Mahmoud Abdel-Aziz, Azza Abdel-Aziz, Mohammed M. El-Arman
Background: Both nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CHC) are frequent causes of chronic liver disease. Questions remain regarding the etiology of steatosis and steatohepatitis in hepatitis C, and its impact on disease progression and treatment outcomes.
Objectives: To estimate the association of NAFLD with CHC and to evaluate the effect of steatosis and non alcoholic steatohepatitis (NASH) on the end treatment virologic response of combined anti-viral therapy in such patients.
Subjects and Methods: Eighty-nine naive PCR and biopsy proven CHC patients were included. Clinical, demographic and laboratory data at the time of liver biopsy were obtained. One pathologist reviewed all pathologic specimens using the modified histological activity index score and the Ishak staging for fibrosis and NAFLD pathologic protocol. All patients received combined antiviral therapy in the form of Pegylated Interferon α 2a plus Ribavirin.
Results: Forty-five (50.6%) out of 89 CHC patients had associated NAFLD among which 11 patients encounter superimposed steatohepatitis (NASH). The overall end treatment virologic response was achieved in 61 cases (68.54%). End treatment virologic response was significantly lower (51%) in NAFLD group compared with 86.36% in group not affected by NAFLD (P=0.000). Variables associated with the NAFLD group were: higher serum levels of Aspartate transaminase AST (P<0.001), Alanine transaminase ALT (P<0.001), gamma glutamyle transferase γ-GT (P=0.003), severity of histolopathologic activity (grading, P=0.018) and extent of fibrosis (staging, P=0.020). In the responder group, body mass index (BMI) was significantly lower compared to nonresponder group (P=0.011). Applying the model of logistic regression analysis revealed that NAFLD can be considered as independent risk factor for poor response to combined pegylated interferon α 2a plus ribavirin therapy (odds ratio 0.039, P=0.002). Conclusion: Overall end treatment virologic response for patients with HCV and significant steatosis or steatohepatitis is considerably lower than that for HCV in absence of NAFLD.
