Review article: blood platelet number and function in chronic liver disease and cirrhosis

Abstract

Summary Background The liver plays a central role in coagulation and fibrinolysis but is also closely intertwined with the function and number of blood platelets. Aim To describe and integrate all literature concerning blood platelets and liver disease by performing a thorough literature research. Methods A thorough literature research on ‘blood platelets’ and ‘liver disease’ was performed. Results Thrombocytopenia is a marked feature of chronic liver disease and cirrhosis. Traditionally, this thrombocytopenia was attributed to passive platelet sequestration in the spleen. More recent insights suggest an increased platelet breakdown and to a lesser extent decreased platelet production plays a more important role. Besides the reduction in number, other studies suggest functional platelet defects. This platelet dysfunction is probably both intrinsic to the platelets and secondary to soluble plasma factors. It reflects not only a decrease in aggregability, but also an activation of the intrinsic inhibitory pathways. The net effect, finally, is a decreased platelet function in the various types of chronic liver diseases and cirrhosis. Finally, recent data suggest that platelets are not only affected by but can also contribute to the liver disease process, as for instance, in viral hepatitis and cholestatic liver disease. Conclusion Platelet research in liver disease is a growing area of investigation and could provide new pathophysiological insights.

The European Hematology Association Roadmap for European Hematology Research: a consensus document

“…[217][218][219] European investigators clarified, in particular, the role of altered platelet formation versus platelet destruction in thrombocytopenia and of in vivo platelet activation, platelet "exhaustion", altered nitric oxide signaling, and enhanced nitric oxide formation in platelet dysfunction. Similarly, the role of uremic toxins and enhanced generation of nitric oxide in uremic platelet dysfunction have been shown by European investigators.…”

Diagnostic non-invasive model of large risky esophageal varices in cirrhotic hepatitis C virus patients

“…An additional proposed underlying mechanism of "platelet exhaustion" states that hyperdynamic circulation causes platelet damage during intravascular activation with consequent hypofunction. However, the presence of splenomegaly in patients with cirrhosis is, in all likelihood, derived from vascular derangement mainly resulting from portal hypertension [25] . Consequently, Giannini et al [26] aimed to chart a new parameter bridging thrombocytopenia to splenomegaly so as to originate a variable that takes into account the diminished platelet count probably due to hypersplenism attributed to portal hypertension.…”

Hematological spectrum in patients with alcoholic liver cirrhosis: a model of end-stage liver disease score based approach

“…Indeed, TPO mRNA levels in the liver are slightly decreased in cirrhosis. 17,18 Liver transplantation is known to resolve thrombocytopenia due to an increase in serum TPO and increased platelet production. 19,20 As splenomegaly is an important feature of portal hypertension, it is not surprising that splenic platelet sequestration is thought to be an important mechanism in the etiology of thrombocytopenia.…”