Short- and long-term effects of therapy with interferon-α and pegylated interferon-α/ribavirin on platelet plug formation and von Willebrand factor release in patients with chronic hepatitis C
Article first published online: 22 DEC 2004
Alimentary Pharmacology & Therapeutics
Volume 21, Issue 1, pages 49–55, January 2005
How to Cite
Homoncik, M., Ferlitsch, A., Ferenci, P., Formann, E., Jilma, B., Gangl, A., Panzer, S. and Peck-Radosavljevic, M. (2005), Short- and long-term effects of therapy with interferon-α and pegylated interferon-α/ribavirin on platelet plug formation and von Willebrand factor release in patients with chronic hepatitis C. Alimentary Pharmacology & Therapeutics, 21: 49–55. doi: 10.1111/j.1365-2036.2004.02305.x
- Issue published online: 22 DEC 2004
- Article first published online: 22 DEC 2004
- Accepted for publication 11 October 2004
Background : A pegylated interferon-alpha-induced decrease in platelet counts may become a limiting factor for continuation of therapy.
Aim : To evaluate the effect of pegylated interferon-α administration on platelet plug formation and von Willebrand factor antigen release in patients with chronic hepatitis C.
Methods : Thirty patients with chronic hepatitis C (genotype 1; fibrosis 1–3: n = 16, cirrhosis: n = 14) received a single dose of 9 MU interferon-α2a, followed by weekly administration of 180 μg of pegylated interferon-α2a/ribavirin for 48 weeks. Platelet counts, platelet function (collagen–epinephrine-induced closure time) and von Willebrand factor antigen were measured.
Results : Platelet counts and collagen–epinephrine-induced closure time decreased by 13% and 16%, respectively, 24 h after the first dose of interferon-α2a, and von Willebrand factor antigen levels increased by 31% (P < 0.01) compared with baseline. During a 48-week observation period, platelet counts decreased by a maximum of 33% (P < 0.001), von Willebrand factor antigen levels increased by 69% (P < 0.001) whereas collagen–epinephrine-induced closure time did not change. In noncirrhotic patients, the increase of von Willebrand factor antigen levels was maintained throughout therapy without a change in collagen–epinephrine-induced closure time. In contrast, in cirrhotics, von Willebrand factor antigen levels did not increase, while collagen–epinephrine-induced closure time was prolonged.
Conclusion : Single-dose interferon-α decreases platelet counts but improves platelet function, possibly by the release of von Willebrand factor antigen. Accordingly, long-term antiviral treatment had no effect on collagen–epinephrine-induced closure time, despite the decrease in platelet count in noncirrhotic patients. Such a compensation of decreased platelet counts by increased von Willebrand factor antigen level did not occur in cirrhotics.