Liver, Pancreas, and Biliary TractThe relation of iron status and hemochromatosis gene mutations in patients with chronic hepatitis C☆
Section snippets
Patients
One hundred eighty-four consecutive patients with chronic HCV infection (127 men [69%] and 57 women [31%]; mean age, 48 years; age range, 20–78 years) were studied. Chronic hepatitis C was diagnosed on the basis of increased serum transaminase levels for longer than 6 months and detection of antibody to HCV (anti-HCV) and HCV RNA by polymerase chain reaction (PCR). Patients with secondary causes of iron elevation were excluded, including patients with ethanol consumption of >60 g/day. Before
Results
Table 1 shows the results of analysis for the C282Y and H63D mutations in 184 patients with chronic hepatitis C and in the control group.
WT, wild-type.Mutation status Patients Controls C282Y/C282Y (%) 5 (2.7) 0 H63D/H63D (%) 3 (1.6) 6 (1.2) C282Y/H63D (%) 2 (1.0) 8 (1.6) C282Y/WT (%) 14 (7.6) 39 (8.0) H63D/WT (%) 35 (19.0) 88 (18.1) WT/WT (%) 125 (67.9) 346 (71.0) Total 184 487
Discussion
The results of this study indicate that mutations of the HFE gene contribute in part to the increase of iron parameters in patients with chronic hepatitis C. About half of the patients with biochemical evidence of iron overload carried either of the two mutations associated with genetic hemochromatosis. Possible influences of HFE gene mutations in response to interferon therapy could not be evaluated because patients either did not receive treatment or are involved in ongoing therapy protocols
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Address requests for reprints to: Peter Ferenci, M.D., Department of Internal Medicine IV, Gastroenterology and Hepatology, Währinger Gürtel 18-20, A-1090 Wien, Austria. Fax: (43) 1-40400-4735.