Debra L. Bogen, MD

General Academic Pediatrics

Children's Hospital of Pittsburgh

Pretest

Q1. You are seeing a 12-month-old boy for routine well child care. If you use the selective screening criteria recommended by the CDC, which of the following scenarios would suggest that he have blood test screening for iron deficiency anemia?

A. He started whole milk last week

B. He has been on a low iron cow's milk based formula since age 7 months

C. He was born at 37 weeks gestation

D. He has Sickle Cell Trait

E. All of the above

Q2. How would you manage a 12 month old, healthy appearing child with the following laboratory results: hemoglobin 10.5g/dL, hematocrit 31.2, MCV 68.0fL, RDW 16.6, ferritin 9ng/ml, lead < 3?g/dL.

A. Recommend an over-the-counter multivitamin with iron and retest in 3 months.

B. Recommend an increase in the amount of meat in her diet

C. Repeat the tests in 2 weeks and include a reticulocyte count, total serum iron and total iron binding capacity (TIBC).

D. Prescribe 3-4 mg/kg/day of elemental iron and retest in one month.

E. Recommend she stop breast feeding, start whole milk now and retest in one month.

Q3. You are seeing a healthy, African American 15-month-old boy for a well child visit. His capillary blood anemia screen at age 12 months was 10.9 g/dL. The results from his venous blood tests today are: Hgb 10.8 g/dL, MCV 68.0 fL, RDW 12.5%, ferritin 45 ?g/L. What is the most likely cause of this child's anemia?

A. Iron deficiency anemia

B. a-thalassemia trait

C. Recent infection

D. B12 deficiency

E. None of the above

Q4. If you practice selective screening, which of the following children would you NOT screen for iron deficiency anemia?

A. 16 year old Tanner 4 male

B. 15 year old Tanner 5 female

C. 12 year old Tanner 4 female athlete

D. 2 year old boy who eats a vegetarian diet

E. 2 year old who consumes 36 ounces of milk per day

Q5. Dietary factors known to impair non-heme iron absorption from the gut include all the following except:

A. Tea

B. Milk

C. Bran

D. Ascorbic acid

E. Calcium

Objectives

At the conclusion of this section, residents will able to:

1. Identify risk factors for iron deficiency.

2. Recognize the physical and psychological consequences of iron deficiency.

3. State the screening and confirmatory tests used to diagnose iron deficiency and iron deficiency anemia and the limitations of each test.

4. Differentiate the laboratory findings in iron deficiency from thalassemia, anemia due to recent infection or chronic disease and lead poisoning.

5. Develop screening and treatment strategies for iron deficiency and iron deficiency anemia.

Facilitator Preparation

For this section, the facilitator should review:

Bogen DL, Duggan AK, Dover GJ, Wilson WH. Screening for iron deficiency anemia by dietary history in a high-risk population. Pediatrics. 2000 Jun;105(6):1254-9

Lozoff B, et al. Behavioral and developmental effects of preventing iron-deficiency in health full term infants. Pediatrics 2003;112:846-54

Lozoff B, Corapci F, Byrden, MJ et al. Preschool-aged children with iron deficiency anemia show altered affect and behavior. J Nutrition 2007 Mar;137(3):683-9

Pediatric Nutrition Handbook, 5th edition. Robert Kleinman, MD editor. Committee on Nutrition, American Academy of Pediatrics, Elk Grove, IL, 2004, pp 299-312.

Recommendations to Prevent and Control Iron Deficiency in the United States: MMWR, April 3, 1998, Vol 47, No. RR -3.

Case Study (part 1)

You are seeing Kim, a 12-month-old African American girl for well child care. She is new to your practice. As part of your routine 1-year visit, you assess risk factors for iron deficiency.

Q1. Can you identify two factors held in common that might place infants, toddlers, adolescent women and pregnant women at high risk for iron deficiency?

The 2 factors in common among infants, toddlers, adolescent women and pregnant women that place that at increased risk for iron deficiency are 1. rapid growth and 2. poor dietary intake. One must also consider the importance of 3. iron storage

Rapid Growth: There is an increased need for dietary iron during times of rapid growth, including infancy, adolescence and pregnancy. Healthy infants should double their birth weight by 4 months, triple by a year and quadruple by 2 years. Some infants have the need for even faster growth than normal and are born with low iron stores - including infants that were born preterm, were growth retarded or born to diabetic mothers. Iron is transferred across the placenta in the last trimester of pregnancy and is proportional to body weight. Adolescent women also have rapid growth at the same time they begin to have monthly blood loss from menstruation. Pregnant women undergo rapid growth and increase their blood volume by one third.

Dietary Intake and Use: The groups that are growing rapidly are the same groups that often have poor dietary intake - toddlers and adolescent women. In general, turnover and loss of iron is mostly from the formation and destruction of red blood cells (RBCs). In adult men, 95% of all iron for RBC production is from recycled iron and 5% is from the diet. In babies only 70% of all iron comes from recycled sources and 30% must come from the diet. Pregnant women are like infants in this respect - more of their iron needs come from dietary sources. Adult men absorb about 1 mg iron per day in order to replace losses from desquamation. Infants ages 4-12 months absorb about 0.8 mg iron per day - but about ¾ of this is needed for growth and ¼ replaces losses.

Iron storage: Iron storage is also important. Men store about 1-1.4 g of iron, women 0.2-0.4 g and children even less. Full-term healthy babies are born with about 75 mg/kg of iron. This is usually adequate to meet the needs of full-term infants until 4 to 6 months. Preterm and low birth weight babies have the same ratio of total body iron to weight, but because they start at a lower weight, they have less total iron. They also grow faster than full term infants to achieve "catch-up" growth. Their iron stores may be used by 2 to 3 months.

Iron storage affects absorption.

Caption: Iron absorption is high when the endothelial cells of the GI tract are ferritin deficient and the transport system (Iron/TIBC) is unsaturated. This enhancing effect does not work well for vegetable sources of iron. These tend to be in the trivalent ferric form.

Derived by Lozoff and Karp from Moore. See Lozoff and Karp, 1993)

Q2. Can you give 3 questions for taking a diet history that would assess Kim's dietary risk for iron deficiency. Explain how your question relates to iron status. Can dietary screening used as a screening test for iron deficiency?

This is an opportunity for a paired role play where residents take one role or the other - parent/provider.

A2. An easy format for taking a diet history in an infant follows (from Part II Section 1; cross link):

1. How many bottles (cups) of formula (milk) does (name of child) drink each day? (If the child is being breastfeeding, it is not necessary for her to quantify the amount, but you can ask about supplementation. What is the size of the bottle (cup)? What kind of milk (iron fortified formula, low iron formula, whole or reduced fat cow milk) does your child drink.

2. How many bottles (cups) of juice?

3. Does your child have a mixed diet with meat, dairy, vegetables, fruit and cereal

4. Are there foods your family or child does not eat?

5. Does your child have soda, chips, cookies or candy? How often?

6. Does your child take any vitamins or nutritional supplements? What kind and how often?

7. Do you worry that you might not be able to feed Kim nutritious foods because they cost too much?

8. Because you are taking a diet history looking for iron deficiency, you want to carefully ask about what Kim drank for her main source of calories during her first year of life?

TEACHING CAPTION: The kind of milk, how much, and other foods are important.

If the infant is drinking cow milk, you want to know when she started it. Introduction of cow milk before 12 months is associated with microscopic blood loss in the stool and therefore a greater risk of iron deficiency.

More than 24 ounces of milk per day is not recommended for a number of reasons. Milk is not a good source of iron. Whole milk is high in calories and therefore very filling.
8 ounces of whole milk has 160 kcal and 2% has 115 kcal. Children who drink a large volume of milk may not eat other foods because they get full from the milk.

Her current diet is also important.

You want to assess her dietary sources of iron - meat, vegetables or both?

Iron comes in two sources. Heme iron is found in meat, poultry and fish and is well absorbed. Non-heme iron is derived from plant-based foods and iron fortifiers and is not well absorbed from the gut.

Iron metabolism is affected by iron store, iron intake and factors affecting absorption and iron losses.

Iron stores are discussed above in Q1.

Dietary histories are essential when anemia has been identified, and certainly, a dairy and junk food replete diet increases risk for ID. Screening tools, however, should be highly sensitive - e.g., no false negatives. Diet screening fails that test. Some infants with reasonable diets still become iron deficient. See Geltman, et al.

Q3. How is iron absorbed?

A3. Iron intake and absorption are regulated in the GI tract by a number of factors. The gut absorption of iron increases when body iron stores are low and when red blood cell production is increased. Absorption decreases when iron stores are high. The amount and kind of iron in the diet also impacts absorption. The amount of iron absorbed in the gut ranges from <1% to as high as 50%, with plant based foods and iron fortifiers (non-heme iron) at the lowest end of the range, dairy products in the middle and meat, poultry and fish (heme iron) and breast milk at the high end.

About 50% of iron is absorbed from breast milk, 4% from fortified formula, and 10% from cow milk and unfortified formula.

The iron content of human breast milk is similar to cow milk, but due to a variety of complementary components in breast milk, such as lactoferrin, up to 50% of iron in breast milk is absorbed. Iron absorption is increased in the presence of enhancers in the diet, such as ascorbic acid. It decreases in the presence of inhibitors in the diet, such as some vegetables, tea, bran and calcium. Calcium is now added to many brands of orange juice - so this may not be a good juice to drink at the same time you are taking iron.

TEACHING CAPTION: From this data it is clear why children given unfortified formulae or cow milk develop iron deficiency. Iron content and absorbed iron are inconsistent. From MMWR, April 3, 1998; Vol 47, No. RR-3.

* Iron losses can be normal, such as from turnover of intestinal mucosa, desquamation of the skin and menstruation.

Q4. Can you pose at least 1 question related to each of the following, family history, past medical history or current history that might help you interpret laboratory results from iron deficiency screening?

This time you can have the residents provide one question for one area on a slip of paper and send it up front without identifiers.

A4. Family History: Family history can be important when trying to assess a child for anemia. You could ask about a family history of anemia or blood problems. The most common abnormalities that result in anemia are thalassemia traits. However, most people with thalassemia traits will not know that is what they have. They will report that they have been anemic their whole life. However, many states now include a screen for hemoglobinopathies in the newborn screen. If that is true in your state, you should be able to identify children with thalassemia trait in infancy and use that information to interpret laboratory evaluation for iron deficiency. The thalassemias are more common among people of Mediterranean and African decent.

Less common familial disorders that are associated with anemia are spherocytosis or eliptocytosis. Sickle cell anemias are also associated with anemia. Sickle cell trait in general is not associated with anemia but there was one study that indicated that children with sickle cell trait have slightly lower hemoglobin values compared to others. G6PD deficiency is extremely common and is associated with intermittent anemia. This is detected in some states on the newborn screen.

Past Medical History: Past medical history is important to assess. 1) Chronic and inflammatory illnesses are associated with normocytic anemia. Children with recurrent otitis media, juvenile rheumatoid arthritis, or other chronic illnesses for example may have low hemoglobin with a normal mean corpuscular volume (MCV). 2) Premature infants may be at increased risk of anemia at 12 months of age compared to full term infants because children are born with iron stores that are proportionate to their birth weight.

History of the Present Illness: It is important to assess recent and current infection prior to screening for anemia. Even mild infection can cause a fall in hemoglobin which can make it hard to interpret the results of screening. It may be better to obtain a CBC rather than hemoglobin alone if you decide to screen at the time of the mild illness. Because ferritin is an acute phase reactant, it can be falsely elevated in the face of infection (see Q12).

The Case study continued (part 2)

HPI: Kim has had a runny nose, congestion and cough for the past 4 days without fever.

Diet: She was exclusively breastfed until 3 months of age when her mother returned to work. From 3 to 11 months, Kim received a combination of breast milk and unfortified cow milk based formulae. Starting at age 12 months, she continued to breastfeed twice a day and drink soy milk from a cup. Her current diet includes table food that she mostly feeds herself, 16 oz of soy milk and 4 oz of juice per day. Her parents are vegetarians and have not offered Kim any meat. Her main protein sources are soy and beans. She drinks about 8 ounces of fruit juice each day.

Social: She attends full time daycare because both her parents work full time outside the home. Her mother has received WIC benefits for Kim since birth

PMH: She was born at 36+ weeks weighing 2680 g. She has had 2 ear infections with colds in the past 4 months. She has not been on any supplemental vitamins or iron.

FH: Kim's mother says that she is not aware of any family history of anemia except that she was anemic when she was pregnant with Kim. There is a family history of sickle cell trait but Kim's newborn screen was normal.

Q5. How do you interpret Kim's current, dietary, past medical and family histories with respect to risk for iron deficiency?

A5.

Current: Kim has a mild illness. Acute and chronic infections are both associated with a fall in hemoglobin (with a normal MCV). Therefore, Kim's current cold symptoms and recent ear infections may make Kim appear mildly anemic if just Hgb or Hct are obtained.

Diet: Kim has one major risk factor for iron deficiency - all iron sources are non-heme. However, she is still drinking some breast milk and drank iron-fortified formula until she was age 1 year.

The following can lead to inadequate iron intake in infants.

Low iron formula
Early introduction (before age 1 year) of cow milk into the diet.
Exclusive breastfeeding past 6 months without an additional source of iron - such as meat, iron fortified cereal or iron supplementation. Although iron is better absorbed from breast milk than cow milk, there is not enough iron in breast milk after age 6 months.
More than 24 ounces of milk per day is not recommended for a number of reasons.

1. Milk is not a good source of iron.

2. Whole milk is high in calories and therefore very filling. 8 ounces of whole milk has 160 kcal and 2% has 115 kcal.

3. Children who drink a large volume of milk may not eat other foods because they get full from the milk.

Past: Kim was born mildly preterm but at a normal birth weight for gestational age.

Most iron is transferred to the infant in-utero during the 3rd trimester of pregnancy. The amount is proportional to the infant's weight. Preterm and low birth weight babies start off with lower iron stores and must grow faster to achieve "catch-up" growth. Their iron stores may be used by 2 to 3 months. Thus Kim is at an additional risk.

See the CDC Recommendations which advise iron supplementation (2-4 mg/kg/day; max 15 mg/day) from age 1-12 months and screening at 9-12 months for former preterm or low-birth weight infants. The Nutrition Handbook Book also gives recommendations for supplementing premature infants.

Family History: The relationship between maternal iron status during pregnancy and child stores is not well studied - and may be an added risk factor for iron deficiency in Kim. The FH of sickle trait does not increase her risk for iron deficiency, although in at least one study, sickle cell trait was associated with a higher rate of mild anemia.

Q6. When in your clinic/practice should children be screened for iron deficiency or iron deficiency anemia and what screening tests are used? Should there be different normative hemoglobin values by race?

A6. Routine screening likely varies by practice type and location.

Practices that serve a low-income, high risk population should follow the CDC recommendations for routine screening.
In our high risk clinic, we routinely screen at 12 and 24 months at a minimum with a CBC because we would like to detect iron deficiency with and without anemia. We obtain a lead at the same time (see lead section).
If either the 12 or 24 month test is abnormal but not likely iron deficiency based on the MCV and RDW - we follow-up with a repeat test - timing may vary.
If a child had iron deficiency at 1 or 2, it is important to continue to screen them yearly until age 4 or 5 years.
Many of our patients are enrolled in WIC - which requires screening annually from 12 months through age 4 years.
Ancestry does affect likelihood of iron deficiency being a cause for reduced hemoglobin. People whose origins are from malarial belts will have a distribution pattern of red cell indices that is lower (perhaps 0.5 g/dL of Hemoglobin). Nevertheless, the same rule applies here as for the first question. Do not pass on an African-American child with a hemoglobin level below 11.0 g/dL on the basis of "race."

The Case study continued (part 3)

You decide that you will screen Kim for iron deficiency at today's visit, despite her current cold symptoms for at least 2 reasons. She is due for her WIC screening and she was premature and did not receive iron supplementation during infancy.

Q7. What screening tests are available to you and what are the pros and cons of each?

A7.

Hemoglobin or hematocrit:

Pros: Hemoglobin (Hgb) is inexpensive, widely available and reproducible and can be done in the office using a HemoCue machine. However, improper technique (squeezing the finger and taking the first drop of blood) can lead to falsely low test results. Hematocrit (Hct) is no longer done at the bedside in most places due to changes in laboratory regulation. However - it is a routine part of the results from the Coulter counter and is inexpensive and reproducible.
Cons: It can only detect late stage of iron deficiency not iron deficiency without anemia

Complete blood count (CBC):

Pros: inexpensive, widely available, reproducible; Includes Hgb/Hct plus MCV and RDW
Cons: can't do in office unless you have an approved lab

MCV (mean corpuscular volume):

is the average volume of the RBC.
Iron deficiency is one cause of microcytic anemia.
MCV is highest at birth, declines until about 6 months then rises again until adulthood so must use age adjusted norms. (see Table of Normal Laboratory Values - end of case)
MCV falls before frank anemia develops so can detect earlier stage of iron deficiency

RDW (red cell distribution width):

measures the variability in RBC volume. If the RBCs are homogeneous, like in thalassemia minor or trait, the RDW will be normal.
If the red cell volume is variable, such as in iron deficiency, the RDW will be elevated
An elevated RDW with a normal MCV is not likely to represent iron deficiency and similarly, a low MCV with a normal RDW is not likely to represent iron deficiency.
However, only a very high RDW (>17) is diagnostic of iron deficiency. An RDW in the 14-16 range is consistent with iron deficiency but not diagnostic (non-specific).

Zinc Protoporphyrin:

Pros: inexpensive, rapid
Cons: no longer widely used, non-specific

Q8. What confirmatory tests are available to evaluate iron status and what are the pros and cons of each?

A8.

Serum ferritin is a measure of circulating iron.

Under normal conditions, there is a direct relationship between serum ferritin and iron stores, where ~ 1 ?g/dL ferritin correlates with 10 mg of stored iron.
Low serum ferritin serves as an early indicator of low iron stores
Serum ferritin is an acute phase reactant and can be falsely elevated in the presence of acute or chronic illness. Cost is about $50.

Erythrocyte protoporphyrin (EP) is the precursor of hemoglobin.

EP accumulates when there is not enough iron available to form hemoglobin.
Infection, inflammation and lead poisoning can also increase EP.
EP is an earlier indicator of impaired erythropoiesis than anemia but not as early as ferritin. Cost is about $10.

Transferrin saturation measures the available iron binding sites. It is calculated from 2 other laboratory measures, serum iron concentration and total iron binding capacity (TIBC).

Transferrin sat (%) = [serum iron](?g/dL)/TIBC(?g/dL) x 100
Transferring sat has a lot of variability due to its component parts. Serum iron concentration is quite variable. It increases after meals, decreases with inflammation, and has a natural diurnal variation. TIBC is also affected by a variety of factors.
Transferrin saturation becomes abnormal only after iron stores are depleted.

Q9. Is there a "gold standard" for measuring iron status?

A9.

No, there is not one single gold standard diagnostic test for iron deficiency.

A 1 g/dL increase in Hgb after one month of daily iron therapy is considered diagnostic
In order to accurately diagnose iron deficiency, it is best to use a combination of tests because each test assesses a different aspect of iron metabolism.
The Third National Health and Nutrition Examination Survey (NHANES III) defined iron deficiency by at least 2 abnormal tests of iron status (MCV, RDW, ferritin, erythrocyte protoporphyrin, and transferrin saturation). Iron deficiency anemia was defined as iron deficiency plus anemia by hemoglobin.
There often isn't complete consistency among the results of the tests of iron status.
Nutrient stores are depleted before the biochemical markers change or there are clinical findings.:

Table 5. From the Pediatric Nutrition Handbook, 5th edition, page 304, summarizes the spectrum of iron status in relations to the major tests available.

Q10. How would a newborn screen of Bart's hemoglobin impact your screening?

A10. Bart's hemoglobin on newborn screen is an indication of ?-thalassemia trait. Bart's hemoglobin is only present in the newborn period.

After that, a diagnosis of ?-thalassemia trait must be made by excluding all other causes of anemia. If you know that a child had FA (fetal and adult hemoglobin) and Bart's hemoglobin on the newborn screen, you should expect the hemoglobin to be mildly low to normal, the MCV to also be low but the RDW should be normal. However, a child can have both thalassemia trait and iron deficiency!

The Case study continues (part 4)

Because Kim has some risk factors for iron deficiency (WIC participant, slightly premature, vegetarian) and she currently has a cold, you obtain a complete blood count rather than just hemoglobin. You also obtain a venous lead sample. The results of the laboratory tests are:

WBC 7.0 (1000/mm3)

Hgb 10.4 g/dL

Hct 32.2 %

MCV 68.0 fl

RDW 15.7 %

Platelets 390 1000/mm3

Lead 6 ug/dL

Q11. What is your assessment of these laboratory findings?

A11.

These results are consistent with iron deficiency anemia but not diagnostic
Wide RDW is suggestive of iron deficiency (but not high enough to be very specific.) Recall that RDW>17 is diagnostic.
MCV is borderline low for age.
Although black children on average have lower Hgb values than white children, there is no good explanation. The CDC and IOM still recommend that the same normative values be used for all children regardless of race.

Q12. What is the differential diagnosis?

A12.

TEACHING CAPTION: Remember Screen for the most dangerous first and evaluate for most common second.

Q13. What is your treatment plan and justify it?

A13. Recommended plan: Treat her with oral iron therapy for 1 month because of the negative consequences of untreated iron deficiency. Have her return in 1 month for repeat testing.

Kim's mother tells you that she is concerned that her daughter will become constipated..

Q14. Will treatment with 3 to 4 mg/kg of elemental iron cause GI symptoms. Is there an association between iron fortification levels in formula and constipation?

A14. Three to four mg/kg is suggested to limit GI symptoms. As for iron fortified formulas, double blind studies have shown no impact of iron fortification whatsoever.

Q15. What are the short and long-term consequences of iron deficiency (ID) and iron deficiency anemia (IDA) in early childhood and adolescence?

A15. Iron deficiency anemia and iron deficiency without anemia can have detrimental effects on the developing brain of infants and toddlers, including lower scores on tests of infant development and later IQ.

Neurological effects of ID and IDA may not be reversible even with early therapy (see articles by Betsy Lozoff if interested).

Anemia is a late manifestation of iron deficiency. The non-hematologic effects of iron deficiency anemia include many body systems:

Impaired growth

Skin and mucous membranes changes include koilonychias, angular stomatitis, and glossitis

Gastrointestinal tract changes include: anorexia, dysphagia with postcricoid webs, gastric achlorhydria, malabsorption, beeturia, exudative enteropathy, occult bleeding

Central nervous system changes include irritability, decreased attention span, and poor performance in standardized developmental testing, breath-holding spells, impaired exercise tolerance and maximal work capacity

Immunologic response include impaired lymphocyte mitogen response, decreased leukocyte killing

Among teens, iron deficiency without anemia is associated with decreased exercise tolerance, shorter attention span and lower scores on verbal learning and memory, aerobic adaptation and muscle fatigability.

Q16. Iron comes in a variety of formulations. Calculate the proper dose of iron for Kim using the 3 available concentrations of iron (ferrous sulfate). Kim weighs 11 kg.

A16.

Children should be prescribed 3 to 4 mg/kg/day of elemental iron. Once a day dosing works well and improves adherence.

(11 kg) x (3 or 4 mg/kg) = 33 to 44 mg Fe/day (can prescribe 45 mg Fe/day)

Using Ferrous Sulfate drops (15 mg Fe/0.6 ml dropper) - write as 1.8 ml/day or 3 droppers/day
Using Ferrous Sulfate syrup (18 mg Fe/5 ml) - write as 10 ml/day or 2 tsp per day
Using Ferrous Sulfate elixir (44 mg Fe/5 ml) - can write as 5 ml/day or 1 tsp per day

Q17. What instructions should you give when you prescribe iron therapy?

A17.

Give mid day with a meal containing fruit or juice but no dairy product.. That is with a source of a Vitamin C and not with calcium, tea, milk or bran. Be culturally aware.

Iron absorption decreases in the presence of inhibitors in the diet, such as some vegetables, tea, bran and calcium. Calcium is now added to many brands of orange juice - so this may not be a good juice to drink when taking iron. Iron is better tolerated when it is taken with a meal.

Liquid iron preparations may stain the teeth (not permanently) so you can suggest it be taken through a straw or with a dropper.

Iron in these doses can cause constipation and make the stools darker.

Iron overdose can be fatal. Therefore, it should be dispensed with a child proof cap. This danger should be discussed with parents so they keep it locked and out of the reach of children.

WARNING: Remind parents that iron is a toxic substance. All iron drops or pills must be in safety bottles to reduce risk for iron toxicity.

Q18. What is the relationship between lead poisoning and iron deficiency?

A18.

[see lead poisoning and nutrition module for a comprehensive overview]

Lead and iron have the same valence (charge) and compete for the same gut transport system.
Therefore, when a child is iron deficient and the body is working hard to absorb iron, any lead in the gut will be readily absorbed.
Similarly, if a child has severe lead poisoning, iron deficiency can develop because the quantity of lead overwhelms the transport system and iron absorption is not adequate.
The same children (low-income and minority) at high risk for lead poisoning are also the ones at high risk of iron deficiency.
Thus, when lead poisoning is detected, it is imperative that the child be evaluated for iron status and treated aggressively for iron deficiency to minimize lead absorption.

The Case study continues (part 5)

Kim returns for follow-up 4 weeks later as you had recommended. Her mother reports that she gave Kim the iron at least 5 times per week. Furthermore, she tells you that Kim's stools were much darker and firmer since starting the iron therapy, just as you had warned her. She has been healthy without any cold symptoms since she last saw you. You obtain the following laboratory results:

WBC 7.0 (1000/mm3)

Hemoglobin 11.4 g/dL

Hematocrit 33.5 %

MCV 73.0 fL

RDW 15.0 %

Platelets 390 (1000/mm3)

Ferritin 20 micrograms /dL

Q19. How do you interpret Kim's current laboratory results?

A19.

Hgb is now in the normal range for age. There was a 1.0 g/dL increase in Hgb which is considered diagnostic for iron deficiency.
Kim's ferritin level is in the low normal range. This is likely due to her 4 weeks of iron therapy.

Q20. What is your treatment and follow-up plan for Kim?

A20.

Recommend that she continue the therapeutic dose of iron for another 2- 3 months in order to replete her stores of iron.
Given her vegetarian status, it would be reasonable to suggest that she receive a multivitamin with iron on a regular basis after she ends her therapeutic iron.
Screen again at age 2 for lead and CBC (This is needed for EPSDT and WIC)

REFERENCES

Bogen DL, Duggan AK, Dover GJ, Wilson WH. Screening for iron deficiency anemia by dietary history in a high-risk population. Pediatrics. 2000 Jun;105(6):1254-9

Boutry M, Needlman R. Use of diet history in the screening of iron deficiency. Pediatrics. 1996 Dec;98(6 Pt 1):1138-42

Geltman PL, Meyers AF, Mehta SD, et al. Daily multivitamins with iron to prevent anemia in high-risk infants: a randomized clinical trial. Pediatrics. 2004 Jul;114(1):86-93.

Looker AC, Dallman PR, Carroll MD, Gunter EW, Johnson CL. Prevalence of iron deficiency in the United States. JAMA. 1997;277:973-976.

Lozoff B, Karp R. (1993) Iron Deficiency among disadvantaged children

(in) Karp RJ (ed) Malnourished Children in the United States: Caught in the Cycle of Poverty. Springer Publishing Co of New York.pp81-90

Lozoff B, et al. Behavioral and developmental effects of preventing iron-deficiency in health full term infants. Pediatrics 2003;112:846-54

Lozoff B, Corapci F, Byrden, MJ et al. Preschool-aged children with iron deficiency anemia show altered affect and behavior. J Nutrition 2007 Mar;137(3):683-9

Oski FA, Naiman JL. (1983) Hematologic Problems in the Newborn, 3rd edition. WP Saunders. Philadelphia.

Pediatric Nutrition Handbook, 5th edition. Robert Kleinman, MD editor. Committee on Nutrition, American Academy of Pediatrics, Elk Grove, IL, 2004, pp 299-312.

Recommendations to Prevent and Control Iron Deficiency in the United States: MMWR, April 3, 1998, Vol 47, No. RR -3.

Serwint JR, Damokosh AI, Berger OG, et al. No difference in iron status between children with low and moderate lead exposure. J Pediatr. 1999;135:108-110.

Annotated Answers:

A1. the answer is B; Of the possibilities listed, only "low-iron" formulae is associated with an increased incidence of iron deficiency. The other choices are sufficiently close to "normal" in clinical experience of pathology. Formulae company representatives tell us that they jeep this unacceptable formulation available at the request of "older" physicians and pediatricians. It is our hope that this demand be eliminated.

A2. the answer is D; You have sufficient evidence to provide therapy. The child is depleted of iron (low ferritin level), has red cell changes associated with iron deficiency (decreased MCV and increased RDW), and actual anemia (HGB level is below standard). Note that the treatment with iron of 3 to 4 mg/kg/day is a bit lower than suggested elsewhere. Iron depleted children absorb ferrous sulfate at an increased rate. Less iron intake is effective with fewer side effects. Giving the 6mg/kg often recommended may result in poor adherence.

A3. The answer is B; These are the classic measurements found in a-thalassemia trait. Unlike the child in the prior scenario, this child has normal RDW and the storage level of iron (ferritin) is quite good. Of course, a-thalassemia trait may be found in association with the other disorders, but a careful history, physical exam and use of appropriate lab tests will show this association.

A4. The answer is A; Nutritional iron deficiency is an unlikely occurrence in boys once they enter adolescence. The energy intake is quite high, and even a marginal diet - one likely to produce iron deficiency in the other children listed - will not be associated with anemia. If anemia is found in males past adolescence, one must always think of intestinal bleeding and evaluate for a bleeding polyp or actual tumor.

A5. The answer is D; Ascorbic acid (Vitamin C) enhances iron absorption by keeping iron in the ferrous state (+2) rather than allowing oxidation to the ferric state (+3). High fiber diets absorb mineral (link to fiber module). Calcium competes with iron for absorption (link to calcium) and because it is consumes at a ration of 100:1 with respect to iron, dairy products should be avoided when consuming iron containing ones or when on iron therapy. Phytic acid in teas is also an inhibitor of iron absorption.