Secondary iron overload is more common than hereditary hemochromatosis and arises from conditions such as transfusions, ineffective erythropoiesis, and chronic liver diseases. Iron absorption is regulated by hepcidin, which suppresses ferroportin when iron levels are high, reducing plasma iron entry.
Secondary iron overload is more common than hereditary hemochromatosis and arises from conditions such as transfusions, ineffective erythropoiesis, and chronic liver diseases. Iron absorption is regulated by hepcidin, which suppresses ferroportin when iron levels are high, reducing plasma iron entry. Diagnosing iron overload involves assessing transferrin saturation (TSAT >45%) and ferritin levels, though ferritin can be elevated due to inflammation or malignancy. Non-invasive imaging, particularly MRI, is preferred for measuring liver iron content, as it correlates well with biopsy results.
Secondary iron overload is linked to various conditions, including iron-loading anemias (e.g., thalassemia, myelodysplastic syndromes, sickle cell disease) and chronic liver diseases (e.g., non-alcoholic fatty liver disease [NAFLD], alcoholic liver disease [ALD], viral hepatitis). Thalassemia is a leading cause due to frequent transfusions and suppressed hepcidin, with risks of fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). NAFLD and ALD are also associated with iron overload, contributing to worse outcomes and advanced fibrosis. Hepatitis C virus (HCV) suppresses hepcidin, increasing iron absorption, while hepatitis B virus (HBV) with HDV co-infection correlates with advanced fibrosis.
Treatment depends on the cause: phlebotomy for hereditary hemochromatosis and post-transplant cases without anemia, and iron chelators for transfusion-dependent conditions like thalassemia. No proven therapies currently exist for NAFLD-, hepatitis-, or ALD-related iron overload.
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