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Iron deficiency anemia



Iron deficiency anemia
Classification & external resources
Red blood cells
ICD-10 D50.
ICD-9 280
DiseasesDB 6947
eMedicine med/1188 
MeSH D018798

For a discussion of iron deficiency more broadly, see the Wikipedia article iron deficiency.

Iron deficiency anemia is the most common type of anemia, and is also 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. The principal cause of iron deficiency anemia in premenopausal women is blood lost during menses.

Iron deficiency anemia is the final 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. 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 by the body is not adequate for growth and development or to replace the amount lost.

Contents

History

A disease believed to be iron deficiency anemia is described in about 1500 B.C. in the Egyptian Ebers papyrus. It was termed chlorosis or green sickness in Medieval Europe, and iron salts were used for treatment in France by the mid-17th century. Thomas Sydenham recommended iron salts as treatment for chlorosis, but treatment with iron was controversial until the 20th century, when its mechanism of action was more fully elucidated.

Symptoms

Iron deficiency anemia is characterized by pallor, 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. Hair loss and lightheadedness can also be associated with iron deficiency anemia.

Other symptoms

Other symptoms patients with iron deficiency anemia have reported are:

  • Constipation
  • Tinnitus
  • Palpitations
  • Seeing Bright Colors
  • Fainting, Feeling faint
  • Depression
  • Weakness
  • Breathlessness
  • Twitching Nerves, Tingling, Numbness
  • Burning sensations
  • Sleep apnea (rare)
  • Missed menstrual cycle
  • heavy menstrual cycle
  • weak/ brittle nails
  • slow social development
  • lethargia
  • hair loss
  • sore/ swollen tongue
  • poor skin color
  • weak immune system
  • exhaustion
  • loss of desire for food

Diagnosis

Anemia will be diagnosed on the basis of suggestive symptoms, or found on the basis of routine testing, which includes a complete blood count (CBC). A sufficiently low hemoglobin or hematocrit value is diagnostic of anemia, and further studies will be undertaken to determine its cause. 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. 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 anaemia. Microcytic anemia can also be the result of malabsorption phenomena associated with gluten-sensitive enteropathy/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.[2]

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 hemachromatosis (accumulation of iron in the liver) A hemoglobin electrophoresis would provide useful evidence in distinguishing these two conditions, along with iron studies.

Gold standard

A definitive diagnosis requires a demonstration of depleted body iron stores by performing a bone marrow aspiration, with the marrow stained for iron. Because this is invasive and painful, while a clinical trial of iron supplementation is inexpensive and non-traumatic, patients are often treated without a definitive diagnosis.

Determination of etiology

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.[3]. In addition to dietary insufficiency, malabsorption, chronic blood loss, diversion of iron to fetal erythropoiesis during pregnancy, intravascular haemolysis and haemoglobinuria or other forms of chronic blood loss should all be considered.

Treatment

If the cause is dietary iron deficiency, iron supplements, usually with iron (II) sulfate, ferrous gluconate, or iron amino acid chelate NaFeEDTA, 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 [4]. 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 100mg of Iron.[5].

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 [6].
  • 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.
  • Some people believe 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 [7].

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 haemodialysis. Parenteral iron involves risks of fever, chills, backache, myalgia, dizziness, syncope, rash, anaphylactic shock[8] and secondary iron overload. Epinephrine is used to counter anaphylactic shock, and Chelation therapy is used to manage secondary iron overload [9].

A follow up blood test is essential to demonstrate whether the treatment has been effective.

Note that iron supplements must be kept out of the reach of children, as iron-containing supplements are a frequent cause of poisoning in the pediatric age group.

See also

References

  1. ^ Brady, P. (2007). Iron deficiency anemia: a call for aggressive diagnostic evaluation. Southern Medical Journal, 10(100), 967. Retrieved December 2, 2007, from EbscoHost Research Databases.
  2. ^ Guyatt G, Patterson C, Ali M, Singer J, Levine M, Turpie I, Meyer R (1990). "Diagnosis of iron-deficiency anemia in the elderly.". Am J Med 88 (3): 205-9. PMID 2178409.
  3. ^ Rockey D, Cello J (1993). "Evaluation of the gastrointestinal tract in patients with iron-deficiency anemia". N Engl J Med 329 (23): 1691-5. PMID 8179652.
  4. ^ Rimon E, Kagansky N, Kagansky M, Mechnick L, Mashiah T, Namir M, Levy S (2005). "Are we giving too much iron? Low-dose iron therapy is effective in octogenarians". Am J Med 118 (10): 1142-7. doi:10.1016/j.amjmed.2005.01.065. PMID 16194646.
  5. ^ Kiesewetter, H., Radtke, H., Rocker, L., Mayer, B., & Salama, A. (2004). Iron supplementation and two-unit red blood cell apheresis. Hemapheresis, (44), 1463. Retrieved December 8, 2007, from EbscoHost Research Databases.
  6. ^ Olivares M, Pizarro F, Pineda O, Name JJ, Hertrampf E, Walter T. (Jul 1997). "Milk inhibits and ascorbic acid favors ferrous bis-glycine chelate bioavailability in humans". J Nutr 127 (7): 1407-11. PMID 9202099.
  7. ^ Fischer, R., Hediger, M., Scholl, T., & Scearer, J. (1992). Anemia vs. iron deficiency. The American Journal of Clinical Nutrition, 8(55). Retrieved December 5, 2007, from EbscoHost Research Databases.
  8. ^ http://www.globalrph.com/irondextran.htm
  9. ^ James P. Kushner, John P. Porter and Nancy F. Olivieri (2001). "Secondary Iron Overload". Hematology. PMID 11722978. http://asheducationbook.hematologylibrary.org/cgi/content/full/2001/1/47


 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Iron_deficiency_anemia". A list of authors is available in Wikipedia.
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