Case Presentation: Most complications of Hepatitis C virus (HCV) infection, such as progressive fibrosis and cirrhosis, hepatic decompensation, and hepatocellular carcinoma (HCC), are related to chronic infection. Upon adequate treatment of HCV with sustained virologic response (SVR), patients without prior bridging fibrosis or cirrhosis are at a lower risk of developing complications. This is a case presentation of an unexpected complication of HCC in a patient with HCV with SVR.
A 64-year-old woman with well-controlled diabetes mellitus and HCV status-post treatment three years ago with subsequent SVR presented with chronic right upper quadrant abdominal pain. She also had intermittent nausea and non-bloody vomiting, which was not related to food intake. She did not have fatigue, fevers, chills, weight changes, recent travel, sick contacts, or known gallstones or biliary disease. Abdominal ultrasound three years prior to admission showed hepatic steatosis without fibrosis.

On arrival to the emergency department, she was afebrile with normal vital signs. Examination was notable for mild tenderness with palpation of the right upper quadrant. There were no peritoneal signs, splenomegaly, icteric sclera, or jaundice. Laboratories were significant for an elevated aspartate aminotransferase (AST) of 119 IU/L (normal 10-42 IU/L), elevated alkaline phosphatase of 141 IU/L (normal 38-127 IU/L), and low albumin of 3.1 g/mL (normal 3.5-4.5 g/mL). Other liver enzymes, electrolytes, blood counts, coagulation studies, and hepatitis serologies were within normal limits. Hepatitis C viral load was undetectable.

Abdominal ultrasound showed hepatomegaly with a heterogenous echotexture read as potentially consistent with space-occupying lesions. Subsequent computer tomography (CT) of the abdomen with liver protocol revealed multiple lesions consistent with HCC. Staging imaging (CT chest, abdomen, and pelvis) revealed enlarged retroperitoneal lymph nodes and spinal lesions. Alpha-fetoprotein was markedly elevated. Oncology was consulted and given the imaging and tumor markers, a diagnosis of metastatic HCC was made. The diagnosis was discussed with the patient who deferred a biopsy and eventually opted for comfort care.

Discussion: This case provides an example of the rare complication of HCC in a patient with adequately-treated HCV. Though there is a strong association between HCV and HCC, most cases of HCC in HCV patients occur in the setting of severe fibrosis or cirrhosis. Furthermore, development of HCC in patients with minimal liver fibrosis usually results in those with active chronic HCV infection with a detectable viral load.

Conclusions: Our patient had neither significant hepatic fibrosis nor a detectable HCV viral load during the preceding three years, yet developed metastatic HCC in this time. This case demonstrates the importance of maintaining a broad differential when evaluating abdominal pain in patients with known hepatic pathology.