Typical adults lose about 1 mg iron (Fe) per day in shed epidermal and gastrointestinal cells; menstruating females lose on average an additional 0.5 to 1 mg/day from menses. This iron loss is balanced by absorption of a portion of the 10 to 20 mg of iron in a typical US diet. Iron absorption is regulated based on the body's iron stores and is usually in balance with the body's needs. However, because there is no physiologic mechanism to remove iron from the body, iron absorbed in excess of bodily needs (or acquired through repeated transfusion) is deposited in tissues.
Hemosiderosis is focal deposition of iron that typically does not cause tissue damage.
Hemochromatosis (iron overload) is a typically systemic process in which iron deposition can cause tissue damage.
Iron overload may result from hereditary hemochromatosis (a genetic disorder of iron metabolism) or from secondary hemochromatosis, an acquired form of the disease that is due to excess oral intake or absorption of iron or to repeated blood transfusions (1, 2). Morbidity is mainly due to iron accumulation in the endocrine organs (especially the pancreas, gonads, and pituitary), liver, and heart.
African iron overload occurs most often in sub-Saharan Africa among people who consume an iron-rich fermented drink. A genetic component is thought to contribute to the pathogenesis of African iron overload, but no gene has yet been identified.
(See also Iron Poisoning and Idiopathic Pulmonary Hemosiderosis.)
General references
1. Bacon BR, Adams PC, Kowdley KV, et al: Diagnosis and management of hemochromatosis: 2011 Practice Guideline by the AASLD. Hepatology 54 (1): 328–343, 2011.
2. Fleming RE, Ponka P: Iron overload in human disease. New Engl J Med 366:348–359, 2012.
