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Iron Deficiency Anaemia

Iron Deficiency Anaemia

NORMAL FERRITIN LEVELS  (NB. Normal values may vary from lab to lab.  and ng/mL = mcg/L)

NB "Normal" does not equal "Optimal"


18-270 nanograms per milliliter (ng/mL) or 18-270micrograms per liter (mcg/L)


18-160 ng/mL or 18-160 mcg/L

Children 6 months to 15 years:

7-142 ng/mL or 7-142 mcg/L

Babies 2 to 5 months:

50-200 ng/mL or 50-200 mcg/L

Babies 1 month:

200-600 ng/mL or 200-600 mcg/L

Newborn babies:

25-200 ng/mL or 25-200 mcg/L

Disease Iron TIBC/Transferrin UIBC



Iron Deficiency Low High High Low Low
Hemochromatosis High Low Low High High
Chronic Illness Low Low Low/Normal Low Normal/High
Hemolytic Anemia High Normal/Low Low/Normal High High
Sideroblastic Anemia Normal/High Normal/Low Low/Normal High High
Iron Poisoning High Normal Low High Normal

Iron Deficiency Anemia in Toddlers.  (CLICK on the diagram below to view it)

Low iron and ferritin are associated with:

"Does timing of iron deficiency matter?
"The previously mentioned studies in human infants of nerve conduction provide some evidence that the effects of iron deficiency on biological neural functioning are irreversible (5, 12). The issue of timing of iron deficiency, therefore, is of great importance. These biological measurements are the first data that directly support the contention that human toddlers with iron deficiency anemia suffer developmental delays due to biological abnormalities. Given the fact that nearly all of the published clinical intervention trials in human infants also fail to show a complete normalization in functioning despite a normalization of iron status, investigators are forced to consider the question of "critical periods" of development that absolutely require adequate iron nutriture for "normal" development. A number of animal studies have been conducted in an attempt to mimic and model the human condition and the timing of nutrient deficiency to coincide with the timing of peak risk of human infant iron deficiency (28). As autopsy data of human infants suffering solely from iron deficiency is nonexistent, we have relied on animal models and imaging methods to argue for the existence of "a critical period". Although the course of development in the rat is more compressed than in humans, in both species there is the same sequence of cell migration, significant myelination, cellular differentiation, and increased expression of neuropeptides. What appears to occur from 3–16 mo postnatal in humans occurs from 7–25 d postnatal in rats (28). Iron deficiency during lactation in the rat results in significant loss of regional brain iron that is distinct from those regions that lose iron with dietary restrictions later in life (22) (Fig. 4). Importantly, the restoration of brain iron with later aggressive dietary iron repletion also resulted in incomplete restoration of abnormalities in dopamine (DA) metabolism and in behaviors related to DA (22, 29, 30); i.e. , the sensitivity of a brain region to loss of iron during development is likely to be related to the regional development requirements for iron during that period. In contrast to the perception that brain iron is "resistant" to iron depletion, these experiments demonstrate quite clearly that in the rodent, dietary treatments can decrease brain iron within 10 d and replete iron within 14 d. Comparative data in human infants or primate models are lacking, thus there remains uncertainty regarding the completeness of brain iron recovery in humans despite full restoration of hematological indices of iron status (5, 12)."

J Pediatr Gastroenterol Nutr. 2009 Mar;48 Suppl 1:S8-15.

Sleep and neurofunctions throughout child development: lasting effects of early iron deficiency.

Peirano PD, Algarín CR, Chamorro R, Reyes S, Garrido MI, Duran S, Lozoff B.

Sleep and Functional Neurobiology Laboratory, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.

Iron-deficiency anemia (IDA) continues to be the most common single nutrient deficiency in the world. Infants are at particular risk due to rapid growth and limited dietary sources of iron. An estimated 20% to 25% of the world's infants have IDA, with at least as many having iron deficiency without anemia. High prevalence is found primarily in developing countries, but also among poor, minority, and immigrant groups in developed ones. Infants with IDA test lower in mental and motor development assessments and show affective differences. After iron therapy, follow-up studies point to long-lasting differences in several domains. Neurofunctional studies showed slower neural transmission in the auditory system despite 1 year of iron therapy in IDA infants; they still had slower transmission in both the auditory and visual systems at preschool age. Different motor activity patterning in all sleep-waking states and several differences in sleep states organization were reported. Persistent sleep and neurofunctional effects could contribute to reduced potential for optimal behavioral and cognitive outcomes in children with a history of IDA.

  • Body Growth
  • Infant Development

"Iron deficiency anemia for infants in their earlier stages of development may have significantly greater consequences than it does for adults. An animal made severely iron deficient during its earlier life cannot recover to normal iron levels even with iron therapy. In contrast, iron deficiency during later stages of development can be compensated with sufficient iron supplements. Iron deficiency anemia affects neurological development by decreasing learning ability, altering motor functions, and permanently reducing the number of dopamine receptors and serotonin levels. Iron deficiency during development can lead to reduced myelination of the spinal cord, as well as a change in myelin composition. Additionally, iron deficiency anemia has a negative effect on physical growth. Growth hormone secretion is related to serum transferrin levels, suggesting a positive correlation between iron-transferrin levels and an increase in height and weight."

  • Psychomotor Development

Cochrane Database Syst Rev. 2001;(2):CD001444.

Iron therapy for improving psychomotor development and cognitive function in children under the age of three with iron deficiency anaemia.

Logan S, Martins S, Gilbert R.

Systematic Reviews Training Unit, Institute of Child Health, 30 Guilford Street, London, UK, WC1N 1EH.

Comment in:

  • Breath Holding Episodes
  • Int J Psychiatry Med. 2008;38(2):195-201.

    Piracetam in severe breath holding spells.

    Azam M, Bhatti N, Shahab N.

    The Children's Hospital, Pakistan Institute of Medical Sciences, Islamabad.

    BACKGROUND: Breath holding spells (BHS) are apparently frightening events occurring in otherwise healthy children. Generally, no medical treatment is recommended and parental reassurance is believed to be enough, however, severe BHS can be very stressful for the parents and a pharmacological agent may be desired in some of these children. OBJECTIVE: In this prospective study aim was to determine the usefulness of piracetam as prophylactic treatment for severe BHS. METHODS: Children were recruited from Neurology Clinic in Children's Hospital, Islamabad between January 2002 to December 2004. Diagnosis of BHS was based on characteristic history and normal physical examination. Piracetam was prescribed to those children who were diagnosed as severe BHS in a dose ranging from 50-100 mg/kg/day. Iron supplements were added if hemoglobin was less than 10 gm%. Patients were seen at 2-4 weeks interval and follow-up was continued until 3 months after the cessation of drug therapy. RESULTS: Fifty-two children were enrolled in the study, 34 boys and 18 girls. Ages ranged from 4 weeks to 5 years with mean age of 17 months. In 81% of children, spells disappeared completely and in 9% frequency was reduced to less than one per month and of much lesser intensity. Prophylaxis was given for 3-6 months (mean 5) duration. CONCLUSIONS: Piracetam is an effective prophylactic treatment for severe BHS.

  • Arch Dis Child. 1999 Sep;81(3):261-2.

    Breath holding spells in 91 children and response to treatment with iron.

    Mocan H, Yildiran A, Orhan F, Erduran E.

    Department of Pediatrics, Faculty of Medicine, Karadeniz (Black Sea) Technical University, Trabzon, Turkey.

    To evaluate the prognosis of breath holding spells (BHS) after iron treatment, 91 children (56 boys, 35 girls) aged between 6 months and 40 months (median, 17) were followed prospectively for a median of 45 months (range, 6-89). In 49 of the children, the frequency of BHS was less than 10 each month, in 22 it was 10-30 each month, and in 20 more than 30 each month. The spells were cyanotic in 60 children. All patients were evaluated initially and during follow up for haematological indices. Electroencephalographic and electrocardiographic abnormalities were also recorded. Sixty three patients were found to have iron deficiency anaemia and were treated with iron (6 mg/kg/day) for three months. Other patients were not given any treatment. After three months, there was a significant difference for correction of cyanotic spells between children who had been treated with iron and those who had not (84.1% v 21.4%). During further follow up, febrile convulsions occurred in 10 children (six were on iron treatment initially). It appears that treating iron deficiency anaemia is effective in reducing the frequency of BHS.

Getting Iron in Your Diet


Iron Chelators
An iron chelator is a substance which binds iron and then eliminates it from the body in the urine and stool.  If the diet includes too many chelators it can produce an iron deficiency.  Of concern for children with Down Syndrome is the fact that Curcumin is an iron chelator as is Ginkgo Biloba.  This raises the concern that children that are being supplemented with these substances might develop an iron deficiency anaemia.  This is of particular concern if the child already has marginal iron stores. 

Iron, really has some affect on thyroid function, although selenium has much more to do with thyroid function. Iron deficiency anemia can cause hypothyroidism and iron and ferritin levels probably need to be monitored in those taking high dose curcumin or Ginkgo. The action of curcumin seems to be a positive excess iron scavenger in the brain and does not seem to have a general negative effect on the body. Ginkgo also does not seem to be a total body iron scavenger and appears to primarily work in the brain. With both of these supplements or herbal products, there may be a dose dependent process going on though none of the studies I have read document what dosage may produce negative iron results. This could be problematic in the long run for using either of them in DS if we then produce iron deficiency anemia. That being said, my experience to date has not documented any significant iron deficiency anemia in any of my patients taking Ginkgo at 5.5mg per kg per day or those using 2000-mg of curcumin and I do look for iron deficiency if anemia occurs.

Dr Lawrence Leichtman


Ginkgo Biloba

Ongoing Research

Priya S. Kishnani, MD
Duke Unversity Medical Center
Associate Professor in Pediatrics and Genetics

Title of  Project:

A pilot study screening for prevalence of iron deficiency in children with Down syndrome

Summary Of Project:

Down Syndrome (DS) is the most common genetic cause of mild to moderate mental retardation. With improved medical care, the average lifespan of individuals with DS is currently >50 years.  Current health supervision guidelines recommend the same well child care as outlined for the general pediatric population as well as preventative health care specific for people with DS.  At the current time testing for iron deficiency /iron deficiency anemia (ID/IDA) in DS is based on a complete blood count (CBC) at 12 months of age, similar to that for the general pediatric population.  A diagnosis of ID or IDA could be missed if a CBC is done as these patients have an underlying macrocytosis. The macrocytosis of RBC's of children and adolescents with DS may thus obscure the diagnosis of ID/IDA. Given the important role of iron in brain development, identification of ID/IDA in the DS population is of paramount importance. The proposed study is a pilot single center, prospective study which involves a one time laboratory evaluation of 100 patients ages > 12 months followed in the Duke Down Syndrome clinic for ID or IDA. These lab indices will be used to determine prevalence of ID/IDA in DS. A CBC, reticulocyte count, serum iron, total iron binding capacity and serum ferritin, will be done on all patients. Causes for IDA such as poor nutrition, comorbidities and a stool sample for occult blood loss will be done. Patients identified with ID/IDA will be matched to controls with DS (age, gender and ethnic backgrounds). Causes for ID/IDA will be evaluated and future studies and recommendations will be planned based on results.

Lay Summary Of Project:

The Duke Down syndrome (DS) clinic was established in 1995 and has seen over 500 patients with DS.  A main purpose of the clinic is to improve the care of children with DS by providing good medical care and advancing our understanding of DS via research.  Iron deficiency (ID) and iron deficiency anemia (IDA) are conditions where a person has inadequate amounts of iron to meet body demands. IDA is a decrease in the amount/size of red cells in the blood caused by having too little iron. At the current time, testing for ID/IDA in DS is based on labs looking at the size of the red blood cells.  However, people with DS can have enlarged red blood cells, therefore, lab results may mask a diagnosis of ID/IDA. Iron is important in brain development; therefore, people with DS and ID or IDA must be identified and treated with oral supplements of iron.  The proposed study will take place at Duke and involves a one time laboratory evaluation of 100 patients with DS 12 months or older to look for ID or IDA. We will look at several blood parameters, including red blood cell measures, low serum ferritin, low serum iron levels, high iron binding capacity in blood, and blood in stool.  Lab results will be used to determine how common ID/IDA is in our DS clinic.  The patients that are diagnosed will be matched to their peers with DS and without ID/IDA to make comparisons and try to determine what factors cause these conditions, which lay the groundwork for future studies.

Paul Doney,
21 Mar 2011, 01:37
Paul Doney,
22 Jul 2010, 20:49