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Pigments dervied from Hemoproteins: click here Primary Hemochromatosis: click here Local accumulations of hemosiderin (hemosiderosis) occur regularly around areas of bruising and hemorrhage and in lungs and spleen subjected to the protracted congestion that accompanies recurrent heart failure. In each instance the pigment is localized in cells of the reticuloendothelial cells. In the lungs hemosiderin-laden macrophages are appropriately referred to as "heart failure cells". The pigment imparts a deep brown colour to tissues and organs when it is present in high concentrations. The generalized form of this condition, also referred to as secondary hemochromatosis, is most commonly encountered in patients who have received repeated blood transfusions or more rarely after prolonged parenteral administration of iron. It can also occur in patients with chronic ineffective erythropoiesis (such as thalassemia major), presumably from increased absorption of dietary iron across the duodenal mucosa.
Alcohol ingestion when carried to extremes can lead to hemosiderosis because of increase of iron uptake by alcohol. Wines, which are rich in iron, place the alcoholic in double jeopardy. In the south African Bantu there is an added interesting facet in that the alcoholic beverages are conventionally prepared in iron pots, which probably serve as an abundant source of additional dietary iron (estimated to be as high as 100 mg per day). Although iron deposition in hemosiderosis is initially limited to the reticuloendothelial system, with time the parenchymal cells of the liver, kidney, and heart are also affected and the condition becomes clinically and pathologically indistinguishable from primary hemochromatosis.
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