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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 .
The human body has protective mechanisms in place to prevent excess free ferric iron from circulating the body. When being transported throughout the body, iron is bound to an iron transporting protein called transferrin to prevent iron from being absorbed into different cells. [6] Any excess iron is stored as ferritin in the liver. [6]
Excessive iron can lead to a condition called hemochromatosis, which may damage organs like the liver, heart and pancreas. Symptoms of iron overload include fatigue, skin discoloration, and joint ...
Haemochromatosis is protean in its manifestations, i.e., often presenting with signs or symptoms suggestive of other diagnoses that affect specific organ systems.Many of the signs and symptoms below are uncommon, and most patients with the hereditary form of haemochromatosis do not show any overt signs of disease nor do they have premature morbidity, if they are diagnosed early, but, more ...
The human body lacks a mechanism to excrete excess iron. Iron accumulation is toxic to many tissues, causing heart failure, cirrhosis, liver cancer, growth retardation and endocrine abnormalities. In the absence of regular iron chelation therapy, the iron loading rates vary.
Siderosis is the deposition of excess iron in body tissue. When used without qualification, it usually refers to an environmental disease of the lung, also known more specifically as pulmonary siderosis or Welder's disease, which is a form of pneumoconiosis.
Iron deficiency can cause a slew of symptoms ... “Too much iron can lead ... You can also pair iron with vitamin C and avoid things that can limit your body’s absorption of iron, like calcium ...
The body has limited ways to store and remove iron. When red blood cells (RBCs) die, they are consumed by macrophages. Transfused RBCs have shorter lifespans that native ones, so they die and are consumed more frequently by the macrophages, which causes the latter to die from excess iron which is then released into the blood. [2]