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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.
This finding is consistent with the concept that excess iron metabolism is a primary cause of haemochromatosis disease. [ 83 ] Finally, in 1976, Marcel Simon and his collaborators confirmed that haemochromatosis is an autosomal recessive disorder that has a link to the human leukocyte antigen (HLA) region of the genome.
Hemosiderin may deposit in diseases associated with iron overload. These diseases are typically diseases in which chronic blood loss requires frequent blood transfusions, such as sickle cell anemia and thalassemia, though beta thalassemia minor has been associated with hemosiderin deposits in the liver in those with non-alcoholic fatty liver ...
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]
Autoimmune diseases that affect the GI tract “can prevent a person from absorbing iron from the foods that they eat, even if they're eating iron-rich foods,” says Dr. Danielle Nance, a ...
For instance, a severe form of iron overload, juvenile hemochromatosis, is a result of severe hepcidin deficiency. The majority of cases are caused by mutations in the hemojuvelin gene (HJV or RGMc/repulsive guidance molecule c). The exceptions, people who have mutations in the gene for ferroportin, prove the rule: these people have plenty of ...
In women, iron deficiency anemia has also been linked to mortality during pregnancy, lower birth rates, difficulty with milk production and possible lower IQs in children if the iron deficiency ...
Type 4 hemochromatosis is caused by mutations of the SLC40A1 gene, located on the long arm of chromosome 2, specifically at 2q32.2. The SLC40A1 gene encodes ferroportin, a protein responsible for exporting iron from cells in the intestine, liver, spleen, and kidney, as well as from reticuloendothelial macrophages and the placenta.