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Hemosiderin or haemosiderin is an iron-storage complex that is composed of partially digested ferritin and lysosomes. The breakdown of heme gives rise to biliverdin and iron. [1] [2] The body then traps the released iron and stores it as hemosiderin in tissues. [3] Hemosiderin is also generated from the abnormal metabolic pathway of ferritin. [3]
Iron in ferritin or hemosiderin can be extracted for release by the RE cells, although hemosiderin is less readily available. Under steady-state conditions, the level of ferritin in the blood serum correlates with total body stores of iron; thus, the serum ferritin FR5Rl is the most convenient laboratory test to estimate iron stores.
Hemosiderin deposition in the lungs is often seen after diffuse alveolar hemorrhage, which occurs in diseases such as Goodpasture's syndrome, granulomatosis with polyangiitis, and idiopathic pulmonary hemosiderosis. Mitral stenosis can also lead to pulmonary hemosiderosis. Hemosiderin collects throughout the body in hemochromatosis.
Iron can be stored in ferritin as ferric iron due to the ferroxidase activity of the ferritin heavy chain. [28] Dysfunctional ferritin may accumulate as hemosiderin, which can be problematic in cases of iron overload. [29] The ferritin storage iron pool is much larger than the labile iron pool, ranging in concentration from 0.7 mM to 3.6 mM. [25]
Iron can be stored in ferritin as ferric iron due to the ferroxidase activity of the ferritin heavy chain. [43] Dysfunctional ferritin may accumulate as hemosiderin, which can be problematic in cases of iron overload. [44] The ferritin storage iron pool is much larger than the labile iron pool, ranging in concentration from 0.7 mM to 3.6 mM. [40]
Blood ferritin may be increased with a number of other conditions, so is less reliable for diagnosis. [4] A liver biopsy may be used, which is the most accurate diagnostic technique. [4] The level of siderosis seen in a liver biopsy can be graded by severity. [2]
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Iron overload (also known as haemochromatosis or hemochromatosis) is the abnormal and increased accumulation of total iron in the body, leading to organ damage. [1] The primary mechanism of organ damage is oxidative stress, as elevated intracellular iron levels increase free radical formation via the Fenton reaction.