Non-alcoholic fatty liver disease and antiviral therapy in hepatitis C.

Sir, I have read the excellent paper by Shifflet and Wu.1 Watanabe et al reported that several metabolic disturbances, such as obesity, insulin resistance, and hepatic steatosis, are significant risk factors for decreased sustained virologic response to interferon and ribavirin combination antiviral therapy in chronic hepatitis C patients.2 It should be noted, for completeness, the influence of non-alcoholic fatty liver disease (NAFLD) on post liver transplantation (LT) antiviral treatment. It is well known that the natural history of recurrent hepatitis C is accelerated after LT. Hepatitis C driven fibrosis response in the allograft leads to the development of graft cirrhosis in approximately 25% of recipients after a follow-up of 5–10 years. More than 10% of patients who undergo transplantation for hepatitis C cirrhosis eventually require retransplantation for hepatitis C related graft failure.3 In relation to organ shortage, Llado et al affirmed that retransplantation is not an option for recurrent hepatitis C cirrhosis after LT.4 For this reason, it is mandatory to protect in the best way the graft by treating with antiviral therapy for recurrent hepatitis C.5 In a substantial proportion of infected recipients, liver injury remains mild despite high viral burden. Several factors have been clearly shown to be associated with fibrosis progression rate. Metabolic conditions and steatosis are emerging as independent cofactors of fibrogenesis. Machicao et al suggested that allograft steatosis is a common occurrence after orthotopic liver transplantation (metabolic alterations, immunosuppression) and is independent of concomitant HCV infection.6 Till now, in our experience, there is evidence for the importance of parameters such as body mass index (BMI, kg/m2), cholesterol (mg/dL), triglycerides (TG, ng/mL) and hepatic percentage of steatosis in response to therapy with pegylated interferon (PEG-IFN) alfa-2b and ribavirin in patients with recurrent hepatitis C after LT.7 Response to therapy was evaluated in relation to virologic response (HCV-RNA assay was performed at 1, 3, 6, 12 and 18 months): sustained virologic response (SVR) was defined as the absence of serum HCV-RNA (virologic remission) and serum alanine aminotransferase (ALT) activity within the reference range for at least 6 months after; sustained biochemical response (SBR) was defined as a decrease in serum ALT activity to within the reference range but with reappearance or persistently detectable serum HCV-RNA; nonresponse (NR) was defined as persistence/relapse at the end of therapy of HCV-RNA and no decrease in ALT activity or relapse at the end of therapy. Ten patients (31.2%) stopped therapy for side effects, SVR was observed in six cases (6/22, 27.2%), SBR in seven cases (7/22, 31.8%) and NR in nine cases (9/22, 40.9%).