Monday, February 21, 2011


Iron Deficiency Anemia
What is Iron Deficiency Anemia?
Iron Deficiency Anemia (also called IDA) is a condition where a person has inadequate amounts of iron to meet body demands. It is a decrease in the amount of red cells in the blood caused by having too little iron. Iron deficiency anemia is usually caused by a diet insufficient in iron or from blood loss. Blood loss can be acute as in hemorrhage or trauma or long term as in heavy menstruation.
Iron deficiency anemia is the most common form of anemia. About 20% of women, 50% of pregnant women, and 3% of men are iron deficient.
Some people with iron deficiency anemia always feel cold. They feel cold because iron plays a role in regulating the body's temperature.
Iron deficiency anemia and sickle cell anemia are VERY DIFFERENT.
Individuals with iron deficiency anemia may also experience pica.
What is Iron?
Iron is an essential component of hemoglobin, the oxygen carrying pigment in the blood. Iron is normally obtained through the food in the diet.
Iron is part of hemoglobin, the oxygen-carrying component of the blood. Iron-deficient people tire easily because their bodies are starved for oxygen. Iron is also part of myoglobin. Myoglobin helps muscle cells store oxygen. Without enough iron, the body's fuel cannot be properly synthesized.
What Causes Iron Deficiency Anemia?
The main causes of iron deficiency are: poor absorption of iron by the body (Vitamin C aides in iron absorption), inadequate daily intake of iron, pregnancy, growth spurts or blood loss due to heavy period or internal bleeding.
Anemia develops slowly after the normal stores of iron have been depleted in the body and in the bone marrow. Women, in general, have smaller stores of iron than men. Women also lose iron more frequently than men because of the blood loss during menstruation.
In men and postmenopausal women, anemia is usually due to gastrointestinal blood loss associated with ulcers, the use of aspirin or nonsteroidal anti-inflammatory medications (NSAIDS), or colon cancer.
Gaucher Disease may also cause anemia.
Am I at Risk for Iron Deficiency Anemia?
High-risk groups include: women of child-bearing age who have blood loss through menstruation; pregnant or lactating women who have an increased requirement for iron; infants, children, and adolescents in rapid growth phases; and people with a poor dietary intake of iron through a diet of little or no meat or eggs for several years. Risk factors related to blood loss are peptic ulcer disease, long term aspirin use, or colon cancer.
Vegetarians are at risk of developing anemia. This usually occurs because they don't eat meat, (especially red meat) which is high in iron. However, vegetarians don't always develop anemia. There are many vegetables that contain iron (such as broccoli and spinach).
Can Anemia be Prevented?
Yes. If your diet is high in iron, you probably won't be anemic. Iron can be found in red meat, liver, raisins, spinach, broccoli, and egg yolks.
What are the Symptoms of Iron Deficiency Anemia?
There are many symptoms of anemia. Each individual will not experience all the symptoms and if the anemia is mild, the symptoms may not be noticeable. Some of the symptoms are: Pale skin color, fatigue, irritability, dizziness, weakness, shortness of breath, sore tongue, brittle nails, decreased appetite (especially in children), headache - frontal.
How will I know if I'm Anemic?
If you believe you may be anemic, ask your doctor and he will perform some tests. The tests are simple. Some of the tests are: red blood cell measures of hemocrit and hemoglobin; size of red blood cells, serum iron level, and iron binding capacity in the blood.
Iron-Deficiency Anemia
What is iron-deficiency anemia?
The most common cause of anemia is iron deficiency. Iron is needed to form hemoglobin. Iron is mostly stored in the body in the hemoglobin. About 30 percent of iron is also stored as ferritin and hemosiderin in the bone marrow, spleen, and liver.
What causes iron-deficiency anemia?
Iron-deficiency anemia may be caused by the following:
·         diets low in iron
Iron is obtained from foods in our diet, however, only 1 mg of iron is absorbed for every 10 to 20 mg of iron ingested. A person unable to have a balanced iron-rich diet may suffer from some degree of iron-deficiency anemia.
·         body changes
An increased iron requirement and increased red blood cell production is required when the body is going through changes such as growth spurts in children and adolescents, or during pregnancy and lactation.
·         gastrointestinal tract abnormalities
Malabsorption of iron is common after some forms of gastrointestinal surgeries. Most of the iron taken in by foods is absorbed in the upper small intestine. Any abnormalities in the gastrointestinal (GI) tract could alter iron absorption and result in iron-deficiency anemia.
·         blood loss
Loss of blood can cause a decrease of iron and result in iron-deficiency anemia. Sources of blood loss may include GI bleeding, menstrual bleeding, or injury.
What are the symptoms of iron-deficiency anemia?
The following are the most common symptoms of iron-deficiency anemia. However, each individual may experience symptoms differently. Symptoms may include:
·         abnormal paleness or lack of color of the skin
·         irritability
·         lack of energy or tiring easily (fatigue)
·         increased heart rate (tachycardia)
·         sore or swollen tongue
·         enlarged spleen
·         a desire to eat peculiar substances such as dirt or ice (a condition called pica)
The symptoms of iron-deficiency anemia may resemble other blood conditions or medical problems. Always consult your physician for a diagnosis.
How is iron-deficiency anemia diagnosed?
Iron-deficiency anemia may be suspected from general findings on a complete medical history and physical examination, such as complaints of tiring easily, abnormal paleness or lack of color of the skin, or a fast heartbeat (tachycardia). Iron-deficiency anemia is usually discovered during a medical examination through a blood test that measures the amount of hemoglobin (number of red blood cells) present, and the amount of iron in the blood. In addition to a complete medical history and physical examination, diagnostic procedures for iron-deficiency anemia may include the following:
·         additional blood tests
·         bone marrow aspiration and biopsy - marrow may be removed by aspiration or a needle biopsy under local anesthesia. In aspiration biopsy, a fluid specimen is removed from the bone marrow. In a needle biopsy, marrow cells (not fluid) are removed. These methods are often used together.
Treatment for iron-deficiency anemia:
Specific treatment for iron-deficiency anemia will be determined by your physician based on:
·         your age, overall health, and medical history
·         extent of the anemia
·         cause of the anemia
·         your tolerance for specific medications, procedures, or therapies
·         expectations for the course of the anemia
·         your opinion or preference
Treatment may include:
·         iron-rich diet
Eating a diet with iron-rich foods can help treat iron-deficiency anemia. Good sources of iron include the following:
o    meats - beef, pork, lamb, liver, and other organ meats
o    poultry - chicken, duck, turkey, liver (especially dark meat)
o    fish - shellfish, including clams, mussels, and oysters, sardines, anchovies
o    leafy greens of the cabbage family, such as broccoli, kale, turnip greens, and collards
o    legumes, such as lima beans and green peas; dry beans and peas, such as pinto beans, black-eyed peas, and canned baked beans
o    yeast-leavened whole-wheat bread and rolls
o    iron-enriched white bread, pasta, rice, and cereals
·         iron supplements
Iron supplements can be taken over several months to increase iron levels in the blood. Iron supplements can cause irritation of the stomach and discoloration of bowel movements. They should be taken on an empty stomach, or with orange juice, to increase absorption.
How does the body process iron?
Iron is present in many foods and absorbed into the body through the stomach. During this process of absorption, oxygen combines with iron and is transported into the plasma portion of blood by binding to transferri. From there, iron and transferri are used in the production of hemoglobin (the molecule that transports oxygen in the blood), stored in the liver, spleen, and bone marrow, and utilized as needed by all body cells.
The following is a list of foods that are good sources of iron. Always consult your physician regarding the recommended daily iron requirements for your particular situation.
Iron-Rich Foods
Quantity
Approximate Iron Content (mg)
Oysters
3 ounces
13.2
Beef liver
3 ounces
7.5
Prune juice
1/2 cup
5.2
Clams
2 ounces
4.2
Walnuts
1/2 cup
3.75
Ground beef
3 ounces
3.0
Chickpeas
1/2 cup
3.0
Bran flakes
1/2 cup
2.8
Pork roast
3 ounces
2.7
Cashew nuts
1/2 cup
2.65
Shrimp
3 ounces
2.6
Raisins
1/2 cup
2.55
Sardines
3 ounces
2.5
Spinach
1/2 cup
2.4
Lima beans
1/2 cup
2.3
Kidney beans
1/2 cup
2.2
Turkey, dark meat
3 ounces
2.0
Prunes
1/2 cup
1.9
Roast beef
3 ounces
1.8
Green peas
1/2 cup
1.5
Peanuts
1/2 cup
1.5
Potato
1
1.1
Sweet potato
1/2 cup
1.0
Green beans
1/2 cup
1.0
Egg
1
1.0
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.

Contents

  • 1 Symptoms and Signs
    • 1.1 Infant development
  • 2 Cause
  • 3 Diagnosis
    • 3.1 Gold standard
  • 4 Treatment
    • 4.1 Effect of vitamin and mineral supplements
  • 5 Epidemiology

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.

Cause

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.

Diagnosis

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.

Treatment

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.
Introduction
Background
Iron deficiency is defined as a decreased total iron body content. Iron deficiency anemia occurs when iron deficiency is sufficiently severe to diminish erythropoiesis and cause the development of anemia. Iron deficiency is the most prevalent single deficiency state on a worldwide basis. It is important economically because it diminishes the capability of individuals who are affected to perform physical labor, and it diminishes both growth and learning in children.
In healthy people, the body concentration of iron (approximately 60 parts per million [ppm]) is regulated carefully by absorptive cells in the proximal small intestine, which alter iron absorption to match body losses of iron (see images below). Persistent errors in iron balance lead to either iron deficiency anemia or hemosiderosis. Both are disorders with potential adverse consequences.
The total body iron in a 70-kg man is about 4 g. ...
The total body iron in a 70-kg man is about 4 g. This is maintained by a balance between absorption and body losses. Although the body only absorbs 1 mg daily to maintain equilibrium, the internal requirement for iron is greater (20-25 mg). An erythrocyte has a lifespan of 120 days so that 0.8% of red blood cells are destroyed and replaced each day. A man with 5 L of blood volume has 2.5 g of iron incorporated into the hemoglobin, with a daily turnover of 20 mg for hemoglobin synthesis and degradation and another 5 mg for other requirements. Most of this iron passes through the plasma for reutilization. Iron in excess of these requirements is deposited in body stores as ferritin or hemosiderin.
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The total body iron in a 70-kg man is about 4 g. ...
The total body iron in a 70-kg man is about 4 g. This is maintained by a balance between absorption and body losses. Although the body only absorbs 1 mg daily to maintain equilibrium, the internal requirement for iron is greater (20-25 mg). An erythrocyte has a lifespan of 120 days so that 0.8% of red blood cells are destroyed and replaced each day. A man with 5 L of blood volume has 2.5 g of iron incorporated into the hemoglobin, with a daily turnover of 20 mg for hemoglobin synthesis and degradation and another 5 mg for other requirements. Most of this iron passes through the plasma for reutilization. Iron in excess of these requirements is deposited in body stores as ferritin or hemosiderin.

Mucosal cells in the proximal small intestine med...
Mucosal cells in the proximal small intestine mediate iron absorption. Intestinal cells are born in the crypts of Lieberkuhn and migrate to the tips of the villi. The cells are sloughed into the intestinal lumen at the end of their 2- to 3-day lifespan. Absorptive cells remain attuned to the body requirement for iron by incorporating proportionate quantities of body iron into the absorptive cells. This iron and recently absorbed iron decrease uptake of iron from the gut lumen by satiation of iron-binding proteins with iron, by stimulating an iron regulatory element, or both. The incorporation of iron into these cells in quantities proportional to body stores of iron also provides a limited method of increasing iron excretion in individuals replete in iron.
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Mucosal cells in the proximal small intestine med...
Mucosal cells in the proximal small intestine mediate iron absorption. Intestinal cells are born in the crypts of Lieberkuhn and migrate to the tips of the villi. The cells are sloughed into the intestinal lumen at the end of their 2- to 3-day lifespan. Absorptive cells remain attuned to the body requirement for iron by incorporating proportionate quantities of body iron into the absorptive cells. This iron and recently absorbed iron decrease uptake of iron from the gut lumen by satiation of iron-binding proteins with iron, by stimulating an iron regulatory element, or both. The incorporation of iron into these cells in quantities proportional to body stores of iron also provides a limited method of increasing iron excretion in individuals replete in iron.

Posthemorrhagic anemia is discussed in this section because it is an important cause of iron deficiency. The acute and potentially catastrophic problems of hypoxia and shock that can occur from significant hemorrhage or severe iron deficiency are discussed elsewhere in the textbook; however, daily blood losses can be small and may be overlooked. Occasionally, patients with severe iron deficiency anemia from slow but persistent gastrointestinal bleeding have repeatedly negative testing of stool for hemoglobin. Therefore, it is important for the clinician to be aware of characteristics of the anemia at all intervals after the onset of bleeding.

Pathophysiology
Iron is vital for all living organisms because it is essential for multiple metabolic processes, including oxygen transport, DNA synthesis, and electron transport. Iron equilibrium in the body is regulated carefully to ensure that sufficient iron is absorbed in order to compensate for body losses of iron.
While body loss of iron quantitatively is as important as absorption in terms of maintaining iron equilibrium, it is a more passive process than absorption. Consistent errors in maintaining this equilibrium lead to either iron deficiency or iron overload.
Iron balance is achieved largely by regulation of iron absorption in the proximal small intestine. Either diminished absorbable dietary iron or excessive loss of body iron can cause iron deficiency. Diminished absorption usually is due to an insufficient intake of dietary iron in an absorbable form.
Hemorrhage is the most common cause of excessive loss of body iron, but it can occur with hemoglobinuria from intravascular hemolysis. Malabsorption of iron is relatively uncommon in the absence of small bowel disease (sprue, celiac disease, regional enteritis) or previous gastrointestinal surgery.
Iron uptake in the proximal small bowel occurs by 3 separate pathways (see image below). These are the heme pathway and separate pathways for ferric and ferrous iron.
Three pathways exist in enterocytes for uptake of...
Three pathways exist in enterocytes for uptake of food iron. In the United States and Europe, most absorbed iron is derived from heme. Heme is digested enzymatically free of globin and enters the enterocyte as a metalloporphyrin. Within the cell iron is released from heme by heme oxygenase to pass into the body as inorganic iron. Most dietary inorganic iron is ferric iron. This can enter the absorptive cell via the integrin-mobilferrin pathway (IMP).
Some dietary iron is reduced in the gut lumen and enters the absorptive cell via the DCT-1 pathway (divalent cation transporter, Nramp-2). The proteins of both pathways interact within the enterocyte with paraferritin, a large protein complex capable of ferrireduction. Excess iron is stored as ferritin to protect the cell from oxidative damage. Iron leaves the cell to enter plasma facilitated by ferroportin and hephaestin, which associate with an apotransferrin receptor. The enterocyte is informed of body requirements for iron by transporting iron from plasma into the cell using a holotransferrin receptor.
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Three pathways exist in enterocytes for uptake of...
Three pathways exist in enterocytes for uptake of food iron. In the United States and Europe, most absorbed iron is derived from heme. Heme is digested enzymatically free of globin and enters the enterocyte as a metalloporphyrin. Within the cell iron is released from heme by heme oxygenase to pass into the body as inorganic iron. Most dietary inorganic iron is ferric iron. This can enter the absorptive cell via the integrin-mobilferrin pathway (IMP).
Some dietary iron is reduced in the gut lumen and enters the absorptive cell via the DCT-1 pathway (divalent cation transporter, Nramp-2). The proteins of both pathways interact within the enterocyte with paraferritin, a large protein complex capable of ferrireduction. Excess iron is stored as ferritin to protect the cell from oxidative damage. Iron leaves the cell to enter plasma facilitated by ferroportin and hephaestin, which associate with an apotransferrin receptor. The enterocyte is informed of body requirements for iron by transporting iron from plasma into the cell using a holotransferrin receptor.

In North America and Europe, one third of dietary iron is heme iron, but two thirds of body iron is derived from dietary myoglobin and hemoglobin. Heme iron is not chelated and precipitated by numerous constituents of the diet that renders nonheme iron nonabsorbable (see image below). Examples are phytates, phosphates, tannates, oxalates, and carbonates. Heme is maintained soluble and available for absorption by globin degradation products produced by pancreatic enzymes. Heme iron and nonheme iron are absorbed into the enterocyte noncompetitively.
Dietary iron contains both heme and nonheme iron....
Dietary iron contains both heme and nonheme iron. Both chemical forms are absorbed noncompetitively into duodenal and jejunal mucosal cells. Many of the factors that alter the absorption of nonheme iron have little effect upon the absorption of heme iron because of the differences in their chemical structures. Iron is released from heme within the intestinal absorptive cell by heme oxygenase and then transferred into the body as nonheme iron. Factors affecting various stages of iron absorption are shown in this diagram. The simplest model of iron absorption must consider intraluminal, mucosal, and corporeal factors.
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Dietary iron contains both heme and nonheme iron....
Dietary iron contains both heme and nonheme iron. Both chemical forms are absorbed noncompetitively into duodenal and jejunal mucosal cells. Many of the factors that alter the absorption of nonheme iron have little effect upon the absorption of heme iron because of the differences in their chemical structures. Iron is released from heme within the intestinal absorptive cell by heme oxygenase and then transferred into the body as nonheme iron. Factors affecting various stages of iron absorption are shown in this diagram. The simplest model of iron absorption must consider intraluminal, mucosal, and corporeal factors.

Heme enters the cell as an intact metalloporphyrin, presumably by a vesicular mechanism. Heme is degraded within the enterocyte by heme oxygenase with release of iron so that it traverses the basolateral cell membrane in competition with nonheme iron to bind transferrin in the plasma.
Ferric iron utilizes a different pathway to enter cells than ferrous iron. This was shown by competitive inhibition studies, the use of blocking antibodies against divalent metal transporter-1 (DMT-1) and beta3-integrin, and transfection experiments using DMT-1 DNA. This indicated that ferric iron utilizes beta3-integrin and mobilferrin, while ferrous iron uses DMT-1 to enter cells.
Which pathway transports most nonheme iron in humans is not known. Most nonheme dietary iron is ferric iron. Iron absorption in mice and rats may involve more ferrous iron because they excrete moderate quantities of ascorbate in intestinal secretions. Contrariwise, humans are a scorbutic species and are unable to synthesize ascorbate to reduce ferric iron.
Other proteins are described that appear related to iron absorption. These are stimulators of iron transport (SFT), which are reported to increase the absorption of both ferric and ferrous iron, and hephaestin, which is postulated to be important in the transfer of iron from enterocytes into the plasma. The relationship and interactions between the newly described proteins is not known at this time and is being explored in a number of laboratories.
The iron concentration within enterocytes varies directly with the body's requirement for iron. Absorptive cells in iron-deficient humans and animals contain little stainable iron, whereas this is increased significantly in subjects who are replete in iron. Untreated phenotypic hemochromatosis creates little stainable iron in the enterocyte, similar to iron deficiency. Iron within the enterocyte may operate by up-regulation of a receptor, saturation of an iron-binding protein, or both. In contrast to findings in iron deficiency, enhanced erythropoiesis, or hypoxia, endotoxin rapidly diminishes iron absorption without altering enterocyte iron concentration. This suggests that endotoxin and, perhaps, cytokines alter iron absorption by a different mechanism.
Most iron delivered to nonintestinal cells is bound to transferrin. Transferrin iron is delivered into nonintestinal cells via 2 pathways, the classical transferrin receptor pathway (high affinity, low capacity) and the pathway independent of the transferrin receptor (low affinity, high capacity). Otherwise, the nonsaturability of transferrin binding to cells cannot be explained.
In the classical transferrin pathway, the transferrin iron complex enters the cell within an endosome. Acidification of the endosome releases the iron from transferrin so that it can enter the cell. The apotransferrin is delivered by the endosome to the plasma for reutilization. The method by which the transferrin receptor–independent pathway delivers iron to the cell is not known.
Nonintestinal cells also possess the mobilferrin integrin and DMT-1 pathways. Their function in the absence of an iron-saturated transferrin is uncertain; however, their presence in nonintestinal cells suggests they may participate in intracellular functions in addition to their capability to facilitate cellular uptake of iron.
Frequency
United States
In North America and Europe, iron deficiency is most common in women of childbearing age and as a manifestation of hemorrhage. Iron deficiency caused solely by diet is uncommon in adults in countries where meat is an important part of the diet. Depending upon the criteria used for the diagnosis of iron deficiency, approximately 4-8% of premenopausal women are iron deficient. In men and postmenopausal women, iron deficiency is uncommon in the absence of bleeding.
International
In countries where little meat is in the diet, iron deficiency anemia is 6-8 times more prevalent than in North America and Europe. This occurs despite consumption of a diet that contains an equivalent amount of total dietary iron because heme iron is absorbed better from the diet than nonheme iron. In certain geographic areas, intestinal parasites, particularly hookworm, worsen the iron deficiency because of blood loss from the gastrointestinal tract. Anemia is more profound among children and premenopausal women in these environs.


Mortality/Morbidity
Chronic iron deficiency anemia is seldom a direct cause of death; however, moderate or severe iron deficiency anemia can produce sufficient hypoxia to aggravate underlying pulmonary and cardiovascular disorders.
  • Hypoxic deaths have been observed in patients who refuse blood transfusions for religious reasons. Obviously, with brisk hemorrhage, patients may die from hypoxia due to posthemorrhagic anemia.
  • While a number of symptoms, such as ice chewing and leg cramps, occur with iron deficiency, the major debility of moderately severe iron deficiency is fatigue and muscular dysfunction that impairs muscular work performance.
  • In children, the growth rate may be slowed, and a decreased capability to learn is reported. In young children, severe iron deficiency anemia is associated with a lower IQ, a diminished capability to learn, and a suboptimal growth rate.
Race
Race probably has no significant effect upon the occurrence of iron deficiency anemia; however, because diet and socioeconomic factors play a role in the prevalence of iron deficiency, it more frequently is observed in people of various racial backgrounds living in poorer areas of the world.
Sex
An adult male absorbs and loses about 1 mg of iron from a diet containing 10-20 mg daily. During childbearing years, an adult female loses an average of 2 mg of iron daily and must absorb a similar quantity of iron in order to maintain equilibrium. Because the average woman eats less than the average man does, she must be more than twice as efficient in absorbing dietary iron in order to maintain equilibrium and avoid developing iron deficiency anemia.
  • Healthy males lose body iron in sloughed epithelium, in secretions from the skin and gut lining, and from small daily losses of blood from the gastrointestinal tract (0.7 mL of blood daily). Cumulatively, this amounts to 1 mg of iron. Males with severe siderosis from blood transfusions can lose a maximum of 4 mg daily via these routes without additional blood loss.
  • A woman loses about 500 mg of iron with each pregnancy. Menstrual losses are highly variable, ranging from 10-250 mL (4-100 mg of iron) per period. These iron losses in women double their need to absorb iron in comparison to males.
Age
Healthy newborn infants have a total body iron of 250 mg (80 ppm), which is obtained from maternal sources. This decreases to approximately 60 ppm in the first 6 months of life, while the baby consumes an iron-deficient milk diet. Infants consuming cow milk have a greater incidence of iron deficiency because bovine milk has a higher concentration of calcium, which competes with iron for absorption. Subsequently, growing children must obtain approximately 0.5 mg more iron daily than is lost in order to maintain a normal body concentration of 60 ppm.
  • During adult life, equilibrium between body loss and gain is maintained. Children are more likely to develop iron deficiency anemia. In certain geographic areas, hookworm adds to the problem. Children are more likely to walk in soil without shoes and develop heavy infestations.
  • During childbearing years, women have a high incidence of iron deficiency anemia because of iron losses sustained with pregnancies and menses.
  • Gastrointestinal neoplasms become increasingly more prevalent with each decade of life. They frequently present with gastrointestinal bleeding that may remain occult for long intervals before it is detected. Usually, bleeding from neoplasms in other organs is not occult, prompting the patient to seek medical attention before developing severe iron depletion.
Clinical
History
While iron deficiency anemia is a laboratory diagnosis, a carefully obtained history can lead to its recognition. The history can be useful in establishing the etiology of the anemia and, perhaps, in estimating its duration.
  • Diet
    • A dietary history is important. Vegetarians are more likely to develop iron deficiency, unless their diet is supplemented with iron. National programs of dietary iron supplementation are initiated in many portions of the world where meat is sparse in the diet and iron deficiency anemia is prevalent. Unfortunately, affluent nations also supplement iron in foodstuffs and vitamins without recognizing the potential contribution of iron to free radical formation and the prevalence of genetic iron overloading disorders.
    • Elderly patients, because of poor economic circumstances, may try to survive on a "tea and toast" diet because they do not wish to seek aid. They may also be hesitant to share this dietary information.
    • Pica can be the etiology of iron deficiency among people who habitually eat either clay or laundry starch. Hippocrates recognized clay eating; however, physicians do not recognize it unless the patient and family are specifically queried. Both substances decrease the absorption of dietary iron. Clay eating occurs worldwide in all races, though it is more common in Asia Minor. Starch eating is a habit in females of African heritage, and it often is started in pregnancy as a treatment for morning sickness.
  • Hemorrhage
    • Two thirds of body iron is present in circulating red blood cells as hemoglobin. Each gram of hemoglobin contains 3.47 mg of iron; thus, each mL of blood lost from the body (hemoglobin 15 g/dL) results in a loss of 0.5 mg of iron. Bleeding is the most common cause of iron deficiency in North America and Europe. Patients report a history of bleeding from most orifices (hematuria, hematemesis, hemoptysis) before they develop chronic iron deficiency anemia; however, gastrointestinal bleeding may go unrecognized, and excessive menstrual losses may be overlooked.
    • Patients often do not understand the significance of a melanotic stool. Unless menstrual flow changes, patients do not seek medical attention. If they do, they report that their menses are normal in response to inquiry for self-evaluation. Because of the marked differences among women with regard to menstrual blood loss (10-250 mL per menses), query the patient about a specific history of clots, cramps, and the use of multiple tampons and pads.
  • Duration
    • Iron deficiency in the absence of anemia is asymptomatic. One half of patients with moderate iron deficiency anemia develop pagophagia. Usually, they crave ice to suck or chew. Occasionally, patients are seen who prefer cold celery or other cold vegetables in lieu of ice. Leg cramps, which occur on climbing stairs, also are common in patients deficient in iron.
    • Often, patients can provide a distinct point in time when these symptoms first occurred, providing an estimate of the duration of the iron deficiency.
  • Symptoms
    • Fatigue and diminished capability to perform hard labor are attributed to the lack of circulating hemoglobin; however, they occur out of proportion to the degree of anemia and probably are due to a depletion of proteins that require iron as a part of their structure.
    • Increasing evidence suggests that deficiency or dysfunction of nonhemoglobin proteins has deleterious effects. These include muscle dysfunction, pagophagia, dysphagia with esophageal webbing, poor scholastic performance, altered resistance to infection, and altered behavior.
Physical
  • Anemia produces nonspecific pallor of the mucous membranes.
  • A number of abnormalities of epithelial tissues are described in association with iron deficiency anemia.
    • These include esophageal webbing, koilonychia, glossitis, angular stomatitis, and gastric atrophy.
    • The exact relationship of these findings to iron deficiency is unclear and may involve other factors. For example, in publications from the United Kingdom, esophageal webbing and atrophic changes of the tongue and the corner of the mouth are reported in as many as 15% of patients with iron deficiency; however, they are much less common in the United States and other portions of the world.
  • Splenomegaly may occur with severe, persistent, untreated iron deficiency anemia. This is uncommon in the United States and Europe.


Causes
  • Diet
    • Meat provides a source of heme iron, which is less affected by the dietary constituents that markedly diminish bioavailability than nonheme iron is. The prevalence of iron deficiency anemia is low in geographic areas where meat is an important constituent of the diet. In areas where meat is sparse, iron deficiency is commonplace.
    • Substances that diminish the absorption of ferrous and ferric iron are phytates, oxalates, phosphates, carbonates, and tannates (see image below). These substances have little effect upon the absorption of heme iron. Similarly, ascorbic acid increases the absorption of ferric and ferrous iron and has little effect upon the absorption of heme iron.
      •  
Both nonheme iron and heme iron have 6 coordinati...
Both nonheme iron and heme iron have 6 coordinating bonds; however, 4 of the bonds in heme bind pyrroles, making them unavailable for chelation by other compounds. Therefore, ascorbic acid chelates nonheme iron to enhance absorption but has no effect upon heme iron. Many dietary components, such as phytates, phosphates, oxalates, and tannates, bind nonheme iron to decrease nonheme iron absorption. They do not affect heme. This explains why heme is so effectively absorbed with foods containing these chelators. Iron hemoglobin structure.
[ CLOSE WINDOW ]
Both nonheme iron and heme iron have 6 coordinati...
Both nonheme iron and heme iron have 6 coordinating bonds; however, 4 of the bonds in heme bind pyrroles, making them unavailable for chelation by other compounds. Therefore, ascorbic acid chelates nonheme iron to enhance absorption but has no effect upon heme iron. Many dietary components, such as phytates, phosphates, oxalates, and tannates, bind nonheme iron to decrease nonheme iron absorption. They do not affect heme. This explains why heme is so effectively absorbed with foods containing these chelators. Iron hemoglobin structure.
    • Purified heme is absorbed poorly because heme polymerizes into macromolecules. Globin degradation products diminish heme polymerization, making it more available for absorption. They also increase the absorption of nonheme iron because the peptides from degraded globin bind the iron to prevent both precipitation and polymerization; thus, absorption of iron in spinach is increased when eaten with meat. Heme and nonheme iron uptake by intestinal absorptive cells is noncompetitive.
  • Hemorrhage
    • Bleeding for any reason produces iron depletion. If sufficient blood loss occurs, iron deficiency anemia ensues (see image below). A single sudden loss of blood produces a posthemorrhagic anemia that is normocytic. The bone marrow is stimulated to increase production of hemoglobin, thereby depleting iron in body stores. Once they are depleted, hemoglobin synthesis is impaired and microcytic hypochromic erythrocytes are produced.
      •  
Sequential changes in laboratory values following...
Sequential changes in laboratory values following blood loss are depicted. A healthy human was bled 5 L in 500-mL increments over 45 days. A moderate anemia ensued, initially with normal cellular indices and serum iron. Subsequently, the mean corpuscular volume (MCV) increased as iron was mobilized from body stores and reticulocytosis occurred. The serum iron decreased, followed by an increase in the total iron-binding capacity. Gradual decreases in the red blood cell indices occurred, with maximal microcytosis and hypochromia present 120 days after bleeding. Values returned to normal approximately 250 days after blood loss. At the end of the experiment, iron was absent from body stores (marrow) because hemoglobin has a first priority for iron. Iron-59 absorption was increased after all values returned to normal in order to replenish the body store with iron. This suggests that the serum iron, total iron-binding capacity, hemoglobin concentration, and indices were not the primary regulators of iron absorption.
[ CLOSE WINDOW ]
Sequential changes in laboratory values following...
Sequential changes in laboratory values following blood loss are depicted. A healthy human was bled 5 L in 500-mL increments over 45 days. A moderate anemia ensued, initially with normal cellular indices and serum iron. Subsequently, the mean corpuscular volume (MCV) increased as iron was mobilized from body stores and reticulocytosis occurred. The serum iron decreased, followed by an increase in the total iron-binding capacity. Gradual decreases in the red blood cell indices occurred, with maximal microcytosis and hypochromia present 120 days after bleeding. Values returned to normal approximately 250 days after blood loss. At the end of the experiment, iron was absent from body stores (marrow) because hemoglobin has a first priority for iron. Iron-59 absorption was increased after all values returned to normal in order to replenish the body store with iron. This suggests that the serum iron, total iron-binding capacity, hemoglobin concentration, and indices were not the primary regulators of iron absorption.
    • Maximal changes in the red blood cell cellular indices occur in approximately 120 days, at a time when all normal erythrocytes produced prior to the hemorrhage are replaced by microcytes. Prior to this time, the peripheral smear shows a dimorphic population of erythrocytes, normocytic cells produced prior to the bleed, and microcytic cells produced after bleeding. This is reflected in the red blood cell distribution width (RDW); thus, the earliest evidence of the development of an iron-deficient erythropoiesis is seen in the peripheral smear and by an increased RDW.
  • Hemosiderinuria, hemoglobinuria, and pulmonary hemosiderosis
    • Iron deficiency anemia can occur from loss of body iron in the urine. If a freshly obtained urine specimen appears bloody but contains no red blood cells, suspect hemoglobinuria. Obtain confirmation in the laboratory that the pigment is hemoglobin and not myoglobin. This can be accomplished easily because 60% ammonium sulfate precipitates hemoglobin but not myoglobin.
    • Hemoglobinuria classically is ascribed to paroxysmal nocturnal hemoglobinuria, but it can occur with any brisk intravascular hemolytic anemia. In the early days of heart surgery with implantation of artificial valves, this mechanism of producing iron deficiency anemia was commonplace in large university hospitals. Today, with better prostheses, it has become a less frequent clinical problem. With less severe hemolytic disorders, there may be no significant hemoglobinuria. Investigate renal loss of iron by staining the urine sediment for iron. Hemosiderin is detected intracellularly. Most of these patients have a low or absent plasma haptoglobin. Similarly, pulmonary hemosiderosis can result in sufficient loss of iron as hemosiderin from the lungs.
  • Malabsorption of iron
    • Prolonged achlorhydria may produce iron deficiency because acidic conditions are required to release ferric iron from food. Then, it can be chelated with mucins and other substances (amino acids, sugars, amino acids, amides) to keep it soluble and available for absorption in the more alkaline duodenum.
    • Starch and clay eating produce malabsorption of iron and iron deficiency anemia. Specific inquiry is required to elicit a history of either starch or clay eating because patients do not volunteer the information.
    • Extensive surgical removal of the proximal small bowel or chronic diseases, such as untreated sprue or celiac syndrome, can diminish iron absorption. Rarely, patients with no history of malabsorption have iron deficiency anemia and fail to respond to oral iron therapy. Most merely are noncompliant with therapy. Before placing these patients on parenteral therapy, document iron malabsorption by either measuring absorption of radioiron or by obtaining a baseline fasting serum-iron concentration and repeating the test one-half hour and 1 hour after administration of a freshly prepared oral solution of ferrous sulfate (50-60 mg of iron) under observation. The serum iron should increase by 50% over the fasting specimen.
    • Genetic abnormalities producing iron deficiency have been shown in rodents (sex-linked anemia [sla] mice, microcytic anemia [mk] mice, Belgrade rat). This has not been clearly demonstrated in humans, and if it exists, it is probably an uncommon cause of iron deficiency anemia.

What Are the Signs and Symptoms of Iron-Deficiency Anemia?

The signs and symptoms of iron-deficiency anemia depend on how serious the condition is. Mild to moderate iron-deficiency anemia may have no signs or symptoms.
When signs and symptoms do occur, they can range from mild to severe. Many of the signs and symptoms of iron-deficiency anemia apply to all types of anemia.

Signs and Symptoms of Anemia

The most common symptom of all types of anemia is fatigue (tiredness). Not having enough hemoglobin in the blood causes fatigue. Hemoglobin is an iron-rich protein in red blood cells that carries oxygen to the body.
Anemia also can cause shortness of breath; dizziness, especially when standing up; headache; coldness in your hands or feet; pale skin, gums, and nail beds; and chest pain.
If you don't have enough hemoglobin-carrying red blood cells, your heart has to work harder to circulate the reduced amount of oxygen in your blood. This can lead to arrhythmia, heart murmur, an enlarged heart, or even heart failure.
In infants and young children, signs of anemia include poor appetite, slowed growth and development, and behavioral problems.

Signs and Symptoms of Iron-Deficiency Anemia

Signs and symptoms of iron-deficiency anemia may include brittle nails, swelling or soreness of the tongue, cracks in the sides of the mouth, an enlarged spleen, and frequent infections.
People who have iron-deficiency anemia may have unusual cravings for nonfood items such as ice, dirt, paint, or starch. This craving is called pica (PI-ka or PE-ka).
Some people who have iron-deficiency anemia develop restless legs syndrome (RLS). RLS is a disorder that causes a strong urge to move your legs. This urge to move often occurs with strange and unpleasant feelings in your legs. People who have RLS often have a hard time sleeping.
Iron-deficiency anemia can put children at greater risk for lead poisoning and infections.
Some signs and symptoms of iron-deficiency anemia are related to the condition's causes. For example, a sign of intestinal bleeding can be bright red blood in the stools or black, tarry-looking stools.
Very heavy menstrual bleeding, long periods, or other vaginal bleeding may suggest that a woman is at risk for iron-deficiency anemia.

The Different Kinds Of Anemia

There are different kinds of anemia. Some forms of this condition are inherited, while others are brought on by poor nutrition.

Iron Deficiency Anemia

The body needs iron to produce the hemoglobin necessary for red blood cell production. In general, most people need just 1 milligram of iron daily. Menstruating women need double that dose.

Vitamin Deficiency Anemias

Vitamin B-12 is also essential in hemoglobin production. Normally, a chemical secreted by the stomach helps the body absorbs this vitamin. However, some people can't readily absorb B-12. The result is B-12 deficiency (pernicious anemia). Because the symptoms develop gradually this condition may not be immediately recognized. Those with thyroid disease or diabetes mellitus are at increased risk for this type of anemia. The condition occurs most often in 40- to 80-year-old northern Europeans with fair skin.
A lack of folic acid, another one of the B vitamins, can also lead to anemia. Folic acid deficiency is a particular problem for alcoholics.

Hemolytic Anemias

Anemia caused by the premature destruction of red blood cells is known as hemolytic anemia. In this type of anemia, antibodies produced by the immune system damage red blood cells. This condition is sometimes associated with disorders such as systemic lupus, or lymphoma.
Toxic materials such as lead, copper, and benzene can also cause the destruction of red blood cells.
Blood transfusions may be necessary for some people with this kind of anemia. Hemolytic anemia can be acquired or inherited. Sickle cell disease and thalassemia are both inherited types of hemolytic anemia.

Sickle Cell Anemia

Sickle cell anemia is also known as Hemoglobin S disease. This is a serious, life-threatening inherited form of anemia. Persons with this disease have sickle-shaped red blood cells that are stiff and unable to squeeze through blood vessels.
Persons with this disease often suffer from pain in the joints and bones. Infections and heart failure can also occur.
The disease occurs in just 0.6 percent of the population, usually in African Americans.

Thalassemia

This is a group of anemias due to the defects in the genes producing hemoglobin. It is most common in people of Mediterranean descent. There are two major forms: thalassemia minor and thalassemia major.
As its name implies, thalassemia minor is mild and those suffering from this condition go on to live a full life. Treatment is often unnecessary. Thalassemia major can be serious, but it is very rare. Transfusions or bone marrow The soft tissue occupying the cavities of many bones, including the breastbone. Marrow is of two types: red and yellow. Red marrow is found in spongy bones, yellow is found in the cavities of the long bones. transplants are usually required. Thalassemia major is also called Cooley's anemia, named after the doctor who first described it in 1925.

Aplastic Anemia

This is one of the deadliest and most rare forms of anemia. Only two to six people per million have this type of anemia. The condition results from an unexplained failure of the bone marrow to produce all types of blood cells. Instead, fat cells replace bone marrow.
Aplastic anemia is usually found in adolescents and young adults. Symptoms can include bleeding in the mucous membranes. Chemicals such as benzene and certain pesticides can also cause this type of anemia.
Definition
Anemia is a condition characterized by abnormally low levels of healthy red blood cells or hemoglobin (the component of red blood cells that delivers oxygen to tissues throughout the body).

Description
The tissues of the human body need a regular supply of oxygen to stay healthy. Red blood cells, which contain hemoglobin that allows them to deliver oxygen throughout the body, live for only about 120 days. When they die, the iron they contain is returned to the bone marrow and used to create new red blood cells. Anemia develops when heavy bleeding causes significant iron loss or when something happens to slow down the production of red blood cells or to increase the rate at which they are destroyed.
Types of anemia
Anemia can be mild, moderate, or severe enough to lead to life-threatening complications. More than 400 different types of anemia have been identified. Many of them are rare.
IRON DEFICIENCY ANEMIA. Iron deficiency anemia is the most common form of anemia in the world. In the United States, iron deficiency anemia affects about 240,000 toddlers between one and two years of age and3.3 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.
The onset of iron deficiency anemia is gradual and, at first, there may not be any symptoms. The deficiency begins when the body loses more iron than it derives from food and other sources. Because depleted iron stores cannot meet the red blood cell's needs, fewer red blood cells develop. In this early stage of anemia, the red blood cells look normal, but they are reduced in number. Then the body tries to compensate for the iron deficiency by producing more red blood cells, which are characteristically small in size. Symptoms develop at this stage.
FOLIC ACID DEFICIENCY ANEMIA. Folic acid deficiency anemia is the most common type of megaloblastic anemia (in which red blood cells are bigger than normal). It is caused by a deficiency of folic acid, a vitamin that the body needs to produce normal cells.
Folic acid anemia is especially common in infants and teenagers. Although this condition usually results from a dietary deficiency, it is sometimes due to inability to absorb enough folic acid from such foods as:
  • cheese
  • eggs
  • fish
  • green vegetables
  • meat
  • milk
  • mushrooms
  • yeast
Smoking raises the risk of developing this condition by interfering with the absorption of Vitamin C, which the body needs to absorb folic acid. Folic acid anemia can be a complication of pregnancy, when a woman's body needs eight times more folic acid than it does otherwise.
VITAMIN B12DEFICIENCY ANEMIA. Less common in this country than folic acid anemia, vitamin B12 deficiency anemia is another type of megaloblastic anemia that develops when the body doesn't absorb enough of this nutrient. Necessary for the creation of red blood cells, B12 is found in meat and vegetables.
Large amounts of B12 are stored in the body, so this condition may not become apparent until as much as four years after B12 absorption stops or slows down. The resulting drop in red blood cell production can cause:
  • loss of muscle control
  • loss of sensation in the legs, hands, and feet
  • soreness or burning of the tongue
  • weight loss
  • yellow-blue color blindness
The most common form of B12 deficiency is pernicious anemia. Since most people who eat meat or eggs get enough B12 in their diets, a deficiency of this vitamin usually means that the body is not absorbing it properly. This can occur among people who have had intestinal surgery or among those who do not produce adequate amounts of intrinsic factor, a chemical secreted by the stomach lining that combines with B12 to help its absorption in the small intestine.
Pernicious anemia usually strikes between the ages of 50–60. Eating disorders or an unbalanced diet increases the risk of developing pernicious anemia. So do:
  • diabetes mellitus
  • gastritis, stomach cancer, or stomach surgery
  • thyroid disease
  • family history of pernicious anemia
VITAMIN C DEFICIENCY ANEMIA. A rare disorder that causes the bone marrow to manufacture abnormally small red blood cells, Vitamin C deficiency anemia results from a severe, long-standing dietary deficiency.
HEMOLYTIC ANEMIA. Some people are born with hemolytic anemia. Some acquire this condition, in which infection or antibodies destroy red blood cells more rapidly than bone marrow can replace them.
Hemolytic anemia can enlarge the spleen, accelerating the destruction of red blood cells (hemolysis). Other complications of hemolytic anemia include:
  • pain
  • shock
  • gallstones and other serious health problems
THALASSEMIAS. An inherited form of hemolytic anemia, thalassemia stems from the body's inability to manufacture as much normal hemoglobin as it needs. There are two categories of thalassemia, depending on which of the amino acid chains is affected. (Hemoglobin is composed of four chains of amino acids.) In alpha-thalassemia, there is an imbalance in the production of the alpha chain of amino acids; in beta-thalassemia, there is an imbalance in the beta chain. Alpha-thalassemias most commonly affect blacks (25% have at least one gene); beta-thalassemias most commonly affect people of Mediterranean ancestry and Southeast Asians.
Characterized by production of red blood cells that are unusually small and fragile, thalassemia only affects people who inherit the gene for it from each parent (auto-somal recessive inheritance).
AUTOIMMUNE HEMOLYTIC ANEMIAS. Warm antibody hemolytic anemia is the most common type of this disorder. This condition occurs when the body produces autoantibodies that coat red blood cells. The coated cells are destroyed by the spleen, liver, or bone marrow.
Warm antibody hemolytic anemia is more common in women than in men. About one-third of patients who have warm antibody hemolytic anemia also have lymphoma, leukemia, lupus, or connective tissue disease.
In cold antibody hemolytic anemia, the body attacks red blood cells at or below normal body temperature. The acute form of this condition frequently develops in people who have had pneumonia, mononeucleosis, or other acute infections. It tends to be mild and short-lived, and disappears without treatment.
Chronic cold antibody hemolytic anemia is most common in women and most often affects those who are over 40 and who have arthritis. This condition usually lasts for a lifetime, generally causing few symptoms. However, exposure to cold temperatures can accelerate red blood cell destruction, causing fatigue, joint aches, and discoloration of the arms and hands.
SICKLE CELL ANEMIA. Sickle cell anemia is a chronic, incurable condition that causes the body to produce defective hemoglobin, which forces red blood cells to assume an abnormal crescent shape. Unlike normal oval cells, fragile sickle cells can't hold enough hemoglobin to nourish body tissues. The deformed shape makes it hard for sickle cells to pass through narrow blood vessels. When capillaries become obstructed, a life-threatening condition called sickle cell crisis is likely to occur.
Sickle cell anemia is hereditary. It almost always affects blacks and people of Mediterranean descent. A child who inherits the sickle cell gene from each parent will have the disease. A child who inherits the sickle cell gene from only one parent carries the sickle cell trait, but does not have the disease.
APLASTIC ANEMIA. Sometimes curable by bone marrow transplant, but potentially fatal, aplastic anemia is characterized by decreased production of red and white blood cells and platelets (disc-shaped cells that allow the blood to clot). This disorder may be inherited or acquired as a result of:
  • recent severe illness
  • long-term exposure to industrial chemicals
  • use of anticancer drugs and certain other medications
ANEMIA OF CHRONIC DISEASE. Cancer, chronic infection or inflammation, and kidney and liver disease often cause mild or moderate anemia. Chronic liver failure generally produces the most severe symptoms.
— Maureen Haggerty

Types of Anemia

Anemia is a condition where there is a dearth of oxygen carrying capacity in the body. Read on to know all about the different types of anemia.
Types of Anemia
Anemia in Greek means lack of blood. Anemia is a condition where there is deficiency of either hemoglobin or of red blood cells. Thus, this leads to a condition where there is insufficient amount of oxygen circulating in the body. Anemia is said to be one of the most common condition affecting the blood. There are many types of anemia, which occur due to many different reasons, and thus, due to these differing etiologies, there have to be different treatment plans chalked out for each. Thus, it is important to first understand and diagnose the condition, so that one can single out one from all the different types of anemia.
Hence, given below are the common types of anemia explained.

Types of Anemia: List

Iron Deficiency Anemia

Iron deficiency anemia is one of the most common types of anemia seen in the world. It is one of the types of anemia in pregnancy, as it is one of the malnutrition diseases. This condition occurs due to deficiency of iron in the body, which is spurred on by a diet that is poor in iron and other nutrients. However, in some cases, this could also occur due to colon cancer, as there is loss of blood in stools. Furthermore, in adults, around 60% of patients suffering from iron deficiency anemia may even have this condition due to gastrointestinal disorders, which leads to chronic blood loss. This leads to typical signs and symptoms, like pallor, weakness, shortness of breath, palpitations, etc. The treatment for iron deficiency anemia will consist of advising the patient to eat iron enriched foods and take in iron supplements.
Sickle Cell Anemia
Sickle cell anemia is a disease where the red blood cells assume an abnormal shape, which is sickle like, as they become flattened and pointed at ends. Thus, this leads to insufficient oxygen carrying capacity of the cells. This sickling occurs due to a point mutation in the hemoglobin gene. Thus, when the red blood cells circulate in the bloodstream, due to their sickled structure, they are very fragile. This leads to excessive breakage of the cells, which in turn leads to a state of hemolysis, which is the actual cause of anemia. The symptoms seen in this condition are the same as those seen in any other anemia, like shortness of breath, anxiety, palpitations, etc. Unfortunately, due to this disease being genetic in its etiology, there is no cure for it. However, certain precautionary measures, like eating food rich in iron and folic acid, etc. can be implemented to prevent the severity of the symptoms. In severe cases, blood transfusion and bone marrow transplants can also be done.

Megaloblastic Anemia
This anemia has a very different type of etiology behind it. In cases of people suffering from atrophic gastritis, there is destruction of the gastric parietal cells. These cells are responsible for absorption of vitamin B12, and hence, this condition is brought on by the inability of the body to absorb and utilize vitamin B12. Furthermore, even the folic acid that is ingested is not absorbed properly. Thus, the only treatment in such cases is to take vitamin B12 and folic acid intravenously.

Aplastic Anemia
Aplastic anemia is a condition where the bone marrow does not produce enough of red blood cells, due to which they are not replaced and replenished on a timely enough basis. Thus, the red blood cells, which have a lifespan of only 120 days, eventually die out, but they aren't replaced, due to which there is a deficiency of red blood cells in the body. In such cases, the only treatment option is bone marrow replacement. Read more on aplastic anemia causes.
Thus, these were common types of anemia that are seen. There are some rare types of anemia as well, like anemia of prematurity, hereditary spherocytosis, myelophthistic anemia, etc. However, most of the symptoms seen in all types of anemia are common, and hence, even if the disease does not have any cure, one must make all possible efforts to at least mitigate the severity of the symptoms.
By Dr. Sumaiya Khan
Published: 2/18/2010
Anemia – What Is Anemia?
In a nutshell, anemia is a condition of less Hemoglobin or Red blood cells in the blood. In simple language, the deficiency of blood cells is called as anemia. Anemia is rarely life threatening until and unless there is bleeding from some where in the body. There are various types of anemia and different factors are there that impact on the development of this condition like, gender, age, environmental factors and diseases.
Anemia –Anemia Kia Hai?
Muktasar alfaaz main, anemia us halat ko kehtey hain jis main Hemoglobin or Red Blood Cells blood main kam hojate hain. Aasaan zabaan main, khoon or blood ke cells or khalyon ki kami ko Anemia kehte hain. Animia intehai kam halation main jan leva hosakta hai agar jism se bleeding ho rahi ho. Anemia ki bohot sari iqsaam hain aur muktalif cheezain anemia ka sabab ban sakti hain jin main Jins, umar, maholiyati asraat aur beemari shamil hai.
Anemia – How To Identify Anemia?
In many of the cases, anemia remains silent and doesn't produce any symptoms. Once the Red blood cell count and Hemoglobin decreases remarkably, the symptoms of anemia starts to appear. Although anemia is a purely medical condition, but still there are certain signs and symptoms via which a simple and lay person can even detect that he or she might be having anemia. Followings are the important signs and symptoms of anemia:
1. Generalized weakness
2. Fatigue
3. Decreased appetite
4. Loss of interest in work
5. Lethargy
6. Vertigo and Dizziness
7. Shortness of breadth
8. Black outs
9. Falls and syncope
10. Change of skin color to pale – white
12. Brittle nails
13. Change of nails shape and texture
14. Smooth tongue
15. Dysphasia
16. Palpitations
17. Pica
18. Jaundice
Anemia –Anemia Ko Kaisy Pehchanain?
Baishter cases main Anemia hone ke bawajood zahir nahi hota aur nahi koi alamaat nazar aati hain. Lekin jab Hemogoblin aur Red Blood Cells kafi ziada kam hojate hain tau Anemia ki alaamat zahir hone lagti hain. Agarche Anemia ek  Tibbi halat hai magar Anemia ki kuch alamaat aesi hain jo ke aik aam admi ko be ye bawar kara sakti hain ke usko Anemia hai. Zail main Anemia ki aham khususyat aur alamaat ka zikr kia jaraha hai.
1. Aaam Jismani Kamzoori
2. Thakawat
3. Bhook na lagna
4. Kam Kaaj main adam dilchaspi
5. Jismani dheela pan
6. Chakar Ana
7. Saans phoolna
8. Ankhon ke aage andhera
9. Behoshi aur girne ke waqiyat
10. Rangat Safaid Mail ya peeli perdh jana
12. Nakhun sakht hojana
13. Nakhunon ke banawat aur shakal main tabdeeli
14. Zabaan ka ghair khurdura hona
15. Khane peene main takleef hona
16. Gabrahat
17. Matti ya ghair fitri cheezon ko khane ki talab hona
18. Yarqaan hona
Anemia – Types Of Anemia
There are various modes of classification of Anemia but for common public the following things should be required to be known by them. The simple types of anemia are as follows:
1.  Iron Deficiency Anemia
2. Blood Loss Anemia
3. Anemia due to Thalassemia
4. Anemia due To Sidroblasts
5. Anemia due to Kidney Failure
6. Anemia due to Liver disease
7. Anemia due to Bone Marrow Problems
8. Anemia due to Hemolysis and breaking of Red Blood Cells
9. Anemia due to Chronic Infection
10. Anemia due to Pregnancy
11. Anemia due to Drugs
12. Dilutional Anemia
13. Anemia due to Folate deficiency
14. Anemia due to B12 deficiency
15. Anemia due to Hypothyroidism
Anemia – Anemia Ki Iqsaam
Anemia ki taqseem ki kae soratay hain lekin aam logon ke lye jin iqsaam ko jis tarhan janna behtar hai wo mundarja zail hian:
1.  Iron ki kami se hone wala Anemia
2. Blood zayan hone se hone wala anemia Anemia
3. Anemia due to Thalassemia
4. Anemia due To Sidroblasts
5. Gurday fail hone ke sorat main hone wala anemia
6. Jigar ki kharabi ka anemia
7. Bone Marrow problems ka anemia
8. Red Blood Cells totne ki waja se hone wala anemia
9. Chronic infection ka anemia
10. Hamal ka anemia
11. Adwayat ki wajah se hone wala anemia
12. Dilutional Anemia
13. Folate ki kami ka anemia
14. B12 ki kami ka anemia
15. Hypothyroidism ki wajah se hone wala anemia
Anemia – Iron Deficiency Anemia ( Iron ki Kami ka Anemia) :
As it is cleared from its name that this anemia is due to iron deficiency. Iron is an integral part of Hemoglobin and hence the deficiency of iron could raise the problem of improper synthesis of Blood cells. Jaisa ke name se zahir hai ke ye Anemia Iron ki kami ki wajah se hota hai. Iron Hemoglobin ka ek aham hisa hai is lye Iron ki kami se Hemoglobin or Red cells sahi tor per nahi bante.
Iron deficiency Anemia is the most common anemia worldwide and there are various factors that leads to deficiency of iron in the body. Following are the common factors responsible for Iron deficiency in the body.
Iron deficiency anemia pori dunya main sab se zyada anemia paye jani ke wajah hai aur iske hone ke kaye ek anasir hain. Mandarja zail wajohaat Iron deficiency ka sabab ban sakti hain:
1.             Infestation of worms in intestine ( pait main keeray hona)
2.             Poor nutritional status ( Namunasib ghiza)
3.             Malabsoption of Iron ( Iron ka jazb nahona)
4.             Stomach and duodenal surgery ( mayday aur chooti aant ki jarrahi)
5.             Menses (Mahwari)
6.             Infections of intestines (Anton ki sozish)
7.             Use of NSAIDS Painkillers (Takleef kush adwiayat NSAIDS ka istemal)
8.             Aspirin ( Aspirin, Dispirin Ka istemal)
9.             Gastric Ulcer and Gastritis (Maiday ka ulcer aur sozish)
10.           Bleeding (Khon ka zaya hona)
11.           Malignancy of intestine (Anton ka Cancer)
12.           Other reasons (Deegar wajohaat)
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