Iron deficiency anemia transfusion

The richest dietary sources of total iron are organ meats (liver and kidney), egg yolk, dried legumes, com, molasses and parsley. Liver is particularly valuable because of the high absorbability of its iron. However, only about 10% of dietary iron is absorbed. Iron deficiency anemia can be treated with soluble iron(II) compounds providing 200 mg in three or four daily divided doses. Oral iron(II) sulfate is the least expensive and is in wide use. Ascorbic acid increases the absorption efficiency of iron(II) sulfate. Parenteral administration of iron is used when oral iron is ineffective. Iron-dextran, a colloid formed from iron(III) chloride and an alkali-modified dextran, is one of several preparations available which has found extensive clinical use. It contains up to 28% Fe by weight and has a structural similarity to ferritin. Transfusion therapy may also be used in severe chronic anemia or acute hemorrhage. 

Under normal circumstances, transferrin is one-fourth to one-third saturated with iron. The level of saturation may decrease in systemic infection or cancer and in iron deficiency anemia, the most common nutritional deficiency in the United States. In individuals with iron deficiency anemia, transferrin levels are increased. The level of saturation with iron increases in iron overload syndromes such as hereditary hemochromatosis or as a result of repeated blood transfusions, as is the case in thalassemia patients. Determinations of total plasma iron (TI) and plasma total iron binding capacity (TIBC) are routinely performed in the clinical biochemistry laboratory. The TIBC value reflects transferrin levels in plasma the amount of iron that can be bound by transferrin is equal to TIBC x 0.7. Total plasma iron levels in iron deficiency anemia become abnormal before hemoglobin levels show any change. 

Surprisingly, individuals with hemoglobin levels as low as 20 to 30 mg Hb/ml can continue to be physically active. This is due to adaptive mechanisms involving an increase in the heart rate and an increase in efficiency of extraction of oxygen from the blood. Experiments with rats have revealed that the decreased work capacity of the iron-deficient animals, as determined by their ability to run, was due to a deficiency in the enzymes of the respiratory chain of muscle, as well as to anemia. In short, transfusion with normal blood failed to restore fully the running capacity of the deficient animals. 

When used in patients without iron overload, deferoxamine can cause iron deficiency (12). In 20 patients, there were falls in ferritin concentrations in six, requiring withdrawal of deferoxamine and parenteral administration of iron dextran (12). Monitoring ferritin concentrations is therefore recommended in patients receiving deferoxamine for aluminium overload. On the other hand, the administration of deferoxamine (500mg/day by subcutaneous infusion) improves chronic anemia in patients with rheumatoid arthritis (77). This effect is thought to be achieved through increased erythropoietin responsiveness, secondary to iron chelation. Iron chelation with deferoxamine also improves hemopoiesis in patients with myelodysplastic syndromes and can reduce transfusion dependency (78). Exactly how deferoxamine works in these patients remains to be explained. 

Secondary hemochromatosis is the consequence of the uicreased administration and absorption of iron. The administration of iron includes that given with the transfusions that are required in certain anemic patients and the ill-advised and unfortunate administration of iron to anemic patients who are not actually iron deficient. The most common causes of secondary hemochromatosis are thalassemia major and acquired myelodysplastic states, but there are many other circumstances in which secondary iron overload occurs, including pyruvate kinase deficiency and congenital dyserythropoietic anemias. 

Albumin (human) Epoetin alfa contains albumin, a derivative of human blood. Based on effective donor screening and product manufacturing processes, it carries an extremely remote risk for transmission of viral diseases. No cases of transmission of viral diseases or Creutzfeldt-Jakob disease have ever been identified for albumin. Anemia Not intended for CRF patients who require correction of severe anemia epoetin alfa may obviate the need for maintenance transfusions but is not a substitute for emergency transfusion. Not indicated for treatment of anemia in HIV-infected patients or cancer patients due to other factors such as iron or folate deficiencies, hemolysis, or Gl bleeding, which should be managed appropriately. Hypertension Up to 80% of patients with CRF have a history of hypertension. Do not treat patients with uncontrolled hypertension monitor blood pressure adequately before initiation of therapy. Hypertensive encephalopathy and seizures have occurred in patients with CRF treated with epoetin. 

In other reports from Canada and the UK, patients typically developed sudden worsening of anemia unresponsive to increasing doses of epoetin alfa or any other form of erythropoietin and became transfusion dependent (85). In patients who develop sudden lack of efficacy or worsening of anemia, typical causes of non-response (for example deficiencies of iron, folate, and vitamin B12, infection or inflammation, blood loss, hemolysis, and aluminium intoxication) should be investigated. If pure red cell aplasia is suspected and no cause can be identified, erythropoietin antibodies should be sought. 

Most patients who require dialysis have a normocytic normochronic anemia and a hypoproliferative bone marrow. As erythropoiesis decreases with advancing renal disease, iron shifts from circulating red cells to the reticuloendothelial system, leading to high serum ferritin levels. Repeated blood transfusion is also a common cause of iron overload and hyperferritinemia. Clearly the most important cause of the anemia of chronic renal failure is decreased erythropoietin production by the kidneys uremic patients have much lower plasma erythropoietin levels than comparably anemic patients with normal renal function (E8). Less important causes are shortened red cell survival, iron or folate deficiency, aluminum intoxication, and osteitis fibrosa cystica (E8). Uremic retention products such as methylguanidine (G10) and spermidine (R2) may also have an adverse effect on erythropoiesis. 

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