some studies show that women pregnant during their teenage years can be at greater risk of iron-deficiency anemia due to an already increased need for iron and other nutrients during adolescent growth spurts. children babies are at increased risk of developing iron deficiency anemia due to their rapid growth. their need for iron is greater than they are getting in their diet. babies are born with iron stores; however, these iron stores typically run out by 4–6 months of age. in addition, infants who are given cow's milk too early can develop anemia due to gastrointestinal blood loss. children who are at risk for iron-deficiency anemia include: preterm infants low birth weight infants infants fed with cow's milk under 12 months of age breastfed infants who have not received iron supplementation after age 6 months, or those receiving non-iron-fortified formulas children between the ages of 1 to 5 years old who receive more than 24 ounces (700 ml) of cow milk per day children with low socioeconomic status children with special health care needs children of hispanic ethnicity children who are overweight blood donation frequent blood donors are also at risk for developing iron deficiency anemia. when whole blood is donated, approximately 200 mg of iron is also lost from the body. the blood bank screens people for anemia before drawing blood for donation. if the patient has anemia, blood is not drawn. less iron is lost if the person is donating platelets or white blood cells. hepcidin decreased levels of serum and urine hepcidin are early indicators of iron deficiency. hepcidin concentrations are also connected to the complex relationship between malaria and iron deficiency. mechanism anemia can result from significant iron deficiency. when the body has sufficient iron to meet its needs (functional iron), the remainder is stored for later use in cells, mostly in the bone marrow and liver. these stores are called ferritin complexes and are part of the human (and other animals) iron metabolism systems. men store about 3.5 g of iron in their body, and women store about 2.5 g. hepcidin is a peptide hormone produced in the liver that is responsible for regulating iron levels in the body. hepcidin decreases the amount of iron available for erythropoesis (red blood cell production). hepcidin binds to and induces the degradation of ferroportin, which is responsible for exporting iron from cells and mobilizing it to the bloodstream. conditions such as high levels of erythropoesis, iron deficiency and tissue hypoxia inhibit hepcidin expression. whereas systemic infection or inflammation (especially involving the cytokine il-6) or increased circulating iron levels stimulate hepcidin expression. iron is a mineral that is important in the formation of red blood cells in the body, particularly as a critical component of hemoglobin. about 70% of the iron found in the body is bound to hemoglobin. iron is primarily absorbed in the small intestine, in particular the duodenum and jejunum. certain factors increase or decrease absorption of iron. for example, taking vitamin c with a source of iron is known to increase absorption. some medications such as tetracyclines and antacids can decrease absorption of iron. after being absorbed in the small intestine, iron travels through blood, bound to transferrin, and eventually ends up in the bone marrow, where it is involved in red blood cell formation. when red blood cells are degraded, the iron is recycled by the body and stored. when the amount of iron needed by the body exceeds the amount of iron that is readily available, the body can use iron stores (ferritin) for a period of time, and red blood cell formation continues normally. however, as these stores continue to be used, iron is eventually depleted to the point that red blood cell formation is abnormal. ultimately, anemia ensues, which by definition is a hemoglobin lab value below normal limits. diagnosis blood smear of a person with iron-deficiency anemia at 40x enhancement conventionally, a definitive diagnosis requires a demonstration of depleted body iron stores obtained by bone marrow aspiration, with the marrow stained for iron. however, with the availability of reliable blood tests that can be more readily collected for iron-deficiency anemia diagnosis, a bone marrow aspiration is usually not obtained. furthermore, a study published april 2009 questions the value of stainable bone marrow iron following parenteral iron therapy. once iron deficiency anemia is confirmed, gastrointestinal blood loss is presumed to be the cause until proven otherwise since it can be caused by an otherwise asymptomatic colon cancer. initial evaluation must include esophagogastroduodenoscopy and colonoscopy to evaluate for cancer or bleeding of the gastrointestinal tract. a thorough medical history is important to the diagnosis of iron-deficiency anemia. the history can help to differentiate common causes of the condition such as a menstruation in woman or the presence of blood in the stool. a travel history to areas in which hookworms and whipworms are endemic may also be helpful in guiding certain stool tests for parasites or their eggs. although symptoms can play a role in identifying iron-deficiency anemia, they are often vague, which may limit their contribution to determining the diagnosis. blood tests change in lab values in iron deficiency anemia change parameter ↓ ferritin, hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin ↑ total iron-binding capacity, transferrin, red blood cell distribution width anemia is often discovered by routine blood tests. a sufficiently low hemoglobin by definition makes the diagnosis of anemia, and a low hematocrit value is also characteristic of anemia. further studies will be undertaken to determine the anemia's cause. if the anemia is due to iron deficiency, one of the first abnormal values to be noted on a complete blood count, as the body's iron stores begin to be depleted, will be a high red blood cell distribution width, reflecting an increased variability in the size of red blood cells. a low mean corpuscular volume also appears during the course of body iron depletion. it indicates a high number of abnormally small red blood cells. a low mean corpuscular volume, a low mean corpuscular hemoglobin or mean corpuscular hemoglobin concentration, and the corresponding appearance of red blood cells on visual examination of a peripheral blood smear narrows the problem to a microcytic anemia (literally, a small red blood cell anemia). the blood smear of a person with iron-deficiency anemia shows many hypochromic (pale, relatively colorless) and small red blood cells, 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 hypochromic, pencil-shaped cells and, occasionally, small numbers of nucleated red blood cells. the platelet count may be slightly above the high limit of normal in iron-deficiency anemia (termed a mild thrombocytosis), but severe cases can present with thrombocytopenia (low platelet count). iron-deficiency anemia is confirmed by tests that include serum ferritin, serum iron level, serum transferrin, and total iron binding capacity. a low serum ferritin is most commonly found. however, serum ferritin can be elevated by any type of chronic inflammation and thus is not consistently decreased in iron-deficiency anemia. serum iron levels may be measured, but serum iron concentration is not as reliable as the measurement of both serum iron and serum iron-binding protein levels. the percentage of iron saturation (or transferrin saturation index or percent) can be measured by dividing the level of serum iron by total iron binding capacity and is a value that can help to confirm the diagnosis of iron-deficiency anemia; however, other conditions must also be considered, including other types of anemia. another finding that can be used is the level of red blood cell distribution width. during haemoglobin synthesis, trace amounts of zinc will be incorporated into protoporphyrin in the place of iron which is lacking. protoporphyrin can be separated from its zinc moiety and measured as free erythrocyte protoporphyrin, providing an indirect measurement of the zinc-protoporphyrin complex. the level of free erythrocyte protoporphyrin is expressed in either μg/dl of whole blood or μg/dl of red blood cells. an iron insufficiency in the bone marrow can be detected very early by a rise in free erythrocyte protoporphyrin. further testing may be necessary to differentiate iron-deficiency anemia from other disorders, such as thalassemia minor. it is very important not to treat people with thalassemia with an iron supplement, as this can lead to hemochromatosis. a hemoglobin electrophoresis provides useful evidence for distinguishing these two conditions, along with iron studies. screening it is unclear if screening pregnant women for iron-deficiency anemia during pregnancy improves outcomes in the united states. the same holds true for screening children who are 6 to 24 months old. even so, screening is a level b recommendation suggested by the us preventative services task force in pregnant women without symptoms and in infants considered high risk. screening is done with either a hemoglobin or hematocrit lab test. treatment