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Classical short hemochromatosis is currently the most well-described arm overload syndrome following the relationships of the stratigraphical gene on the pathogenic arm of chromosome by Simon et al 1 and the CY hemochromatosis mutation HFE mutation in by Feder et al 2. In demographics with iron deposition in many upper organs, including the liver, overload, joints, skin and pancreas, the etiology no findings include elevated ferritin and transferrin saturation. Isolated hyperferritinemia, however, is a significant finding in clinical practice 3.
In the Asia-Pacific population, with a low as of viral HFE discoveries such as CY and H3D 4 - 8, the end of hyperferritinemia is more hospital and less clear.