Iron and iron deficiency anemia: what therapists need to know.
Iron is a trace element in humans, but this is a deceptive statement. Of the 3 to 5 grams of iron in the body, only about 2 to 2.5 grams is in hemoglobin, which is contained mostly in red blood cells either in the blood or as precursors in the bone marrow. A moderate amount of iron (about 130 mg) is in myoglobin, the oxygen-carrying protein of muscle. A small (8 mg), but extremely important pool is in tissue where iron is bound to several enzymes that require iron for full activity. These include peroxidases, cytochromes, and many of the Krebs cycle enzymes.
Iron is also stored as ferritin and hemosiderin, primarily in the bone marrow, spleen and liver. This critical pool of iron may be the first to become diminished in iron deficient states.
Iron deficiency is one of the most prevalent disorders known, with 15 percent of the worldwide population affected. Iron deficiency anemia may result from at least four conditions:
1. Nutritional deficiency in which not enough iron is consumed to meet the normal, daily required amount (1 mg in males, higher in females and pregnancy).
2. Faulty or incomplete iron absorption (e.g., achlorhydria in certain disorders or following gastric resection; chronic diarrhea associate with disorders such as celiac disease, sprue or resection of the small bowel; and the absence of factors needed for iron absorption).
3. Increased demand for iron that is not met (e.g., during pregnancy, the growth years, or periods of increased blood regeneration).
4. Excessive loss of iron (e.g., acute or chronic hemorrhage, or heavy menstruation); adult males and postmenopausal females with iron deficiency must be evaluated for abnormal occult bleeding, especially gastrointestinal bleeding.
Iron deficiency may result from several other less commonly occurring conditions, including a disorder of iron utilization, sideroblastic anemia, selected hemoglobinopathies, anemia related to chronic disorders, chronic inflammation, parasitic infections such as hookworm, and a deficiency of the plasma iron transporting protein, transferrin.
Absorption of iron from the intestine is the primary means of regulating the amount of iron within the body. In fact, only about 10 percent of the daily dietary iron is typically absorbed. To be absorbed by intestinal cells, iron must be in the ferrous oxidation state and bound to protein.
Because ferric iron is the predominant form of iron in foods, it must first be reduced to ferrous by agents such as vitamin C before it can be absorbed. In the intestinal mucosal cell, ferrous iron is bound by apoferritin and then oxidized by ceruloplasmin to ferric iron bound to ferritin.
From there, iron is absorbed into the blood by apotransferrin, which becomes transferrin as it binds two ferrous ions. In plasma, transferrin carries and releases iron to the bone marrow, where it is incorporated into hemoglobin of red blood cells. After about four months in circulation, red cells are degraded by the spleen, liver, and macrophages, which return iron to the circulation where it is bound and carried by tranferrin for reuse.
When intracellular iron concentration is low, an iron regulatory protein inhibits the synthesis of apoferritin and promotes the synthesis of transferrin receptor. Newly absorbed iron, or iron released from ferritin, is converted from ferrous to ferric iron by ceruloplasmin, transferred to apotransferrin in the cell, and then released into the circulation as transferrin.
In normal states, both intracellular ferritin and circulating transferrin are only partially saturated. The small amount of circulating ferritin is mostly apoferritin that contains little iron. Transferrin delivers iron to tissue such as bone marrow for synthesis of heme for erythrocytes.
Because this anemia is a condition of low iron, on the patient's chart you would fine the following information: decreased levels of serum iron, percent saturation, ferritin and an increase in transferrin. Because these red blood cells are missing significant amounts of hemoglobin, the cells will appear very "washed out" or hypochromic, and small in size or microcytic. The hemoglobin and hematocrit will also be in the low range with hemoglobin's less than 11 gm%, and hematocrit in the low 30s or less are common.
In closing, consider the following case study as a classic example of iron deficiency anemia. A 10-month old Central American child was seen by a pediatrician. The child was very pale and listless. The following tests were ordered: CBC, platelet count, reticulocyte count, total serum billirubin, total serum iron and total iron-binding capacity (TIBC), and a stool examination for occult blood, ova, and parasites.
The results were as follows: Hemoglobin 5.6 g/dL, Hct 17 percent, RBC 3.5X1012/L, WBC 10.5X109/L, MCV 68.6 fl, MCH 16 pg and MCHC %. Peripheral smear revealed significant anisocytosis, microcytosis, hypochromia and poikilocytosis. There was also normal distribution of platelets.
Additional lab data included platelet count 200X109/L, reticulocyte count 0.5 percent, total serum bilirubin 0.9 mg/dl, serum iron 40 micrograms/dL, and percent saturation of transferrin 8.6 percent. The demonstration of hypochromic, microcytic erythrocytes in a peripheral blood film suggests iron deficiency anemia.
The RBC indices reveal both a decreased MCV and MCH. These findings support the RBC morphology observations of microcytosis and hypochromia. A decreased serum iron and percent saturation were present, along with an increased TIBC. The serum bilirubin and reticulocyte count were normal. No evidence of bleeding or parasitic infections was detected. The most probable cause of this patient's anemia is iron deficiency.
Small children are among the most frequent victims of inadequate dietary iron. The newborn begins life with 350 to 500 mg of iron. A daily intake of 1 mg/kg of body weight is needed during infancy to keep pace with growth. Some iron-poor foods such as milk never become useful sources for the absorption of iron.
Children in underdeveloped countries frequently suffer from a combination of poor diet and parasitic infections. Iron deficiency anemia is a frequent by-product of a dietary consisting largely of milk and unsupplemented by fortified food products during the early years of development.
Don Steinert is an Associate Professor in the Department of Nursing and a faculty member in the RT Program at the Univ. of the District of Columbia.
Don Steinert MA, RRT, MT, CLS
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|Title Annotation:||CLINICAL LABORATORY MEDICINE|
|Publication:||FOCUS: Journal for Respiratory Care & Sleep Medicine|
|Date:||Jan 1, 2010|
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