Spontaneous Resolution of a Large Multifocal Hepatocellular Carcinoma in a Patient with Chronic Hepatitis B and C

Abstract

Hepatocellular carcinoma (HCC) has a poor prognosis and for an unresectable tumor the course is rapidly fatal. Spontaneous regression of HCC has been described but appears to be a rare phenomenon. We report a patient with a large multifocal HCC with portal vein invasion, who had a complete spontaneous resolution of the tumor. Case: A 56 years old man was referred for abdominal pain and feeling a lump in his abdomen in Nov, 05. He was diagnosed with HCV two years ago. His PMH was significant for COPD and HTN. Current meds included diltiazem, propanolol and oral inhalers. His HCV risks included a tattoo. He smokes 4 cig and drinks 5 beers/day. He had no cutaneous stigma of liver disease. A firm mass was palpable in the epigastric area. His AFP levels were markedly elevated at 2854 ng/ml. A CBC and synthetic functions were normal. ALT slightly elevated to 44 iu/ml. HIV was negative, HBSAb positive, HBSAg negative and HBcAb (total) positive. HCV RNA was 14500000 iu/mL (2b). An US showed a solid mass encompassing the entire L. lobe and PV thrombosis. A CT noted a 7.5cm mass at the anterior aspect of the L. hepatic lobe extending to the R. hepatic lobe, a 3.6 cm mass within the PV and several small lesions. A CT biopsy confirmed a mod. diff HCC. In feb, 2006, he presented with chills, sweats and abd. distension, no ascites was appreciated. The previously palpated mass was not felt. He had leukocytosis with a left shift. AFP normalized to 6.6 ng/mL. He denied using OTC/herbal medicine. An MRI, a CT and an US failed to show the tumor. PV was patent. His HBSAg turned positive in april, 06 but two months later is negative again. Current LFTs are normal, HBcAb-M is negative, HBeAg and HBV-DNA are pending. Discussion: Among 28 cases of HCC undergoing a complete spontaneous regression our patient is the first reported case in the setting of chronic infection with both HCV and HBV, with a suspected HBV reactivation and subsequent clearance. In our patient HBV could have been responsible for tumor production. A clear mechanism for spontaneous regression is not well understood. A variety of proposed theories include; immune, genetic and hormonal mechanisms; withdrawal from estrogen, alcohol and carcinogens; local or systemic infections and tumor infarction due to a compromised blood supply. In our case, the last two mechanisms might be responsible for the tumor disappearance. More in depth analysis is needed to find the common characteristics among this group of unique individuals.