Antiviral therapy decreases GpIIb/IIIa activation of platelets in patients with chronic hepatitis C
Wolfgang Sieghart1,2, Monika Homoncik 1 , Bernd Jilma2 , Elisabeth Formann 1 , Peter Ferenci1 , Alfred Gangl 1 , Markus Peck-Radosavljevic1
1 Department of Internal Medicine IV, Division of Gastroenterology and Hepatology and 2 Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
Summary
Interferon alpha (IFN-a ) is used to treat haematological andsolid malignancies and is the gold standard therapy for chronichepatitis C infection in combination with ribavirin. It has a wellknown platelet lowering effect and was recently shown to impairplatelet aggregation in the presence of various agonists andhas been accused to increase patients’ bleeding risk duringIFN-a therapy. Thus, we hypothesised that antiviral treatmentdecreases GpIIb/IIIa activation and affects global platelet function.In a prospective clinical trial, we examined the effects ofcombination therapy with pegylated IFN-a 2a (PegIFN-a 2a)and ribavirin on platelet GpIIb/IIIa activation and platelet secretionin 20 patients with chronic hepatitis C at week 2, 4, 8 and 12after the beginning of therapy. In addition, we determined global platelet function (CEPI-CT) with the PFA-100 and vWF-Ag levels.Antiviral therapy significantly decreased GpIIb/IIIa activationin a time dependent manner, whereas markers of platelet secretion(P-selectin, ß -thromboglobulin) remained unchanged. Despitea marked elevation of vWF-Ag levels, CEPI-CT did notchange compared to baseline levels. Antiviral therapy significantlydecreases GpIIb/IIIa activation in patients with chronichepatitis C, while vWG-Antigen levels are markedly increasedand a -granule secretion is not affected.This does not result in analteration of global platelet function as assessed by the PFA-100,because elevated vWF-Antigen levels might compensate for theacquired defect. Keywords
von Willebrand factor, Platelet activation markers, clinical / epidemiological studies
DOI
http://dx.doi.org/10.1160/TH05-12-0781