African iron overload (Bantu siderosis) results from the combination of a dietary component (a traditional beer that contains iron) and an unknown susceptibility gene. Mutations in the HFE
C-termini are denoted (N and C). The residue lengths of the loops are denoted by numbers adjacent to each loop. Mutations are clustered at either end of TM helices 1 and 3 or at the extracellular loop at the C-terminal end of the helix (from Worwood 2004 with permission).
gene have been excluded but mutations of the ferroportin gene may play a role (see above). Iron deposition, as in type 4 haemochromatosis, occurs both in hepatocytes and in reticu-loendothelial cells. Serum ferritin is usually elevated, but transferrin saturation may be normal. The condition occurs in sub-Saharan Africa. It is a cause of hepatic fibrosis and cirrhosis, and associations with diabetes mellitus, peritonitis, scurvy and osteoporosis have been described. The iron overload is associated with a poor outcome in tuberculosis, an infection that is highly prevalent in sub-Saharan Africa.
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