Hepatic Iron Accumulation Is An Independent Risk Factor For The Development Of Hepatocellular Carcinoma After Interferon Therapy In Patients With Chronic Hepatitis C
     Namiki Izumi, Yasuhiro Asahina, Masakatsu Uchihara, Noguchi Osamu, Nobuhiko Kanazawa, Jun Itakura, Shozo Miyake, Takahiro Sakai, Musashino Red-Cross Hosp, Tokyo Japan

Note: Iron levels can be measured in blood. However, dietary restrictions on the amount of red meat intake are controversial. There is concern among patients that eating red meat can raise iron stores in liver and cause harm. But, there is little evidence this is true. If a person has decompensated cirrhosis and encepholopathy, limiting protein intake is generally recommended. In other circumstances, hepatitis treating physicians do not in general recommend eliminating red meat from diet in HCV-infected patients. But, drawing blood to test iron levels can be done. As there may be individual circumstances in which diet changes may be appropriate. See "Diet & Hepatitis C" article written for NATAP by Jocelyn Rodriguez, MPH, RD, CDN.

Hepatocellular carcinoma (HCC) is a life-threatening complication in patients with chronic hepatitis C, even after interferon (IFN) therapy. Hepatic iron has been shown to be associated with an decreased efficacy of IFN therapy, the relationship between hepatic iron accumulation and the development of HCC has not been adequately examined. We carried out a cohort study whether hepatic iron accumulation is an independent risk for the development of HCC in patients with hepatitis C treated with high dose of IFN.178 patients with chronic hepatitis C without cirrhosis were included in the present study. Hepatic iron content was measured by atomic absorption spectroscopy after homogenization of the biopsied materials before initiating IFN therapy. All patients were treated with a total doses of IFN-alfa exceeding 480 MU and their clinical course was greater than three years after IFN therapy. Twelve risk factors including gender, age, plasma HCV-RNA level, genotype of HCV, total dose of administered IFN, ALT and platelet count before IFN therapy, history of drinking alcohol more than 80 g per day, fibrosis and activity score of the liver, virological outcome of IFN therapy and hepatic iron content were evaluated for HCC. HCC developed in 14 of 178 patients studied. Univariate Kalpan-Meier method and Logrank test revealed that HCC-free survival was greater in the patients with low hepatic iron content less than 457 microêg/g liver (the mean of this cohort of patients), mild to moderate fibrosis of the liver then with severe fibrosis, age less than 54 years (the mean of this cohort of patients), and virological sustained responder to IFN therapy than with non-responder. Stepwise Cox regression analysis revealed that hepatic iron content, the fibrosis of the liver, and age greater than 55 years, were independent risk factors for the development of HCC in these patients. In conclusion, hepatic iron content is an independent risk for the development of HCC in chronic hepatitis C infection, even in the context of IFN therapy. Aggressive phlebotomy should be considered as a preventative measure in patients with chronic HCV infection who do not respond to IFN therapy and show elevated hepatic iron stores.