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The term hemochromatosis was initially used to refer to what is now more specifically called hemochromatosis type 1 (or HFE-related hereditary hemochromatosis). Currently, hemochromatosis (without further specification) is mostly defined as iron overload with a hereditary or primary cause, [11] [12] or originating from a metabolic disorder. [13]
There are five types of hereditary hemochromatosis: type 1, 2 (2A, 2B), 3, 4 [9] and 5, [10] all caused by mutated genes. Hereditary hemochromatosis type 1 is the most frequent, and uniquely related to the HFE gene. It is most common among those of Northern European ancestry, in particular those of Celtic descent. [11]
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Over time, iron stores increase, and individuals with type 4A hemochromatosis may develop hepatic fibrosis. [3] The symptoms of type 4B hemochromatosis tend to be more severe. They resemble the symptoms of hemochromatosis types 1, 2, and 3. Plasma iron concentration is elevated, and symptoms include joint pain, diabetes, and arrhythmia.
The gene involved with patients diagnosed with type 3 hemochromatosis is TFR2 ( or HFE3). HFE (not the same as HFE3) is most often the cause of hereditary hemochromatosis. [14] The HFE gene provides instructions for producing a protein that is located on the surface of cells, primarily liver and intestinal cells.
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[20] [21] The homozygous H63D variant is an indicator of the iron metabolism disorder hemochromatosis, which may increase the risk of developing a fatty liver. [22] In patients with a cirrhotic liver, the mutation can increase the rate of liver cancer. [6] [23] [24]