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Hereditary Hemochromatosis (HH) is called Bronze Diabetes as the skin of the sufferers of this disease turns bronze due to iron overload that usually accompanies this disease. Healthy people usually store up to 4 grams of iron in their body while patients with hemochromatosis exceed this limit. This extra iron distributes all over the body staring with liver and ending with pancreas, heart, pituitary glands and skin. The most common clinical symptoms of the disease include, deep fatigue, joint pain, erectile dysfunction, diabetes, cardiomegaly, Jaundice, cirrhotic liver and cancer. Bronze diabetes is diagnosed phenotypically by the detection of ferritin, total binding and transferrin saturation in serum samples. Bronze diabetes is treated by phelobotomy which means draining the blood from the body. Phelobotomies are carried out on weeky basis until the serum levels of ferritin are down as well as the transferrin saturation. Once this goal is achieved, this process is repeated every few months. In this study, we are attempting to highlight the role of transferrin oxidative modification and carbonyl atress in pathophysiology of HH.
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