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?
REFERENCES
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.
None declared