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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 .
Chelation therapy removes iron from the blood. [5] This involves delivering iron chelating agents such as deferoxamine, deferiprone or deferasirox. [5] If iron overload has caused damage to end-organs, this is generally irreversible and may require transplantation. [clarification needed]
There are five types of hereditary hemochromatosis: type 1, 2 (2A, 2B), 3, 4 [9] and 5, [10] all caused by mutated genes. Hereditary hemochromatosis type 1 is the most frequent, and uniquely related to the HFE gene. It is most common among those of Northern European ancestry, in particular those of Celtic descent. [11]
Treatment for hemochromatosis type 3 may include reducing iron levels by removing blood (phlebotomy), iron chelation therapy, diet changes, and treatment for complications of the disease. The purpose of the treatment is to reduce the amount of iron in the body to normal levels, prevent or delay organ damage from excess iron, and maintain normal ...
Ask your doc about an iron infusion. Iron infusions are for people who don’t tolerate supplements well, have a tough time absorbing iron, or for people who need to boost their levels quickly.
In hemochromatosis, this entails frequent phlebotomy granulomatosis, immune suppression is required. Limiting blood transfusions and institution of iron chelation therapy when iron overload is detected are important when managing sickle-cell anemia and other chronic hemolytic anemias.
After the first stage, gastrointestinal symptoms appear to resolve in the latent phase and individuals may show signs of improvement. [2] Following this stage, the iron begins to affect the cells of the body's organs which manifests as numerous systemic signs and symptoms developing after 6 to 72 hours, in the metabolic acidosis phase.
Hepcidin is the master regulator of iron metabolism and, therefore, most genetic forms of iron overload can be thought of as relative hepcidin deficiency in one way or another. For instance, a severe form of iron overload, juvenile hemochromatosis, is a result of severe hepcidin deficiency.