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Secondary iron overload can result from thalassemias or sideroblastic anemias, both disorders of erythropoiesis. Secondary acquired iron overload can occur after exogenous iron administration, repeated or unusually massive transfusion, or iron-dextran treatments. Each unit of blood transfused provides 250 mg of iron. Significant tissue deposition is likely with ≥ 20 g (ie, about 80 units of blood). Overload also can occur in conditions of defective erythropoiesis, such as thalassemia, sideroblastic anemia, hemoglobinopathies, and RBC enzyme defects. With defective erythropoiesis, iron absorption increases, possibly mediated by hepcidin. These conditions of defective erythropoiesis themselves can usually be identified by clinical history. Iron overload is identified by the elevations in serum iron, transferrin saturation, and serum ferritin.
Phlebotomy may not be helpful, because these disorders sometimes cause anemia, thereby limiting the ability to remove enough blood. If anemia is present, deferoxamine (1 to 2 g once/day over 8 to 24 h in adults; 20 to 40 mg/kg/day over 8 to 12 h in children) should be given as a slow IV infusion overnight through a small portable subcutaneous pump for 5 to 7 days/wk; this process effectively reduces iron stores. Because tachyphylaxis occurs with deferoxamine therapy, continued efficacy must be evaluated (usually by urine iron measurement). Alternatively, salmon-colored urine confirms > 50 mg/day of iron in the urine. Treatment goals and monitoring (with serum iron levels and transferrin) are the same as for primary hemochromatosis (see Iron Overload: Primary Hemochromatosis).
Overload
of Unknown Origin
Parenchymal liver diseases, especially alcoholic liver disease, nonalcoholic steatohepatitis, and chronic hepatitis C infection, can be associated with increased iron storage. The mechanisms are unknown, although primary hemochromatosis can exist simultaneously and should be excluded. Reducing iron stores does not appear to relieve liver dysfunction if these patients do not have primary hemochromatosis.
Last full review/revision November 2005
Content last modified November 2005
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