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Treatment of neuroferritinopathy is focused on managing symptoms associated with chorea and dystonia using standard medications for each. [2] The disorder is progressive and symptoms become worse with age. Fewer than 100 cases of neuroferritinopathy have been reported since its identification in 2001. [2]
The ideal is to increase the body's iron deposits, measured as levels of ferritin in serum, with the aim of reaching a ferritin value between 30 and 100 ng/mL. Another clinical study has shown an increase in ferritin levels in those taking iron compared with others receiving a placebo from persons with LID. [11]
Treatment includes the use of iron chelating agents (such as desferrioxamine) to lower brain and liver iron stores, and to prevent progression of neurologic symptoms. This, combined with fresh-frozen human plasma (FFP) works effectively in decreasing liver iron content. Repetitive use of FFP can even improve neurologic symptoms.
Iron-deficiency anemia is confirmed by tests that include serum ferritin, serum iron level, serum transferrin, and total iron binding capacity. [59] A low serum ferritin is most commonly found. However, serum ferritin can be elevated by any type of chronic inflammation and thus is not consistently decreased in iron-deficiency anemia. [23]
Those with low iron levels are often not discovered because doctors often test only for anemia, rather than the level of ferritin, a blood protein that contains iron and is a marker for stored ...
Iron deficiency, or sideropenia, is the state in which a body lacks enough iron to supply its needs. Iron is present in all cells in the human body and has several vital functions, such as carrying oxygen to the tissues from the lungs as a key component of the hemoglobin protein, acting as a transport medium for electrons within the cells in the form of cytochromes, and facilitating oxygen ...
Diagnosis is based upon identification of symptoms, medical history, family history, and laboratory tests. Blood tests may show high levels of ferritin and low, normal, or high levels of transferrin saturation, depending on the form of hemochromatosis. The diagnosis must be confirmed by genetic testing for SLC40A1 mutations. [14]
Hypochromic anemia may be caused by vitamin B6 deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections (e.g. hookworms) or other diseases (i.e. anemia of chronic disease), therapeutic drugs, copper toxicity, and lead poisoning.