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6404Iron Accumulation in HCV?? Is it Dangerous?

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  • claudine intexas
    Jun 30, 2001
      NATAP - www.natap.org

      Iron Accumulation in HCV?? Is it Dangerous?

      This question appears to remain unanswered but the
      study below suggests
      iron
      accumulation is not an issue. This question raises the
      issue of dietary
      intake of red meat. Some HCV patients eliminate red
      meat from their
      diet due
      at least in part to concern about iron accumulation.
      Is there enough
      data or
      research to support such an action? I think it is
      accepted that for
      people
      with decompensated liver disease eliminating red meat
      may be
      appropriate.
      What about people with less advanced HCV? For people
      with HCV/HIV
      coinfection
      eliminating red meat may not be healthy considering
      their diet needs:
      anemia,
      red blood cell counts, and hemoglobin.

      Hepatic iron and nonalcoholic fatty liver disease

      Hepatology 1999 Oct;30(4):847-50
      Younossi ZM, Gramlich T, Bacon BR, Matteoni CA,
      Boparai N, O'Neill R,
      McCullough AJ
      Department of Gastroenterology, Cleveland, OH, USA.

      Increased iron is suspected to enhance hepatic injury
      associated with
      nonalcoholic fatty liver disease (NAFL). We evaluated
      the impact of
      iron
      accumulation on the outcome of NAFL. Patients with
      NAFL were identified
      from
      our database. Twenty-two clinicodemographic and 19
      pathological
      features were
      available for each patient. Histological staining
      (Perls' Prussian
      blue),
      hepatic iron concentration (HIC), and hepatic iron
      index (HII) were
      determined. Data on follow-up, mortality, and cause of
      death were
      analyzed.
      In 65 patients with available liver biopsy blocks, HIC
      and HII were
      1,171 +/-
      717 microgram/g dry weight and 0.43 +/- 0.30
      micromol/g/yr,
      respectively.
      Males had more iron accumulation (HIC: 1,514 +/- 836
      vs. 859 +/- 389, P
      =.0001; and HII: 0.58 +/- 0.35 vs. 0.29 +/- 0.16, P
      =.0001). In type II
      diabetics, both HIC (977 +/- 769 vs. 1,301 +/- 659; P
      <.05) and HII
      (0.30 +/-
      0.23 vs. 0.52 +/- 0.32; P <.05) were lower. Iron
      accumulation was not
      related
      to other variables analyzed. Increased iron was not
      seen in those with
      higher
      grades of fibrosis or other pathological features
      associated with the
      aggressive form of NAFL (hepatocyte necrosis,
      fibrosis, ballooning
      degeneration, and Mallory hyaline). Iron accumulation
      was not
      associated with
      increased overall mortality, liver-related mortality,
      or development of
      cirrhosis. In summary, in most patients with NAFL,
      significant iron
      accumulation is not seen. Additionally, in our series
      of patients with
      NAFL,
      iron is not associated with poor clinical or
      pathological outcomes.

      Comment in: Hepatology 2000 Feb;31(2):549-50
      PMID: 10498632, UI: 99428426

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