Increased Soluble P-Selectin Levels in Hepatitis C Virus-Related Chronic Hepatitis: Correlation with Viral Load

Abstract

The results obtained in this study support the hypothesis that HCV infection might be directly responsible for a condition of in vivo platelet activation in patients with chronic C hepatitis.

Platelet Function: the Janus face of haemostasis in cirrhosis

“…Moreover, sP-s levels were even higher in patients with a platelet count lower than 110 x 10 3 μL, independently of the presence of plateletassociated immunoglobulins [6]. In addition, a likely direct HCV activation of platelets could be hypothesized based on a strong positive correlation between sP-s/platelet levels and HCV viral load [6]. All together, these results suggested that in vivo platelet activation and degranulation might take place as a direct consequence of HCV infection, leading to the presence of exhausted platelets (not responding to further in vitro stimulation) that are subsequently removed from the circulation with resultant TCP.…”

“…Scheuer Score equal to 4) had higher levels of plasma sP-s, normalized by platelet counts (sP-s/platelet), compared with those with mild-moderate disease [6]. Moreover, sP-s levels were even higher in patients with a platelet count lower than 110 x 10 3 μL, independently of the presence of plateletassociated immunoglobulins [6].…”

“…TCP, in fact, represents a critical issue in cirrhotic patients with or without HCC, and it results from an imbalance between platelet production and platelet survival. The process accounting for TCP in cirrhosis is multifactorial including bone marrow suppression induced by hepatitis virus C (HCV) and alcohol, defective hepatic thrombopoietin metabolism, hypersplenism, removal of platelets from the circulation due to platelet-associated antibodies, or secondary to platelet hyperactivation/activation [4,6]. Thereby, when in vivo markers of platelet function are measured in this clinical setting, it is methodologically mandatory to perform, as Alkozai EM et al did, a platelet count correction to avoid any bias related to low platelet count.…”

“…Scheuer Score equal to 4) had higher levels of plasma sP-s, normalized by platelet counts (sP-s/platelet), compared with those with mild-moderate disease [6]. Moreover, sP-s levels were even higher in patients with a platelet count lower than 110 x 10 3 μL, independently of the presence of plateletassociated immunoglobulins [6]. In addition, a likely direct HCV activation of platelets could be hypothesized based on a strong positive correlation between sP-s/platelet levels and HCV viral load [6].…”

Patients with liver cirrhosis suffer from primary haemostatic defects? Fact or fiction?

“…Although this interpretation cannot be fully supported by the data of 11-deydro-TxB2 urinary excretion as it only partly reflects the activation of platelet COX1 [130], other studies also seem to support the existence of enhanced platelet activation in cirrhosis. Soluble P-selectin (sPs), which is an in vivo marker of platelet activation is consistently elevated in plasma particularly in cases of severe liver disease and correlated with markers of hepatic protein synthesis and low platelet counts [131][132][133].…”