Journal of Hepatology
Volume 48, Issue 4 , Pages 657-665, April 2008

Environmental factors as disease accelerators during chronic hepatitis C

Department of Hepatology and Gastroenterology, INSERM U841, Groupe hospitalier Henri Mondor-Albert Chenevier, Créteil F-94000, France

AP-HP, Groupe hospitalier Henri Mondor-Albert Chenevier, Service d’Hépatologie et de Gastroentérologie, Créteil F-94000, France

Université Paris 12, Faculté de Médecine, Créteil F-94000, France

published online 28 January 2008.

Associate Editor: M.U. Mondelli

Progression of chronic hepatitis is highly variable among individuals, as the result of several host, viral and environmental factors. The latter have been extensively investigated in order to ameliorate hepatitis C outcome, particularly in difficult-to-treat patients. Over the last decade, several studies have shown that a combination of HCV infection and high levels of alcohol abuse results in synergistic acceleration of liver fibrogenesis. In addition, recent data indicate that light alcohol intake may also exacerbate fibrosis progression. It has also been suggested that cigarette smoking may enhance activity grade in patients with chronic hepatitis C, thereby increasing progression of fibrosis. This assumption mostly relies on epidemiological evidences in the absence of pathogenic studies. Finally, cannabis use is increasingly emerging as a novel co-morbidity in patients with chronic hepatitis C. Indeed, regular cannabis smoking is an independent predictor of both fibrosis and steatosis severity in infected patients. In addition, experimental studies have shown that cannabinoid CB1 receptors enhance liver fibrogenesis and steatogenesis by distinct mechanisms, therefore strongly supporting epidemiological findings. Altogether, patients should be informed of the deleterious impact of alcohol, tobacco and cannabis use and should be offered appropriate support to achieve abstinence.

Keywords: Alcohol, Tobacco, Hepatitis C virus, Chronic hepatitis C, Cannabis, CB1 receptor, CB2 receptor, Cannabinoid

 

 The authors declare that they do not have anything to disclose regarding funding from industries or conflict of interest with respect to this manuscript. This work was supported by Inserm, the University Paris-Val-de-Marne and by grants of the Agence Nationale de la Recherche, the Fondation pour la Recherche Medicale and Sanofi-Aventis. Some of these data were presented at the 42nd EASL Annual Meeting, Barcelona, Spain, April 2007.

PII: S0168-8278(08)00049-4

doi:10.1016/j.jhep.2008.01.004

Journal of Hepatology
Volume 48, Issue 4 , Pages 657-665, April 2008