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Brief Communication: The Relationship of Regression of Cirrhosis to Outcome in Chronic Hepatitis C

Vincent Mallet, MD, PhD; Hélène Gilgenkrantz, MD, PhD; Jeanne Serpaggi, MD; Virginie Verkarre, MD, PhD; Anaïs Vallet-Pichard, MD; Hélène Fontaine, MD; and Stanislas Pol, MD, PhD
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From Université Paris Descartes; Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, INSERM U 567; and Assistance Publique-Hôpitaux de Paris, Hôpital Necker—Enfants Malades, Paris, France.

Acknowledgment: The authors thank Dr. Mehran Monchi for help with statistics.

Potential Financial Conflicts of Interest:Honoraria: V. Mallet (Schering-Plough, Bristol-Myers Squibb), S. Pol (Bristol-Myers Squibb, Schering-Plough, Wyeth, Roche, Novartis, Gilead, Tibotec, Boehringer Ingelheim).

Reproducible Research Statement:Study protocol and statistical code: Not available. Data set: Available from Dr. Mallet (e-mail, vincent.mallet@cch.aphp.fr) after establishing written agreement with the authors.

Requests for Single Reprints: Stanislas Pol, MD, PhD, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Hépatologie, 27 rue du Faubourg Saint Jacques, 75014 Paris, France; e-mail, stanislas.pol@cch.aphp.fr.

Current Author Addresses: Drs. Mallet, Gilgenkrantz, Vallet-Pichard, Fontaine, and Pol: Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Hépatologie, 27 rue du Faubourg Saint Jacques, 75014 Paris, France.

Dr. Serpaggi: Centre Hospitalier de Dreux, Hépatogastroentérologie, 44 avenue Kennedy, BP 69, 28102 Dreux, France.

Dr. Verkarre: Assistance Publique-Hôpitaux de Paris, Hôpital Necker—Enfants Malades, Anatomopathologie, 149 rue de Sèvres, 75015 Paris, France.

Author Contributions: Conception and design: V. Mallet, H. Gilgenkrantz, J. Serpaggi, A. Vallet-Pichard, S. Pol.

Analysis and interpretation of the data: V. Mallet, H. Gilgenkrantz, J. Serpaggi, V. Verkarre, A. Vallet-Pichard, H. Fontaine, S. Pol.

Drafting of the article: V. Mallet, H. Gilgenkrantz, A. Vallet-Pichard, S. Pol.

Critical revision of the article for important intellectual content: V. Mallet, H. Gilgenkrantz, A. Vallet-Pichard, H. Fontaine, S. Pol.

Final approval of the article: V. Mallet, H. Gilgenkrantz, J. Serpaggi, V. Verkarre, A. Vallet-Pichard, H. Fontaine, S. Pol.

Provision of study materials or patients: V. Mallet, H. Fontaine, S. Pol.

Ann Intern Med. 2008;149(6):399-403. doi:10.7326/0003-4819-149-6-200809160-00006
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During more than 10 years of follow-up in 96 patients with treated hepatitis C–related cirrhosis, 18 patients achieved histologically proven regression. The absence of liver-related morbidity and mortality in these patients supports the concept of cirrhosis reversal. Persistence of cirrhosis carries a risk for hepatocellular carcinoma, which warrants regular screening.

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Grahic Jump Location
Kaplan–Meier estimates of time to a liver-related event and death in patients with or without a sustained virologic response (top) and in patients with or without regression of cirrhosis (bottom).

“Liver-related events” were hepatocellular carcinoma, hepatic encephalopathy, variceal bleeding, ascites, spontaneous bacterial peritonitis, and liver transplantation.

Grahic Jump Location




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The relationship of regression of cirrhosis to outcome in chronic hepatitis C
Posted on September 27, 2008
Ze-Zhou Song
The First Affiliated Hospital£¬College of Medicine£¬Zhejiang University,Hangzhou,China
Conflict of Interest: None Declared

To the editor: I read with great interest the study by Dr Mallet et al,(1) which concluded that regression of cirrhosis is associated with decreased disease-related morbidity and improved survival. The methods and interpretation of the results, however, raise several concerns: Recent years have seen a surge of interest in complementary food and chemopreventers to treat various liver diseases including cirrhosis. Diet influences body mass index (BMI), iron content in the liver, insulin, enzyme activities, substrate reserves, and metabolic pathways in hepatocytes, and many foods have been reported to exert protective or toxic effects on the liver in animal models and humans (2, 3). In addition, it is well established that HCV genotype influences both response to therapy and disease severity as well as the viral-host interactions (4) and that patients infected with HCV genotypes 2 or 3 respond more favourably than genotype 1 to pegylated Á2a-Interferon and ribavirin anti-viral therapy (5). In the study by Dr Mallet et al, (1) however, the above-mentioned factors were not well described. And then, could the results of the study by Dr Mallet et al1 be affected by the above-mentioned factors?


1. Mallet V, Gilgenkrantz H, Serpaggi J, et al. The Relationship of Regression of Cirrhosis to Outcome in Chronic Hepatitis C. Ann Intern Med 2008; 149: 399-403.

2. Musso G, Gambino R, De Michieli F, et al. Dietary habits and their relations to insulin resistance and postprandial lipemia in non alcoholic steatohepatitis. Hepatology 2003; 37: 909¨C916.

3. Loguercio C, Cuomo A, Tuccillo C, et al. Liver p53 expression in patients with HCV-related chronic hepatitis. J Viral Hepatol 2003; 10: 266¨C270.

4. Farci P, Strazzera R, Alter HJ, et al. Early changes in hepatitis C viral quasispecies during interferon therapy predict the therapeutic outcome. Proc Natl Acad Sci USA. 2002; 99: 3081¨C3086.

5. Hu KQ, Vierling JM, Redeker AG. Viral, host and interferon-related factors modulating the effect of interferon therapy for hepatitis C virus infection. J Viral Hepat. 2001; 8: 1¨C18.

Conflict of Interest:

None declared

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