The mechanism of excessive iron storage in patients with hereditary 
hemochromatosis caused by mutations of the HFE gene seems to be a failure to 
up-regulate hepcidin in the face of increased body iron. Since the cytokines 
IL-1 and IL-6 stimulate hepcidin transcription in the absence of HFE, chronic 
inflammatory states might counteract the effect of HFE mutations. We measured 
the pre-phlebotomy plasma levels of C reactive protein (CRP) and of interleukin 
6 (IL-6) in homozygotes for the C282Y mutation of HFE. There was no difference 
in these levels in subjects with high iron stores than in those with low iron 
stores, suggesting that the phenotypic differences between such homozygotes is 
not appreciably affected by ongoing chronic inflammation.