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Iron deficiency anemia
Classification and external resources

Red blood cells
ICD-10 D50.
ICD-9 280
DiseasesDB 6947
eMedicine med/1188
MeSH D018798

Iron deficiency anemia is a common type of anemia, and is known as sideropenic anemia. It is the most common cause of microcytic anemia.

Iron deficiency anemia occurs when the dietary intake or absorption of iron is insufficient, and hemoglobin, which contains iron, cannot be formed.[1] In the United States, 20% of all women of childbearing age have iron deficiency anemia, compared with only 2% of adult men.[citation needed] The principal cause of iron deficiency anemia in premenopausal women is blood lost during menses. Iron deficiency anemia can be caused by parasitic infections, such as hookworms. Intestinal bleeding caused by hookworms can lead to fecal blood loss and heme/iron deficiency.[2] Chronic inflammation caused by parasitic infections contributes to anemia during pregnancy in most developing countries.[3]

Iron deficiency anemia is an advanced stage of iron deficiency. When the body has sufficient iron to meet its needs (functional iron), the remainder is stored for later use in the bone marrow, liver, and spleen as part of a finely tuned system of human iron metabolism. Iron deficiency ranges from iron depletion, which yields little physiological damage, to iron deficiency anemia, which can affect the function of numerous organ systems. Iron depletion causes the amount of stored iron to be reduced, but has no effect on the functional iron. However, a person with no stored iron has no reserves to use if the body requires more iron. In essence, the amount of iron absorbed and stored by the body is not adequate for growth and development or to replace the amount lost.


Symptoms and Signs

Iron deficiency anemia is characterized by pallor (reduced amount of oxyhemoglobin in skin or mucous membrane), fatigue and weakness. Because it tends to develop slowly, adaptation occurs and the disease often goes unrecognized for some time. In severe cases, dyspnea (trouble breathing) can occur. Unusual obsessive food cravings, known as pica, may develop. Pagophagia or pica for ice is a very specific symptom and may disappear with correction of iron deficiency anemia. Hair loss and lightheadedness can also be associated with iron deficiency anemia..

Other symptoms and signs of iron deficiency anemia include:


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.


The diagnosis of iron deficiency anemia requires further investigation as to its cause. It can be a sign of other disease, such as colon cancer, which will cause the loss of blood in the stool. In adults, 60% of patients with iron deficiency anemia may have underlying gastrointestinal disorders leading to chronic blood loss. In addition to dietary insufficiency, malabsorption, chronic blood loss, diversion of iron to fetal erythropoiesis during pregnancy, intravascular hemolysis and hemoglobinuria or other forms of chronic blood loss should all be considered.


Anemia may be diagnosed from symptoms and signs, but when anemia is mild it may not be diagnosed from mild non-specific symptoms. Anemia is often first shown by routine blood tests, which generally include a complete blood count (CBC). A sufficiently low hemoglobin (HGB) or hematocrit (HCT) value is characteristic of anemia, and further studies will be undertaken to determine its cause and the exact diagnosis. One of the first abnormal values to be noted on a CBC will be a high red blood cell distribution width (RDW), reflecting a varied size distribution of red blood cells (RBCs). A low MCV, MCH or MCHC, and the appearance of the RBCs on visual examination of a peripheral blood smear will narrow the diagnosis to a microcytic anemia. The blood smear of a patient with iron deficiency shows many hypochromatic and rather small RBCs, and may also show poikilocytosis (variation in shape) and anisocytosis (variation in size). With more severe iron deficiency anemia the peripheral blood smear may show target cells, hypochromic pencil-shaped cells, and occasionally small numbers of nucleated red blood cells.[4] Microcytic anemia can also be the result of malabsorption phenomena associated with coeliac disease.

The diagnosis of iron deficiency anemia will be suggested by appropriate history (e.g., anemia in a menstruating woman), and by such diagnostic tests as a low serum ferritin, a low serum iron level, an elevated serum transferrin and a high total iron binding capacity (TIBC). Serum ferritin is the most sensitive lab test for iron deficiency anemia.

Change in lab values in iron deficiency anemia
Change Parameter
Decrease ferritin, hemoglobin, MCV
Increase TIBC, transferrin, RDW

Iron deficient anemia and thalassemia minor present with many of the same lab results. It is very important not to treat a patient with thalassemia with an iron supplement as this can lead to hemochromatosis (accumulation of iron in various organs especially liver). A hemoglobin electrophoresis would provide useful evidence in distinguishing these two conditions, along with iron studies.

Gold standard

Traditionally, a definitive diagnosis requires a demonstration of depleted body iron stores by performing a bone marrow aspiration, with the marrow stained for iron [5] [6]. Because this is invasive and painful, while a clinical trial of iron supplementation is inexpensive and non-traumatic, patients are often treated based on clinical history and serum ferritin levels without a bone marrow biopsy. Furthermore, a study published April 2009 [7] questions the value of stainable bone marrow iron following parenteral iron therapy.


If the cause is dietary iron deficiency, iron supplements, usually with iron (II) sulfate, ferrous gluconate, or iron amino acid chelate ferrous bisglycinate, synthetic chelate NaFerredetate, EDTA will usually correct the anemia.

Recent research suggests the replacement dose of iron, at least in the elderly with iron deficiency, may be as little as 15 mg per day of elemental iron. An experiment done in a group of 130 anemia patients showed a 98% increase in iron count when using an iron supplement with an average of 100 mg of iron. Women who develop iron deficiency anemia in mid-pregnancy can be effectively treated with low doses of iron (20–40 mg per day). The lower dose is effective and produces fewer gastrointestinal complaints.

Many tests have shown that iron supplementation can lead to an increase in infectious disease morbidity in areas where bacterial infections are common. For example, children receiving iron-enriched foods have demonstrated an increased rate in diarrhea overall and enteropathogen shedding. Iron deficiency protects against infection by creating an unfavorable environment for bacterial growth. Nevertheless, while iron deficiency might lessen infections by certain pathogenic diseases, it also leads to a reduction in resistance to other strains of viral or bacterial infections, such as Salmonella typhimurium or Entamoeba histolytica. Overall, it may be concluded that iron supplementation can be both beneficial and harmful to an individual in an environment that is prone to many infectious diseases.

There can be a great difference between iron intake and iron absorption, also known as bioavailability. Scientific studies indicate iron absorption problems when iron is taken in conjunction with milk, tea, coffee and other substances. There are already a number of proven solutions for this problem, including:

  • Fortification with ascorbic acid, which increases bioavailability in both presence and absence of inhibiting substances, but which is subject to deterioration from moisture or heat. Ascorbic acid fortification is usually limited to sealed dried foods, but individuals can easily take ascorbic acid with basic iron supplement for the same benefits.
  • Microencapsulation with lecithin, which binds and protects the iron particles from the action of inhibiting substances. The primary benefit over ascorbic acid is durability and shelf life, particularly for products like milk which undergo heat treatment.
  • Using an iron amino acid chelate, such as NaFeEDTA, which similarly binds and protects the iron particles. A study performed by the Hematology Unit of the University of Chile indicates that chelated iron (ferrous bis-glycine chelate) can work with ascorbic acid to achieve even higher absorption levels
  • Separating intake of iron and inhibiting substances by a couple of hours.
  • Using goats' milk instead of cows' milk.
  • Gluten-free diet resolves some instances of iron-deficiency anemia, especially if the anemia is a result of celiac disease.
  • It is believed[8][9] that "heme iron”, found only in animal foods such as meat, fish and poultry, is more easily absorbed than "non-heme" iron, found in plant foods and supplements.

Iron bioavailability comparisons require stringent controls, because the largest factor affecting bioavailability is the subject's existing iron levels. Informal studies on bioavailability usually do not take this factor into account, so exaggerated claims from health supplement companies based on this sort of evidence should be ignored. Scientific studies are still in progress to determine which approaches yield the best results and the lowest costs.

If anemia does not respond to oral treatments, it may be necessary to administer iron parenterally (e.g., as iron dextran) using a drip or hemodialysis. Parenteral iron involves risks of fever, chills, backache, myalgia, dizziness, syncope, rash and anaphylactic shock. A follow up blood test is essential to demonstrate whether the treatment has been effective.

Iron supplements should be kept out of the reach of children, as iron-containing supplements are a frequent cause of poisoning in children.

Effect of vitamin and mineral supplements

There is an observed correlation between serum retinol and hemoglobin levels. Women with a low serum retinol concentration are more likely to be iron-deficient and anemic, compared to those with normal to high levels of retinol. While vitamin A deficiency has an adverse effect on hemoglobin synthesis, even a slight increase in vitamin A intake can lead to a significant rise in hemoglobin levels. However, vitamin A is less effective in alleviating severe iron-deficiency anemia. Low levels of iron in the body cannot be relieved by vitamin A supplementation alone. Additionally, a low ascorbic acid stores in the body causes an impairment in the release of stored iron in the reticuloendothelial cells. Copper is necessary for iron uptake, and a copper deficiency can result in iron deficiency. Copper deficiency can sometimes be caused by excessive zinc or vitamin C supplementation.


Disability-adjusted life year for iron-deficiency anemia per 100,000 inhabitants in 2002.[10]
     no data      less than 50      50-100      100-150      150-200      200-250      250-300      300-350      350-400      400-450      450-500      500-1000      more than 1000

See also


  1. ^ Brady PG (2007). "Iron deficiency anemia: a call for aggressive diagnostic evaluation". South. Med. J. 100 (10): 966–7. doi:10.1097/SMJ.0b013e3181520699 (inactive 2010-01-09). PMID 17943034. 
  2. ^ Calis JC, Phiri KS, Faragher EB, et al. (2008). "Severe anemia in Malawian children". N. Engl. J. Med. 358 (9): 888–99. doi:10.1056/NEJMoa072727. PMID 18305266. 
  3. ^ Dreyfuss ML, Stoltzfus RJ, Shrestha JB, et al. (2000). "Hookworms, malaria and vitamin A deficiency contribute to anemia and iron deficiency among pregnant women in the plains of Nepal". J. Nutr. 130 (10): 2527–36. PMID 11015485. 
  4. ^ Stephen J. McPhee, Maxine A. Papadakis. Current medical diagnosis and treatment 2009 page.428
  5. ^ Mazza, J.; Barr, R. M.; McDonald, J. W.; and Valberg, L. S.; (21 October 1978). "Usefulness of the serum ferritin concentration in the detection of iron deficiency in a general hospital". Canadian Medical Association Journal 119 (8): 884–886. PMID 737638.& PMC 1819106. Retrieved 2009-05-04. 
  6. ^ Kis, AM; Carnes, M (July 1998). "Detecting iron deficiency in anemic patients with concomitant medical problems.". J Gen Intern Med. 13 (7): 455–61. doi:10.1046/j.1525-1497.1998.00134.x. PMID 9686711. 
  7. ^ Thomason, Ronald W.; Almiski, Muhamad S. (April 2009). "Evidence That Stainable Bone Marrow Iron Following Parenteral Iron Therapy Does Not Correlate With Serum Iron Studies and May Not Represent Readily Available Storage Iron". American Journal of Clinical Pathology 131 (4): 580–585. doi:10.1309/AJCPBAY9KRZF8NUC. PMID 19289594. Retrieved 2009-05-04. 
  8. ^ Health Canada. "Dietary Sources of Iron". Government of Canada. Retrieved 2009-03-30. 
  9. ^ National Institutes of Health. "Dietary Supplement Fact Sheet: Iron". United States of America, Department of Health and Human Services. Retrieved 2009-03-30. 
  10. ^ "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002. 

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