal pregnancy with and without iron supplements. Acta Obstet. Gynecol Scand. Suppl. 95:43-51. Reeves, J.D., R. Yip, V. Kiley, and P.R. Dallman. 1984. Iron deficiency in infants, the influence of antecedent infection. J. Pediatr. 105:874-879. Romslo, I., K. Haram, N. Sagen, and K. Augensen. 1983. Iron requirements in normal pregnancy as assessed by serum ferritin, serum transferrin saturation, and erythrocyte protoporphyrin determinations. Br. J. Obstet. Gynaecol. 90:101-107. Rossander, L., L. Hallberg, and E. Björn-Rasmussen. 1979. Absorption of iron from breakfast meals. Am. J. Clin. Nutr. 32:2484-2489. Salonen, J.T., K. Nyysönen, H. Korpela, J. Tuomilehto, R. Seppänen, and R. Salonen. 1992. High stored iron levels are associated with excess risk of myocardial infarction in Eastern Finnish men . Circulation 86:803-811. Schifman, R.B., J.E. Thomasson, and J.M. Evers. 1987. Red blood cell zinc protoporphyrin testing for iron deficiency anemia in pregnancy. Am. J. Obstet. Gynecol. 157:304-307. Scholl, T.O., M.L. Hediger, R.L. Fischer, and J.W. Shearer. 1992. Anemia vs. iron deficiency: Increased risk of preterm delivery in a prospective study. Am. J. Clin. Nutr. 55:985-988. Seligman, P.A., J.H. Caskey, J.L. Frazier, R.M. Zucker, E.R. Podell, and R.H. Alien. 1983. Measurements of iron absorption from prenatal multivitamin-mineral supplements. Obstet. Gynecol. 61:356-362. Sheldon, W.L., M.O. Aspillaga, P.A. Smith, and T. Lind. 1985. The effects of oral iron supplementation on zinc and magnesium levels during pregnancy. Br. J. Obstet. Gynaecol. 92:892-898. Siegenberg, D., R.D. Baynes, T.H. Bothwell, B.J. MacFarlane, R.D. Lamparelli, N.G. Car, P. McPhail, U. Schmidt, A. Tal, and F. Mayet. 1991. Ascorbic acid prevents the dose dependent inhibitory effects of polyphenols and phytates on non-heme iron absorption. Am. J. Clin. Nutr. 53:537-541. Siimes, M.A., L. Salmenperä, and J. Perheentupa. 1984. Exclusively breast-feeding for nine months: Risk of iron deficiency. J. Pediatr. 104:196-199. Sjöstedt, J.E., P. Manner, S. Nummi, and G. Ekenved. 1977. Oral iron prophylaxis during pregnancy: A comparative study on different dosage regimens. Acta Obstet. Gynecol. Scand. Suppl. 60:3-9. Sölvell, L. 1970. Oral iron therapy-side effects. Pp. 573-583 in Iron Deficiency: Pathogenesis, Clinical Aspects, Therapy, L. Hallberg, H.G. Harwerth, and A. Vannotti, eds. London: Academic Press. Subar, A.F., and G. Block. 1990. Use of vitamin and mineral supplements: Demographics and amounts of nutrients consumed. Am J. Epidemiol. 132:1091-1101. Svanberg, B., B. Arvidsson, A. Norrby, G. Rybo, and L. Sölvell. 1976. Absorption of supplemental iron during pregnancy—A longitudinal study with repeated

OCR for page 98
--> bone-marrow studies and absorption measurements. Acta Obstet. Gynecol. Scand Suppl. 48:87-108. Swiss, L.D., and G.H. Beaton. 1974. A prediction of the effects of iron fortification. Am. J. Clin. Nutr. 27:373-379. Taylor, D.J., C. Mallen, N. McDougall, and T. Lind. 1982. Effect of iron supplementation on serum ferritin levels during and after pregnancy. Br. J. Obstet. Gynecol. 89:1011-1017. Tunnessen, W.W., and F.A. Oski. 1987. Consequences of starting whole cow milk at 6 months of age. J. Pediatr. 111:813-816. Uchida, T., M. Yoshida, K. Sakai, K. Kokubun, T. Igarashi, T. Tanaka, and S. Kariyone. 1988. Prevalence of iron deficiency in Japanese women. Acta Haematol. Jpn. 51:24-27. Ulmer, H.U., and E. Goepel. 1988. Anemia, ferritin and preterm labor. J. Perinat. Med. 16:459-465. Wallenburg, H.C.S., and H.G. van Eijk. 1984. Effect of oral iron supplementation during pregnancy on maternal and fetal iron status. J. Perinat. Med. 12:7-11. Walter, T., I. De Andraca, P. Chadud, and C.G. Perales. 1989. Iron deficiency anemia: Adverse effects on infant psychomotor development. Pediatrics 84:7-17. Walter, T., P.R. Dallman, F. Pizarro, L. Veloso, G. Peña, S. Bartholmey, E. Hertrampf, M. Olivares, A. Letelier, and M. Arredondo. 1993. Effectiveness of iron-fortified infant cereal in prevention of iron deficiency anemia. Pediatrics 91:976-982. Weinberg, E.D. 1984. Iron withholding. Physiol. Rev. 64:65-102. Weinberg, E.D. 1992. Roles of iron in neoplasia. Biol. Trace Element Res. 34:123-140. Widholm, O., E. Vartiainen, and T. Tenhunen. 1967. On iron requirements in menstruating teen-age girls. Acta Obstet. Gynecol. Scand. 46(Suppl. 1):31-46. Yip, R. 1989. The changing characteristics of childhood iron nutritional status in the United States. Pp. 37-56 in Dietary Iron: Birth to Two Years, L.J. Filer, Jr., ed. New York: Raven Press. Yip, R., S. Schwartz, and A.S. Deinard. 1984. Hematocrit values in white, black, and American Indian children with comparable iron status: Evidence to support uniform diagnostic criteria for anemia among all races. Am. J. Dis. Child. 138:824-827. Yip, R., K.M. Walsh, M.G. Goldfarb, and N.J. Binkin. 1987a. Declining prevalence of anemia in childhood in a middle-class setting: A pediatric success story? Pediatrics 80:330-334. Yip, R., N.J. Binkin, L. Fleshood, and F.L. Trowbridge. 1987b. Declining prevalence of anemia among low-income children in the United States. J. Am. Med. Assoc. 258:1619-1623. Ziegler, E.E., S.J. Fomon, S.E. Nelson, C.J. Rebouche, B.B. Edwards, R.R. Rogers, and L.J. Lehman. 1990. Cow milk feeding in infancy: Further observations on blood loss from the gastrointestinal tract. J. Pediatr. I 16:11-18.

Representative terms from entire chapter:

deficiency anemia