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J Hepatol. 2013 Nov;59(5):1135-8. doi: 10.1016/j.jhep.2013.05.040. Epub 2013 Jun 4.

Anti-platelet therapy in the prevention of hepatitis B virus-associated hepatocellular carcinoma.

Author information

1
Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan 20132, Italy.

Abstract

Previous studies in mouse models of self-limited viral hepatitis showed that platelets contribute to acute liver damage by promoting the intrahepatic accumulation of virus-specific CD8 T cells and, secondarily, virus-non-specific inflammatory cells. Built on these observations, a recent preclinical study took advantage of a previously established hepatitis B virus (HBV) transgenic mouse model of immune-mediated chronic hepatitis that progresses to hepatocellular carcinoma (HCC), to demonstrate that clinically achievable doses of the anti-platelet drugs aspirin and clopidogrel - administered continuously after the onset of liver disease - can prevent hepatocarcinogenesis and greatly improve overall survival. These outcomes were preceded by and associated with reduced hepatic accumulation of virus-specific CD8 T cells and virus-non-specific inflammatory cells, reduced hepatocellular injury and hepatocellular proliferation, and reduced severity of liver fibrosis. The observation that anti-platelet therapy inhibits HCC development identifies platelets as key players in the pathogenesis of HBV-associated liver cancer and supports the notion that a sustained immune-mediated necroinflammatory liver disease is sufficient to trigger HCC. The results abovementioned and their clinical implications are discussed in this report.

KEYWORDS:

Anti-platelet drugs; CD8 T cells; Hepatitis B virus; Hepatocellular carcinoma; Platelets; Viral hepatitis

PMID:
23742914
DOI:
10.1016/j.jhep.2013.05.040
[Indexed for MEDLINE]
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