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A case of hereditary haemochromatosis in a patient with extrapyramidal syndrome.

Hereditary haemochromatosis (HH) is a genetic disorder characterised by a progressive accumulation of iron in the body, which can cause progressive tissue damage with dysfunction and failure of the organs involved. The overload of iron is due to changes in the mechanisms regulating the homeostasis of absorption and elimination of iron. Four distinct forms of HH are currently recognised, of which three are transmitted as autosomal recessive disorders and one has a dominant transmission1. The most common form of haemochromatosis (type 1) is due to changes in the HFE gene located on chromosome 6 (p21.3): two mutations, C282Y and H63D, are responsible for most cases of the disease. Subjects homozygous for the C282Y mutation have considerable iron overload and this is the most severe form of the disease. If diagnosed early, haemochromatosis can be successfully treated by removing the excess iron, either by phlebotomy or iron-chelating drugs. 
 
Deposition of iron in the brain has been associated with chronic neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). However, studies carried out so far on a possible correlation between mutations of the HFE gene of HH and the aetiopathogenesis of neurodegenerative diseases, such as AD and PD, have given contradictory results. Here we present the case of a patient with C282Y homozygous HH associated with an extrapyramidal hemisyndrome.