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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.
Elevated levels of methemoglobin in the blood are caused when the mechanisms that defend against oxidative stress within the red blood cell are overwhelmed and the oxygen carrying ferrous ion (Fe 2+) of the heme group of the hemoglobin molecule is oxidized to the ferric state (Fe 3+). This converts hemoglobin to methemoglobin, resulting in a ...
Both these phenomena occur in thalassaemias, with blood transfusion therapy being the major cause of iron overload in thalassaemia major and increased GI absorption being more important in patients with intermedia thalassaemia who are not frequently transfused. Each unit of blood contains about 200 mg iron.
In sideroblastic anemia, the body has iron available but cannot incorporate it into hemoglobin, which red blood cells need in order to transport oxygen efficiently. The disorder may be caused either by a genetic disorder or indirectly as part of myelodysplastic syndrome , [ 2 ] which can develop into hematological malignancies (especially acute ...
Hemolytic anemia or haemolytic anaemia is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), either in the blood vessels (intravascular hemolysis) or elsewhere in the human body (extravascular). [2]
Normally, HFE facilitates the binding of transferrin, which is iron's carrier protein in the blood. Transferrin levels are typically elevated at times of iron depletion (low ferritin stimulates the release of transferrin from the liver). When transferrin is high, HFE works to increase the intestinal release of iron into the blood.
However, a varied size distribution of red blood cells is a hallmark of iron deficiency anemia, and as such shows an increased RDW in virtually all cases. In the case of both iron and B 12 deficiencies, there will normally be a mix of both large cells and small cells, causing the RDW to be elevated.
The structure of cytochrome b5 reductase, the enzyme that converts methemoglobin to hemoglobin. [1]Methemoglobin (British: methaemoglobin, shortened MetHb) (pronounced "met-hemoglobin") is a hemoglobin in the form of metalloprotein, in which the iron in the heme group is in the Fe 3+ state, not the Fe 2+ of normal hemoglobin.
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