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HEPATIC IRON ACCUMULATION IS AN INDEPENDENT RISK FACTOR FOR THE

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    NATAP - www.natap.org DDW Conference May 2001, Atlanta Reported by Jules Levin HEPATIC IRON ACCUMULATION IS AN INDEPENDENT RISK FACTOR FOR THE DEVELOPMENT OF
    Message 1 of 1 , Jul 10, 2001
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      NATAP - www.natap.org

      DDW Conference
      May 2001, Atlanta
      Reported by Jules Levin

      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

      comments: These study findings suggest that iron
      accumulation in the
      liver
      can increase the risk for liver disease progression.
      This raises the
      question
      of how and if diet is related to iron accumulation in
      the liver and to
      disease progression, is it clinically relevant? A
      person's diet
      selection
      should be based on their individual situation based on
      blood work,
      current
      dietary needs, and HIV status. Some patients with HIV
      have anemia or
      predispisition to anemia and this should be
      considered. Is it
      appropriate to
      eliminate all red meat if a HCV-infected patient does
      not have
      decompensated
      cirrhosis? Such a decision may be extreme but each
      person's individual
      situation should be evaluated by an appropriate and
      knowledgeable care
      provider.

      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
      469 micro�g/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. The author showed a
      slide where
      Hepatic
      Liver Content of 620 or less after IFN treatment
      showed improved HCC
      free
      survival compared to HIC of more than 621 (p<0.005).
      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. In
      addition to Hepatic Liver Content, the authors found
      age (>55) and
      fibrosis
      (stage F3 or cirrhosis (after IFN treatment) were
      independent risk
      factors
      for the development of HCC.

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