Hemosiderin is an iron storage complex found in cells as opposed to circulating in the blood. Hemosiderin is usually found in macrophages and abundant in situations following hemorrhage but can accumulate in different organs in hemochromatosis.
Primary hemochromatosis is caused by a mutation in the HFE gene on chromosome 6. This mutation is inherited in an autosomal recessive fashion.
There is a higher frequency of HLA A3 serotypes in individuals with hemochromatosis.
Excessive iron accumulation can also occur secondary to parenteral iron administration for example with multiple transfusion therapies. Individuals at high risk for secondary hemochromatosis include individuals with chronic blood disorders like beta thalassemia major.
Hemochromatosis is a disease characterized by excessive accumulation of iron in the body, most of which becomes deposited in organs such as the liver, pancreas, joints and heart.
Ferritin is a protein that stores and releases iron. Because hemochromatosis is characterized by increased iron absorption, there is increased ferritin levels in the body.
Transferrins are blood plasma glycoproteins that bind iron and control the level of free iron in biological fluids. When there are increased iron stores in the body, transferrin levels decrease. Furthermore, an increase in iron means that transferrin is fully saturated, leading to a decreased total iron binding capacity in the blood (TIBC). Thus, patients have decreased transferrin levels, decreased TIBC, but increased transferrin saturation percentage.
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