An interesting exception to this is the testes. Despite the common occurrence of gonadal failure, these organs have a relatively low iron content. Testicular atrophy is generally attributed to pituitary gland involvement. In early stages of the disease, iron deposits in the liver are found mainly in periportal parenchymal cells, especially within lysosomes in the pericanalicular cytoplasm of the hepatocytes. Eventually iron deposition involves hepatocytes in all zones of the liver.
Inflammatory cells are relatively few.
Even in extensive disease, however, foci of iron free hepatocytes may be identified. The finding of iron free foci in patients with hereditary hemochromatosis is considered to be pre-neoplastic. The common denominator of all presentations of hereditary hemochromatosis is excessive iron deposition in parenchymal tissues. This is an important feature when differentiating this condition from forms of secondary iron overload, which are more likely to show a predominance of reticuloendothelial cell iron overload. Confirmation of liver, cardiac, pancreatic, or other disease processes consistent with hemochromatosis should be made on physical exam.