Reduced platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis

Abstract

Results from previous studies regarding platelet function in liver cirrhosis are discordant. The aim was to investigate platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis. We included 27 patients with alcoholic liver cirrhosis and 22 healthy individuals. A recently established flow cytometric approach was used to measure platelet activation and platelet aggregation independent of sample platelet count. Platelet aggregation was further investigated using light transmission aggregometry (LTA) (for platelet count >100 × 10⁹/L). Platelet agonists were adenosine diphosphate, thrombin receptor-activating peptide, arachidonic acid, collagen, and collagen-related peptide. Patients had lower median platelet count than healthy individuals, 125 × 10⁹/L (interquartile range [IQR] 90˗185) versus 240 × 10⁹ (IQR 204˗285), p < 0.001. Platelet activation levels in stimulated samples were lower in patients versus healthy individuals, e.g., after collagen-related peptide stimulation, the median percentage of platelets positive for activated glycoprotein IIb/IIIa was 85% (IQR 70–94) in patients versus 97% (IQR 94–99) in healthy individuals, p < 0.001; lower platelet activation capacity being associated with low platelet count and Child–Pugh class B/C cirrhosis. Flow cytometric platelet aggregation was reduced in patients for collagen-related peptide and for adenosine diphosphate, e.g., platelet aggregation (mean ± standard deviation) was 57% ± 4 in patients versus 70% ± 1 in healthy individuals for collagen-related peptide, p = 0.01. Light LTA showed reduced collagen-induced platelet aggregation in some patients compared with healthy individuals. In conclusion, platelet function was reduced in some patients with alcoholic liver cirrhosis and the severity was associated with platelet count and severity of liver cirrhosis.

Keywords:

• Alcohol
• liver cirrhosis
• platelet function
• platelet count

Acknowledgments

The study was funded by Lily Benthine Lunds foundation, Krista and Viggo Petersen foundation, A.P. Møller foundation (Fonden til lægevidenskabens fremme), and the foundation of 17–12–1981. The supporting sources were not involved in the study. We would like to thank MD Linda Møller for recruiting patients for the study.

Declaration of interest

Hvas AM has received speaker fees from CSL Behring, Leo Pharma, Bayer Health care, Bristol-Myers Squibb, and Boehringer-Ingelheim and research support from CSL Behring, Octapharma, and Leo Pharma. Vinholt PJ has received speaker’s fee from Bristol-Myers Squibb. The other authors have no conflicts of interest.