Literature DB >> 21335007

Iron levels in hepatocytes and portal tract cells predict progression and outcomes of patients with advanced chronic hepatitis C.

Richard W Lambrecht1, Richard K Sterling, Deepa Naishadham, Anne M Stoddard, Thomas Rogers, Chihiro Morishima, Timothy R Morgan, Herbert L Bonkovsky.   

Abstract

BACKGROUND & AIMS: Iron may influence severity and progression of non-hemochromatotic liver diseases. Our aim was to assess the relationship of iron and HFE genetic variations to progression and outcomes in the HALT-C Trial and whether PegIFN therapy influenced iron variables.
METHODS: Participants were randomized to receive long-term PegIFN [n = 400] or no therapy [n = 413] for 3.5 y, with follow-up for up to 8.7 y [median 6.0 y]. Associations of patient characteristics with iron variables at baseline and over time were carried out using Kaplan-Meier analyses, Cox regression models, and repeated measures analysis of covariance.
RESULTS: Participants who developed clinical outcomes [CTP > 7, ascites, encephalopathy, variceal bleeding, SBP, HCC, death] had significantly higher baseline scores for stainable iron in hepatocytes and in portal tract cells than those without. There were significant direct correlations between stainable iron in portal triads and lobular and total Ishak inflammatory and fibrosis scores [P < 0.0001]. Iron in triads at baseline increased risk of outcomes (HR = 1.35, P = 0.02). Stainable iron in hepatocytes decreased, whereas that in portal stromal cells increased significantly [P < 0.0001] over time. Serum iron and TIBC fell significantly over time [P < 0.0001], as did serum ferritin [P = 0.0003]. Chronic PegIFN treatment did not affect stainable iron. HFE genetic variations did not correlate with outcomes, including development of hepatocellular carcinoma.
CONCLUSIONS: Stainable iron in hepatocytes and portal tract cells is a predictor of progression and clinical and histological outcomes in advanced chronic hepatitis C. Chronic low-dose PegIFN therapy did not improve outcomes, nor iron variables.
Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.

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Year:  2011        PMID: 21335007      PMCID: PMC3081953          DOI: 10.1053/j.gastro.2011.01.053

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  36 in total

1.  Liver iron concentration and distribution in chronic hepatitis C before and after interferon treatment.

Authors:  E Boucher; A Bourienne; P Adams; B Turlin; P Brissot; Y Deugnier
Journal:  Gut       Date:  1997-07       Impact factor: 23.059

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Journal:  Gastroenterology       Date:  2005-08       Impact factor: 22.682

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Review 5.  Iron in nonhemochromatotic liver disorders.

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Journal:  Hepatology       Date:  1998-06       Impact factor: 17.425

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Review 10.  Iron as a co-morbid factor in nonhemochromatotic liver disease.

Authors:  Herbert L Bonkovsky; Richard W Lambrecht; Ying Shan
Journal:  Alcohol       Date:  2003-06       Impact factor: 2.405

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1.  Inhibition of hepcidin transcription by growth factors.

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2.  Iron metabolic disorder in chronic hepatitis C: insights from recent evidence.

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Review 3.  Genetic risk markers for hepatocellular carcinoma in patients with alcoholic liver disease.

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10.  Initial serum ferritin predicts number of therapeutic phlebotomies to iron depletion in secondary iron overload.

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