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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]
[7] [8] Risk factors for the development of arthritis in those with hemochromatosis include elevated iron levels (ferritin greater than 1000 or transferrin saturation greater than 50%) for an extended period of time, increasing age and concurrent advanced liver fibrosis. [7] skin: melanoderma (darkening or 'bronzing' of the skin). [8] [9]
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 ...
Fasting transferrin saturation is a better test to detect HH. [14] [55] Transferrin saturation greater than 62% is suggestive of homozygosity for mutations in the HFE gene. [56] Ferritin, a protein synthesized by the liver, is the primary form of iron storage within cells and tissues.
Transfusional hemosiderosis can be inferred with a blood transferrin test. Blood ferritin may be increased with a number of other conditions, so is less reliable for diagnosis. [4] A liver biopsy may be used, which is the most accurate diagnostic technique. [4] The level of siderosis seen in a liver biopsy can be graded by severity. [2]
Elevated serum ferritin, an indicator of blood iron levels, and transferrin saturation, which is involved with absorption of iron from the gut, are very common. [2] [3] Transferrin saturation may approach or reach 100%, where a normal value would lie between 16% and 45%. If transferrin saturation is normal, juvenile hemochromatosis can be ruled ...
Transferrin and TIBC Percent transferrin saturation; Iron deficiency anemia: Low High. The liver produces more transferrin, presumably attempting to maximize use of the little iron that is available. Low, as there is insufficient iron. Anemia of chronic disease: Low, as the body holds iron intracellularly with ferritin. Low.
The typical constellation of findings is indicative: The patients show a postprandial non-responsive and too low and static transferrin level (hypotransferrinemia) with high transferrin saturation (usually > 55 %) and low ferritin value. Multiple tests are obligatory due to physiologically induced fluctuations.