Thrombopoietin serum levels are elevated in patients with hepatitis B/C infection compared to other causes of chronic liver disease
Article first published online: 23 JAN 2009
Volume 22, Issue 2, pages 114–120, April 2002
How to Cite
Schöffski, P., Tacke, F., Trautwein, C., Martin, M. U., Caselitz, M., Hecker, H., Peter Manns, M. and Ganser, A. (2002), Thrombopoietin serum levels are elevated in patients with hepatitis B/C infection compared to other causes of chronic liver disease. Liver, 22: 114–120. doi: 10.1034/j.1600-0676.2002.01547.x
- Issue published online: 23 JAN 2009
- Article first published online: 23 JAN 2009
- Received 28 February, accepted 19 July 2001
- liver diseases;
- liver cirrhosis
Abstract: Background/aims: Thrombocytopenia in patients with advanced liver disease may stem from a deficient hepatic thrombopoietin production.
Methods: We determined the relationship between thrombopoietin, thrombocytopenia, aetiology and extent of liver damage by incorporating serum thrombopoietin measurements in the pretransplant evaluation of 111 patients with liver disease.
Results: The extent of thrombocytopenia was related to the underlying cause of disease. The platelet count directly correlated with factor V, II, fibrinogen, and PTT, and a negative correlation was found for splenic size and Child's stage. The thrombopoietin concentrations were age-dependent, and no significant difference resulted between the median thrombopoietin level of liver disease patients with age-matched healthy controls. Thrombopoietin concentrations and platelet counts were not correlated. Although noncirrhotic patients had higher platelet counts than those with Child's A–C cirrhosis (p < 0.001, U-test), no such difference was found in thrombopoietin levels. Patients with hepatitis B and/or C had lower platelet counts compared to patients with nonviral diseases (p < 0.001), and their median thrombopoietin concentrations were significantly higher (p < 0.001).
Conclusion: We conclude that thrombocytopenia in patients with liver disease is unlikely to be explained only based on a deficient hepatic production of thrombopoietin. Patients with chronic viral hepatitis have significantly elevated thrombopoietin levels; the involved pathomechanisms require further study.