Hepatocellular carcinoma (HCC) is the fastest growing cause of cancer mortality. Interferon/ribavirin and direct acting antiviral (DAA) therapy have successfully treated HCV infection and may halt the..
Hepatocellular carcinoma (HCC) is the fastest growing cause of cancer mortality. Interferon/ribavirin and direct acting antiviral (DAA) therapy have successfully treated HCV infection and may halt the progression of fibrosis. It is generally believed that HCC primarily occurs in the background of HCV- related cirrhosis; theoretically, achieving sustained viral response (SVR) could decrease the incidence of HCC by slowing down fibrosing process; hence preventing progression of cirrhosis. Here, we present a case of 64-year-old female who was successfully treated for HCV infection with interferon in 1994. Patient achieved sustained viral response (SVR) and has been in remission for 23 years. In June 2017, she presented with abdominal pain and CT scan revealed a liver mass which was subsequently biopsied and proved to be HCC. Patient was treated with partial hepatectomy and histologic examination of the resected liver mass revealed well-differentiated HCC; non-neoplastic liver demonstrated features of regression of cirrhosis/fibrosis with fibrous expansion of few portal tracts and scattered very fine curvilinear fibrous septa; no portal/lobular inflammation was present. The patient developed HCC 23 years after achieving SVR. Significant regression of cirrhosis/fibrosis in the non-neoplastic liver argues against the usual course of HCC development in cirrhotic/advanced fibrotic setting, and suggests the possibility of an alternative phenomenon, e.g., latency of HCV and/or oncologic potential of HCV at the genomic level. This rare event raises certain questions which have not been properly investigated in the course of HCC development, such as: 1) Relationship between regression of cirrhosis/fibrosis and developing HCC; 2) If absence and regression of cirrhosis/fibrosis carries the same value; 3) Necessity of updating the surveillance criteria in patient with SVR lacking cirrhosis; and 4) Oncologic potential of HCV acquired at the genomic level; these questions/issues are currently under investigation.