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There are two main types of hemochromatosis, primary and secondary, as well as two subtypes, juvenile and neonatal. Primary hemochromatosis is by far the most common variety of this disease and goes by the names of classic hereditary hemochromatosis, HFE-related hemochromatosis, hemochromatosis type I, and bronze diabetes. This type of hemochromatosis is usually inherited from an individual’s parents and the accumulation of iron occurs slowly over time. Moreover,  primary hemochromatosis affects white people of northern European descent more often than it affects individuals of other ethnicities. That is to say, Hispanics, African Americans, Asians, and Pacific Islanders are less prone to the disorder. Because primary hemochromatosis is hereditary, those with first-degree relatives who suffer from hemochromatosis should get tested to see if they themselves carry the gene.

Secondary hemochromatosis differs from primary hemochromatosis in that it is caused by various conditions rather than genetic factors. These conditions generally include chronic liver disease, frequent blood transfusions, excess oral intake of iron, kidney dialysis, myelodysplastic syndrome, and certain kinds of anemia. Individuals with erythropoiesis disorders are at a heightened risk of secondary hemochromatosis since the production of red blood cells in these people is altered. Disorders of the erythropoiesis system include sickle cell anemia, thalassemia, X-linked sideroblastic anemia, hereditary spherocytosis, congenital dyserythropoietic anemia, and pyruvate kinase deficiency. Another difference between primary and secondary hemochromatosis is that phlebotomy is not a treatment option for the latter. Instead, the oral iron-chelating agent called deferasirox is often used to treat iron overload in patients with secondary hemochromatosis.

Juvenile hemochromatosis is a rare condition that mainly affects individuals between 10 and 30 years of age, though symptoms vary greatly from one sufferer to the next. This type of hemochromatosis looks very similar to primary hemochromatosis, but affects individuals earlier in life and is accompanied by more severe symptoms. As such, complications can quickly become life-threatening if left untreated. The gene mutations that cause juvenile hemochromatosis are different from those that cause classic hereditary hemochromatosis in that the mutations must occur in the HJV or HAMP genes, or both. One of the most common symptoms associated with juvenile hemochromatosis is hypogonadotropic hypogonadism, which means that little to no sex hormone is produced by the primary reproductive organs due to issues with the hypothalamus or pituitary gland.

Neonatal hemochromatosis affects both fetuses and newborns, the cause of which is not entirely understood but is most likely related to a severe form of fetal liver disease. While the fetus develops in the womb during pregnancy, liver damage occurs and causes abnormal accumulation of iron, resulting in stillbirth, growth delays, and premature birth. Neonatal hemochromatosis affects equal numbers of males and females, though doctors have yet to determine why some have only mild symptoms and others are more severely affected. Interestingly enough, a woman who gives birth to a child with neonatal hemochromatosis will likely have another child with the same condition, which points to the fact that this type of hemochromatosis is not inherited, but rather familial and congenital.