Sarcomatoid Hepatocellular Carcinoma in a HIV and HCV-Positive Patient Without History of Prior Antineoplastic Treatment

Abstract

Sarcomatoid Hepatocellular Carcinoma is a rare neoplasm. It is seen more in the context of HCC undergoing sarcomatoid transformation following treatment with chemotherapy or transcatherial embolization(TAE). Here we present a case of sarcomatoid HCC that developed without prior antineoplastic intervention. 54 M with PMH of HIV on HAART who presented to our hospital with complain of abdominal pain, nausea and vomiting. Patient had been on HAART therapy for 1 year with an absolute CD4 count of 547. He underwent a CT abdomen which showed a 5.1 x 5.6 x 5.7 cm complex, ill-defined mass in segment 8 of the liver. He subsequently underwent an abdominal MRI with liver protocol which showed 4.8 cm lesion in the liver, without enhancement. Given that the radiological finding were more consistent with an abscess patient underwent an IR guided drainage. No drainable fluid was present and the mass was solid. The patient underwent a biopsy which showed sarcomatoid carcinoma. Immunohistochemistry were positive for CAM5.2, keratin AE1/AE3, and vimentin. Focal to rare positivity was seen with CD31 and S100. Tumor cells are negative for desmin, SMA, LCA, CD34, Arginase-1, Hep-Par1, glypican-3, HHV8, and CD117. Tumor makers-CA 19-9, CEA and Alpha feto protein were negative. Patient tested postive for Hepatitis C antibody with very high RNA titires. He tested negative for Hepatitis A and B. The pathogenesis of sacrcomatoid change in HCC is unclear but is believed to be due to the degeneration and regeneration of carcinomas cells due to anticancer therapy and TAE. This causes HCC cells to become multi potent immature stem cells. But in our patient this was not the case. We propose a different mechanism. HIV and HCV are RNA viruses. HIV and HCV have both shown to cause epithelial-mesenchymal transition (EMT) of cells in vivo. EMT is a biologic process that allows a polarized epithelial cell, which normally interacts with basement membrane via its basal surface, to undergo multiple biochemical changes that enable it to assume a multi potent mesenchymal cell phenotype. Therefore we believe confections of HCV and HIV may have induced a EMT transition in HCC cells leading to sarcomatoid carcimanoma.Figure 1Figure 2