Iron deficiency anemia

(medicine) Hypochromic microcytic anemia due to excessive loss, deficient intake, or poor absorption of iron. Also known as nutritional hypochromic anemia.

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Definition

Iron deficiency anemia refers to anemia that is caused by lower than normal levels of iron. This type of anemia is caused by deficient erythropoiesis, the ongoing process of the bone marrow to produce healthy red blood cells (RBCs). It is characterized by the production of small (microcytic) RBCs. When examined under a microscope, the RBCs also appear pale or light colored from the absence of heme, the major component of hemoglobin, which is the iron-bearing protein and coloring pigment in RBCs. Anemia resulting from a deficiency of iron is also called microcytic anemia.

Description

Anemia is a blood disorder characterized by abnormally low levels of healthy RBCs or reduced levels of hemoglobin (Hgb), the iron-bearing protein in RBCs that delivers oxygen to tissues throughout the body. Blood cell volume (hematocrit) may also be reduced in some anemias, but not necessarily in iron deficiency anemia. The reduction of any or all of these blood parameters reduces the essential delivery of oxygen through the bloodstream to the organs of the body. Iron is a mineral found in the bloodstream that is essential for growth, enzyme development and function, a healthy immune system, energy levels, and muscle strength. It is an important component of hemoglobin and myoglobin, the type of hemoglobin in muscle tissue.

Iron deficiency anemia is the most common type of anemia throughout the world, although it occurs to a lesser extent in the United States because of the higher consumption of iron-rich red meat and the practice of food fortification (addition of iron to foods by manufacturers). In developing countries in tropical climates, the most common cause of iron deficiency anemia is infestation with hookworm.

The onset of iron deficiency anemia is gradual and may not have early symptoms. The deficiency begins when the body's store of iron is depleted and more iron is being lost through bleeding or malabsorption than is derived from food and other sources. Because depleted iron stores cannot meet the red blood cells' needs, fewer red blood cells develop. In this early stage of anemia, the red blood cells look normal, but they are reduced in number. Eventually the body tries to compensate for the iron deficiency by producing more red blood cells, which are characteristically small in size (spherocytosis). Symptoms of anemia, especially weakness and fatigue, develop at this stage.

Causes and Symptoms

Iron is an essential component of the production of healthy RBCs, and iron stores must be maintained for the ongoing production of RBCs by the bone marrow. Iron deficiency anemia can develop as a result of depleted iron stores from chronic blood loss, increased demands for iron as seen in periods of growth (e.g., in infancy and adolescence), or malabsorption of iron even when foods or supplements are supplying adequate amounts. It is accepted that iron is hard to absorb; this, in combination with diets that may not meet daily requirements, is a common route to iron deficiency and iron deficiency anemia. Iron can also be lost through strenuous exercise and heavy perspiration, poor digestion, frequent consumption of antacids, long-term illness, heavy menstrual cycles, and other causes.

Infancy is a period of increased risk for iron deficiency because dietary iron may not be adequate for the rapid growth of the child in the first two years of life, an example of increased demand. The human infant is born with a built-in supply of iron, which can be tapped during periods of drinking low-iron milk or formula. Both human milk and cow milk contain rather low levels of iron (0.5–1.0 mg iron/liter). However, the iron in the mother's breast milk is about 50 percent absorbed by the infant, while the iron of cow milk is only 10 percent absorbed. During the first six months of life, growth of the infant is made possible by the milk in the diet and by the infant's built-in supply of iron. However, premature infants have a lower supply of iron and, for this reason, it is recommended that pre-term infants, beginning at two months of age, be given oral supplements of 7 mg iron/day, as ferrous sulfate. Iron deficiency can be provoked where infants are fed formulas based on unfortified cow milk. For example, unfortified cow milk is given free of charge to mothers in Chile. This practice has the fortunate result of preventing general malnutrition, but the unfortunate result of allowing the development of mild iron deficiency.

Children have a great need for iron as they grow, and in most cases, the diet will provide replacement iron for the iron used in growth. Children seem to stay in balance unless a bleeding disorder of some kind exists, either hereditary (hemophilia or von Willebrand's) or related to hookworm infection or another illness. In adolescence, girls have an increased requirement for iron because of increased growth and the start of menstruation. Adolescent boys also experience a major growth spurt that demands more iron; iron stores are worn thin especially when healthy red cell function is needed for adequate oxygenation of exercising muscles and developing organs. Teenagers are also not noted for making healthy food choices; often they are losing iron stores and not replenishing iron through diet.

Iron deficiency occurs most often through chronic blood loss, more often in adults than in children, although the sources of bleeding can apply to people of all ages. Blood losses from gastrointestinal bleeding, excessive menstrual bleeding, and infection with hookworm can deplete iron and lead to iron deficiency anemia. In hookworm infection, a parasitic worm that thrives in warm climates, including in the southern United States, enters the body through the skin, such as through bare feet. The hookworm then migrates to the small intestines where it attaches itself to small sausage-shaped structures in the intestines (villi) that help with the absorption of all nutrients. The hookworm damages the villi, resulting in blood loss; they simultaneously produce anti-coagulants that promote continued bleeding. Each worm can initiate losses of up to 0.25 ml of blood per day.

Chronic blood losses through gradual bleeding in the gastrointestinal tract can be provoked by other conditions such as hemorrhoids, bleeding ulcers, anal fissures, irritable bowel syndrome, aspirin-induced bleeding, blood clotting disorders, and diverticulosis (a condition caused by an abnormal opening from the intestine or bladder). Several genetic diseases also lead to bleeding disorders. These include the coagulation disorders hemophilia A and hemophilia B, and von Willebrand's disease, a bleeding disorder caused by a deficiency in von Willebrand factor, an essential component of the coagulation system. All three genetic diseases can produce symptoms and be diagnosed in childhood.

The symptoms of iron deficiency anemia appear slowly and typically include weakness and fatigue. These symptoms result because of the reduced oxygen carrying capacity of RBCs and the reduced ability of the RBCs to carry iron to working muscles. Iron deficiency can also affect other tissues, including the tongue and fingernails. Prolonged iron deficiency can result in a smooth, shiny, and reddened tongue, a condition called glossitis. The fingernails may grow abnormally and acquire a spoon-shaped appearance.

When to Call the Doctor

Weakness, dizziness, listlessness, or fatigue may be the first signs of iron deficiency anemia. A compulsion to chew on ice cubes or to eat soil is also an indication of iron deficiency. The pediatrician should be consulted if the child is extremely pale, with little or no color in the gums, nail beds, creases of the palm, or lining of the eyelids.

Demographics

In the United States, iron deficiency anemia affects thousands of toddlers between one and two years of age and more than 3 million women of childbearing age. This condition is less common in older children and in adults over 50 and rarely occurs in teenage boys and young men.

Diagnosis

Diagnosing iron deficiency anemia begins with the pediatrician taking a careful history, including the child's age, symptoms, illnesses, general state of health, and a family history of anemias. Symptoms noticed in children by their parents may include fatigue, weight loss, inability to concentrate, loss of appetite, and light-headedness when standing up. The physical examination may reveal paleness, and lack of color in the creases of the palms, in gums, and in the linings of the eyelids.

Diagnostic testing starts with a complete blood count (CBC) and differential, counting RBCs, white blood cells (WBCs) and measuring hemoglobin (Hgb), hematocrit (Hct), and other factors. In iron deficiency anemia, the RBC count can be normal or elevated and hemoglobin will be abnormally low. In infants, iron deficiency anemia is defined as having a hemoglobin level below 109 mg/ml when measured in whole blood, and a hematocrit of less than 33 percent. In the microscopic examination of a stained blood smear (differential), red cells may appear smaller than normal. The mean corpuscular volume (MCV) will be measured to compare the size of RBCs with normal RBCs. A reticulocyte (young RBCs) count will help determine if anemia is caused by impaired RBC production, as in iron deficiency anemia, or increased RBC destruction as in some other types of anemia. Iron, vitamin C or vitamin B₁₂, and folate levels will be measured in blood serum to identify possible deficiencies. In addition to measuring iron itself (Fe) and total iron-binding capacity (TIBC), transferrin and transferrin saturation tests may be performed to evaluate iron metabolism. Different types of hemoglobin may be measured by a diagnostic testing method called hemoglobin electrophoresis. Protoporphyrin IX, a component of hemoglobin, may be measured to help confirm a diagnosis of iron deficiency anemia. Confirmation may also be obtained by taking a bone marrow sample (bone marrow biopsy) for microscopic examination. Kidney function tests, coagulation tests, and stool examinations for occult (hidden) blood may also be performed.

The presence of occult blood found in a stool examination may indicate gastrointestinal bleeding or other causes of bleeding such as aspirin-induced or a bleeding ulcer. The physician then needs to examine the gastrointestinal tract to determine the cause and location of bleeding. In this case, a diagnosis of iron deficiency anemia may include examination with a sigmoidoscope, a flexible, tube-like instrument with a light source that permits examination of the colon. A barium-enhanced x ray of the intestines may also be used to detect abnormalities that can cause bleeding.

The diagnosis of iron deficiency anemia may include a test for oral iron absorption, especially when evidence suggests that oral iron supplements have failed to raise hemoglobin. The oral iron absorption test is conducted by injecting 64 mg iron (325 mg ferrous sulfate) in a single dose. Blood samples are then taken after two hours and four hours. The iron content of the blood serum is then measured. The concentration of iron should rise by about 22 micromolar, when iron absorption is normal. Lesser increases in concentration mean that iron absorption is abnormal and that more effective therapy may involve injections or infusions of iron.

Treatment

The goal of treatment for iron deficiency anemia is to restore iron levels and the production of healthy RBCs and increase the essential flow of oxygen to tissues. Iron preparations may be given by injection or, in older children, as oral supplements. Taking vitamin C along with oral iron supplementation is accepted as a way to achieve better absorption of the iron. Taking iron supplements can result in constipation, diarrhea, cramps, or vomiting in sensitive individuals. Injections and infusions of iron can be given to individuals with poor iron absorption. Treatment of iron deficiency anemia sometimes requires more than iron supplementation. When iron deficiency is provoked by hemorrhoids or gastrointestinal bleeding, for example, surgery may be required to prevent recurrent iron deficiency anemia. When iron deficiency is provoked by bleeding due to aspirin ingestion, aspirin is discontinued. Iron deficiency caused by hookworm infection requires drug therapy to eliminate the parasite; prevention includes wearing shoes when walking in soil known to be infested with hookworms.

Alternative Treatment

Vitamin C is noted for helping to absorb iron in the diet and iron supplements. Cooking in a cast iron skillet may leach small amounts of absorbable iron into the diet. Besides the iron found in eggs, fish, liver, meat, poultry, green leafy vegetables, whole grains, and enriched or whole grain breads and cereals, good food sources of iron include blackstrap molasses, brewer's yeast, and certain types of sea vegetable (e.g., hijiki, kelp, dulse). Herbal supplements that benefit individuals who have iron deficiency anemia include alfalfa, burdock root, dandelion, dong quai, mullein, nettle, raspberry leaf, shepherd's purse, and yellow dock. Herbs are available as tinctures and teas or in capsules.

Nutritional Concerns

Decreased dietary iron intake is a contributing factor in iron deficiency and iron deficiency anemia. Deciding how to add enough iron to the diet, however, depends not just on which foods contain it, but in which foods iron is most available for absorption and use by the body. Bioavailability describes the percent of dietary iron that is successfully absorbed via the gastrointestinal tract to the bloodstream. Non-absorbed iron is lost in the feces. Generally, iron bioavailability in fruits, vegetables, and grains is lower than the iron availability of meat. The availability of iron in plants ranges from only 1 to 10 percent, with some exceptions, while that in meat, fish, chicken, and liver is consistently 20–30 percent. In the following list, the iron content is given parenthetically for each food.

• cabbage (1.6 mg/kg)
• spinach (33 mg/kg)
• lima beans (15 mg/kg)
• potatoes (14 mg/kg)
• tomatoes (3 mg/kg)
• apples (1.5 mg/kg)
• peanut butter (6.0 mg/kg)
• raisins (20 mg/kg)
• whole wheat bread (43 mg/kg)
• eggs (20 mg/kg)
• canned tuna (13 mg/kg)
• chicken (11 mg/kg)
• beef (28 mg/kg)

It is easy to see that apples, tomatoes, and peanut butter are relatively low in iron, while spinach, whole wheat bread, and beef are relatively high in iron. Red meat sources reliably replace the heme component of red blood cells, raising hemoglobin levels and helping to correct iron deficiency. For infants and toddlers, the most available source of iron is human milk (50% availability).

The assessment of whether a food is low or high in iron can also be made by comparing the amount of that food eaten per day with the recommended dietary allowance (RDA) for iron. The RDA for iron for the adult male is 10 mg/day, while that for the adult woman is 15 mg/day. The RDA during pregnancy is 30 mg/day. The RDA for infants five months of age or younger is 6 mg/day, while that for infants of five months to one year of age is 10 mg/day. RDA values are based on the assumption that people eat a mixture of plant and animal foods.

Prognosis

The prognosis for treating and curing iron deficiency anemia is excellent, particularly when those affected take iron supplements as advised and are able to assimilate the iron. A number of studies have shown that iron deficiency anemia in infancy can result in reduced intelligence, when intelligence was measured in early childhood. It is not certain if iron supplementation of children with reduced intelligence, due to iron-deficiency anemia in infancy, has any influence in allowing a "catch-up" in intellectual development.

Prevention

In the healthy population, mineral deficiencies can be prevented by the consumption of inorganic nutrients at levels defined by the RDA. Iron deficiency anemia in infants and young children can be prevented by breast-feeding, consuming good dietary sources of iron, and using fortified foods. Liquid cow milk-based infant formulas are generally supplemented with iron (12 mg/L). The iron in liquid formulas is added as ferrous sulfate or ferrous gluconate. Commercial infant cereals are also fortified with iron, adding small particles of elemental iron. The levels used are about 0.5 gram iron/kg dry cereal. This amount of iron is about 10-fold greater than that of the iron naturally present in the cereal. Iron supplementation is not recommended for all infants, and children and pediatricians should be consulted before giving supplements. Vitamin C is recommended to improve the assimilation of iron in the body, especially when iron is obtained from non-food sources.

Nutritional Concerns

The average diet in the United States contains about 6 mg of iron per calorie of food, which is sufficient for maintaining iron stores. Only 1 mg of iron, however, is absorbed for every 10 mg. consumed, which mean sources of iron must be carefully chosen. The bioavailability of iron in foods varies, influencing the amounts that can be absorbed through the intestines. Absorption is best when the food contains heme, just as in human red cells. That makes meat the best choice as a source of iron and iron-rich vegetables and fruits such as spinach and apricots the next best choice. Certain other plant foods that contain fiber, such as bran, actually reduce the absorption of non-heme iron; so do antacid medications, often taken to relieve the upset stomach associated with taking oral iron supplements. Additionally, food interactions reduce bioavailability. Ascorbic acid (vitamin C) is the only food constituent known to increase the availability of non-heme iron, such as in vegetables and also in food supplements.

Parental Concerns

Understanding iron metabolism and the ways to ensure that iron deficiency anemia in infants and children can be successfully treated and prevented from recurring may be concerns of parents. It is important to remember that although iron deficiency anemia is common in infants and toddlers, it is easily corrected by feeding infants mother's milk or iron-fortified formulas. In older children, the diet usually balances iron usage and replacement. In teenage years, when demands for iron increase for rapid growth and to compensate for menstruation in girls, parents will need to pay attention once again to providing adequate food sources. However, supplementation of iron should only be done with a doctor's recommendation.

Resources

Books

"Blood Disorders." The Merck Manual of Medical Information, 2nd Home Edition. Edited by Mark H. Beers et al. White House Station, NJ: Merck & Co., 2003.

Floyd, B. A. Anemia. Bloomington, IN: AuthorHouse, 2002.

Lark, Susan. Heavy Menstrual Flow and Anemia Self Help Book. Berkeley, CA: Celestial Arts Publishing, 2004.

Ross, Allison J. Everything You Need to Know about Anemia. New York: Rosen Publishing Group, 2001.

Organizations

National Heart, Lung, and Blood Institute (NHLBI). 6701 Rockledge Drive, PO Box 30105, Bethesda, MD 20824–0105. Web site: www.nhlbi.nih.gov.

[Article by: L. Lee Culvert Tom Brody, PhD]

An anemia resulting from a deficiency of iron, characterized by hypochromic microcytic erythrocytes and a normoblastic reaction of the bone marrow. Iron deficiency may result from an increased demand during growth or repeated pregnancies, chronic or recurrent hemorrhage such as from menstrual abnormalities, hemorrhoids, or peptic ulcer, a low intake of iron, or impaired absorption, as often occurs with chronic diarrhea.

This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (July 2007)

Iron deficiency anemia
Classification and external resources
Red blood cells
ICD-10	D50
ICD-9	280
DiseasesDB	6947
eMedicine	med/1188
MeSH	D01

Iron-deficiency anemia (or iron-deficiency anaemia) is a common anemia that occurs when iron loss (often from intestinal bleeding or menses) occurs, and/or the dietary intake or absorption of iron is insufficient. In iron deficiency, hemoglobin, which contains iron, cannot be formed.^[1]

Iron deficiency is the most common single cause of anemia worldwide, accounting for about half of all anemia cases. It is more common in women than men. Estimates of iron deficiency worldwide range very widely, but the number almost certainly exceeds one billion persons globally.^[2] Worldwide, the most important cause of iron-deficiency anemia is parasitic infection caused by hookworms, whipworms, and roundworms, in which intestinal bleeding caused by the worms may lead to undetected blood loss in the stool. These are especially important problems in growing children.^[3] Malaria infections that destroy red blood cells (although the iron is recycled) and chronic blood loss caused by hookworms (where the iron is lost) contribute to anemia during pregnancy in most developing countries.^[4] In adults of post-menopausal age (over 50 years old) the most common cause of iron-deficiency anemia is chronic gastrointestinal bleeding from nonparasitic causes, such as from gastric ulcer, duodenal ulcer or a gastrointestinal cancer.

In the developed world, where intestinal worm parasite burden is less than in many undeveloped countries, about 20% of all women of childbearing age have iron-deficiency anemia, compared with only 3% of adult men.^[5] The principal cause of iron-deficiency anemia in these countries is blood lost during menses in premenopausal women and not compensated by intake from food and supplements.

Iron-deficiency anemia is one result of advanced-stage iron deficiency, which is even more common. When the body has sufficient iron to meet its needs (functional iron), the remainder is stored for later use, mostly in the bone marrow, liver, and spleen (although all cells store some iron) as part of a finely tuned system of human iron metabolism. The store of iron present in all animal cells is deposited mostly in ferritin complexes. In humans each of these are made up of 24 subunit protein molecules of two different types, with each ferritin complex carrying about 4500 iron atoms, as ferrous ions.

Iron deficiency ranges from iron depletion, which produces 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 enters a state in which it requires more iron than is being absorbed from the diet.

Contents 1 Symptoms and signs 1.1 Infant development 2 Cause 3 Diagnosis 3.1 Gold standard 4 Treatment 4.1 Iron supplementation and infection risk 4.2 Effect of vitamin and mineral supplements 5 Epidemiology 6 See also 7 References 8 External links

Symptoms and signs

Iron-deficiency anemia is characterized by pallor (reduced oxyhemoglobin in skin or mucous membranes), 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:

• Anxiety often resulting in OCD type compulsions and obsessions
• Irritability or a low feeling
• Angina
• Constipation
• Sleepiness
• Tinnitus
• Mouth ulcers
• Palpitations
• Hair loss
• Fainting or feeling faint
• Depression
• Breathlessness on exertion.
• Twitching muscles
• Tingling, numbness, or burning sensations
• Missed menstrual cycle
• Heavy menstrual period
• Slow social development
• Glossitis (inflammation or infection of the tongue)
• Angular cheilitis (inflammatory lesions at the mouth's corners)
• Koilonychia (spoon-shaped nails) or nails that are weak or brittle
• Poor appetite
• Pruritus (Itchiness)
• Dysphagia due to formation of esophageal webs (Plummer-vinson syndrome).
• Restless Legs Syndrome^[6]

Infant development

Iron-deficiency anemia for infants in their earlier stages of development may have 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. This is also linked to pica as it can be a cause.

Cause

The diagnosis of iron-deficiency anemia requires further investigation as to its cause. Iron deficiency can be caused by increased iron demand or decreased iron intake,^[7] and can occur in both children and adults.

The most important cause of iron deficiency worldwide is infestation with parasitic worms (hookworms, whipworms, roundworms). Estimates of infection in the world population vary from a minimum of a billion humans to as many as 5 of 6 billion.^[2] In addition to parasitosis, 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, according to the patient's sex, age, and history. Other common causes include gastrointestinal blood loss due to drug therapy (often in the case of NSAIDs or aspirin), and hypochlorhydria/achlorhydria (often due to long-term proton pump inhibitor therapy). In babies and adolescents, rapid growth may outpace dietary intake of iron, and result in deficiency without disease or grossly abnormal diet.^[7] In women of childbearing age, heavy or long menstrual periods can also cause mild iron-deficiency anemia.

Especially in adults over the age of 50, iron deficiency is often a sign of other disease in the gastrointestinal tract, such as chronic bleeding from any cause (for example, a colon cancer) that causes loss of blood in the stool. Such loss is often undetectable, except with special testing. In adults, 60% of patients with iron-deficiency anemia have underlying gastrointestinal disorders leading to chronic blood loss, and this percentage increases with patient age. Iron deficiency in adult men from purely dietary causes is quite rare, and in such cases other causes of iron loss must be vigorously sought until found.

Diagnosis

Anemia may be diagnosed from symptoms and signs, but when anemia is mild it may not be diagnosed from mild non-specific symptoms. Pica, an abnormal craving for dirt, ice, or other "odd" foods occurs variably in iron and zinc deficiency, but is neither sensitive or specific to the problem so is of little diagnostic help.^{[citation needed]}

Anemia is often first shown by routine blood tests, which generally include a complete blood count (CBC) which is performed by an instrument which gives an output as a series of index numbers. A sufficiently low hemoglobin (HGB) by definition makes the diagnosis of anemia, and a low hematocrit (HCT) value is also characteristic of anemia. Further studies will be undertaken to determine the anemia's cause. If the anemia is due to iron deficiency, one of the first abnormal values to be noted on a CBC, as the body's iron stores begin to be depleted, will be a high red blood cell distribution width (RDW), reflecting an increased variability in the size of red blood cells (RBCs). In the course of slowly depleted iron status, an increasing RDW normally appears even before anemia appears.

A low mean corpuscular volume (abbreviated MCV) often appears next during the course of body iron depletion. It corresponds to a high number of abnormally small red blood cells. A low MCV, a low mean corpuscular hemoglobin (MCH) and/or Mean corpuscular hemoglobin concentration (MCHC), and the appearance of the RBCs on visual examination of a peripheral blood smear narrows the problem to a microcytic anemia (literally, a "small red blood cell" anemia). The numerical values for red blood count, blood hemoglobin, MCV, MCH, MCHC are all calculated by modern laboratory equipment.

The blood smear of a patient with iron deficiency shows many hypochromic (pale and relatively colorless) 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.^[8] Very commonly, the platelet count is slightly above the high limit of normal in iron deficiency anemia (this is mild thrombocytosis). This effect was classically postulated to be due to high erythropoietin levels in the body as a result of anemia, cross-reacting to activate thrombopoietin receptors in the precursor cells that make platelets; however, this mechanistic effect has been searched for and not corroborated. Such slightly increased platelet counts present no danger, but remain valuable as an indicator even if their mechanistic origin is not yet known.

The diagnosis of iron-deficiency anemia will be suggested by appropriate history (e.g., anemia in a menstruating woman or an athlete engaged in long distance running), the presence of occult blood (i.e., hidden blood) in the stool, and often by other history. For example, known celiac disease can cause malabsorption of iron. A travel history to areas in which hookworm and whipworm are endemic may be helpful in guiding certain stool tests for parasites or their eggs.

Body-store iron deficiency is diagnosed by diagnostic tests as a low serum ferritin, a low serum iron level, an elevated serum transferrin and a high total iron binding capacity (TIBC). A low serum ferritin is the most sensitive lab test for iron deficiency anemia. However, serum ferritin can be elevated by any type of chronic inflammation and so is not always a reliable test of iron status if it is within normal limits (i.e., this test is meaningful if abnormally low, but less meaningful if normal).

Serum iron levels (i.e., iron not part of the hemoglobin in red cells) may be measured directly in the blood, but these levels increase immediately with iron supplementation (the patient must stop supplements for 24 hours), and pure blood-serum iron concentration in any case is not as sensitive as a combination of total serum iron, along with a measure of the serum iron-binding protein levels (total iron binding capacity or TIBC). The ratio of serum iron to TIBC (called iron saturation or transferrin saturation index or percent) is the most specific indicator of iron deficiency, when it is sufficiently low. The iron saturation (or transferrin saturation) of < 5% almost always indicates iron deficiency, while levels from 5% to 10% make the diagnosis of iron deficiency possible but not definitive. Saturations over 12% (taken alone) make the diagnosis unlikely. Normal saturations are usually slightly higher for women (>12%) than for men (>15%), but this may indicate simply an overall slightly poorer iron status for women in the "normal" population.

Change in lab values in iron deficiency anemia

Change	Parameter
Decrease	ferritin, hemoglobin, MCV
Increase	TIBC, transferrin, RDW

Iron-deficiency 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 the liver). A hemoglobin electrophoresis provides useful evidence for distinguishing these two conditions, along with iron studies.

Gold standard

Conventionally, a definitive diagnosis requires a demonstration of depleted body iron stores obtained by bone marrow aspiration, with the marrow stained for iron.^[9][10] 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^[11] questions the value of stainable bone marrow iron following parenteral iron therapy.

Treatment

If the cause is dietary iron deficiency, eating more iron-rich foods such as beans and lentils or taking 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. There is evidence that the body adapts to oral iron supplementation, so that iron is often effectively started at a comparatively low dose, then slowly increased.

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 non-dairy milk (such as soy, rice, or almond milk) or 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^[12][13] 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 supplementation and infection risk

Because one of the functions of elevated ferritin (an acute phase reaction protein) in acute infections is thought to be to sequester iron from bacteria, it is generally thought that iron supplementation (which circumvents this mechanism) should be avoided in patients who have active bacterial infections. Replacement of iron stores is seldom such an emergency situation that it cannot wait for such infections to be treated.

Some studies have found 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 is sometimes difficult to decide whether iron supplementation will be beneficial or harmful to an individual in an environment that is prone to many infectious diseases; however this is a different question than the question of supplementation in individuals who are already ill with a bacterial infection.

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.

Epidemiology

Disability-adjusted life year for iron-deficiency anemia per 100,000 inhabitants in 2002.^[14]

  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

• Human iron metabolism
• Iron supplements
• Hematogen
• Iron deficiency

References

1. ^ Brady PG (2007). "Iron deficiency anemia: a call for". South. Med. J. 100 (10): 966–7. doi:10.1097/SMJ.0b013e3181520699 (inactive 2010-01-09). PMID 17943034. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?doi=10.1097/SMJ.0b013e3181520699. 
2. ^ ^{a b} [1] Review of numbers of infections
3. ^ 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. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=18305266&promo=ONFLNS19. 
4. ^ 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. 
5. ^ Medline Plus. "Iron deficiency anemia encyclopedia article". Iron deficiency anemia encyclopedia article. http://www.nlm.nih.gov/medlineplus/ency/article/000584.htm. 
6. ^ Rangarajan, Sunad; D'Souza, George Albert. (April 2007). "Restless legs syndrome in Indian patients having iron deficiency anemia in a tertiary care hospital". Sleep Medicine. 8 (3): 247–51. doi:10.1016/j.sleep.2006.10.004. PMID 17368978. 
7. ^ ^{a b} "NPS News 70: Iron deficiency anaemia". NPS Medicines Wise. October 1, 2010. http://www.nps.org.au/health_professionals/publications/nps_news/current/iron_anaemia. Retrieved November 5, 2010. 
8. ^ Stephen J. McPhee, Maxine A. Papadakis. Current medical diagnosis and treatment 2009 page.428
9. ^ 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. PMC 1819106. PMID 737638. http://www.cmaj.ca/cgi/content/abstract/119/8/884. Retrieved 2009-05-04. 
10. ^ 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. PMC 1496985. PMID 9686711. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1496985. 
11. ^ 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. http://ajcp.ascpjournals.org/content/131/4/580.full. Retrieved 2009-05-04. 
12. ^ Health Canada. "Dietary Sources of Iron". Government of Canada. http://www.hc-sc.gc.ca/fn-an/nutrition/prenatal/national_guidelines-lignes_directrices_nationales-07-table2-eng.php. Retrieved 2009-03-30. ^{[dead link]}
13. ^ National Institutes of Health. "Dietary Supplement Fact Sheet: Iron". United States of America, Department of Health and Human Services. http://ods.od.nih.gov/factsheets/iron.asp. Retrieved 2009-03-30. 
14. ^ "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002. http://www.who.int/entity/healthinfo/statistics/bodgbddeathdalyestimates.xls. 

External links

• Iron deficiency textbook IronTherapy.Org
• Establishing the cause of anemia – AnaemiaWorld.com
• Handout: Iron Deficiency Anemia – National Anemia Action Council
• Simplified decision guide for treating iron deficiency anemia – Section: Iron Therapy at Monofer.com
• NPS News 70: Iron deficiency anaemia: NPS – Better choices, Better health – 2011 National Prescribing Service Limited
• 1993342985 at GPnotebook
• Simple Guide to Iron Deficiency Anemia

v d e Pathology: hematology · hematologic diseases of RBCs and megakaryocytes / MEP (D50-69,74, 280-287) Red blood cells ↑ Poly- cythemia Polycythemia vera ↓ Anemia Nutritional Micro-: Iron deficiency anemia (Plummer-Vinson syndrome) Macro-: Megaloblastic anemia (Pernicious anemia) Hemolytic (mostly Normo-) Hereditary enzymopathy: G6PD · glycolysis (PK, TI, HK) hemoglobinopathy: Thalassemia (alpha, beta, delta)  · Sickle-cell disease/trait · HPFH membrane: Hereditary spherocytosis (Minkowski-Chauffard syndrome) · Hereditary elliptocytosis (Southeast Asian ovalocytosis) · Hereditary stomatocytosis Acquired Autoimmune (WAHA, CAD, PCH) membrane (PNH) MAHA · TM (HUS) Drug-induced autoimmune · Drug-induced nonautoimmune Hemolytic disease of the newborn Aplastic (mostly Normo-) Hereditary: Fanconi anemia · Diamond–Blackfan anemia Acquired: PRCA · Sideroblastic anemia · Myelophthisic Blood tests MCV (Normocytic, Microcytic, Macrocytic) · MCHC (Normochromic, Hypochromic) Other Methemoglobinemia · Sulfhemoglobinemia · Reticulocytopenia Coagulation/ coagulopathy ↑ Hyper- coagulability primary: Antithrombin III deficiency · Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden · Prothrombin G20210A acquired:Thrombocytosis (essential) · DIC (Congenital afibrinogenemia, Purpura fulminans) · autoimmune (Antiphospholipid) ↓ Hypo- coagulability Thrombocytopenia Thrombocytopenic purpura: ITP (Evans syndrome) · TM (TTP) Heparin-induced thrombocytopenia · May-Hegglin anomaly Platelet function adhesion (Bernard–Soulier syndrome) · aggregation (Glanzmann's thrombasthenia) · platelet storage pool deficiency (Hermansky–Pudlak syndrome, Gray platelet syndrome) Clotting factor Hemophilia (A/VIII, B/IX, C/XI) • von Willebrand disease • Hypoprothrombinemia/II · XIII · Dysfibrinogenemia M: MYL cell/phys (coag, heme, immu, gran), csfs rbmg/mogr/tumr/hist, sysi/epon, btst drug (B1/2/3+5+6), btst, trns

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