Evaluation of platelet dysfunction in viral liver cirrhosis: relationship to disease severity

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Hepatitis C virus (HCV) is a major health problem in Egypt, which has the highest HCV prevalence worldwide. Cirrhotic patients are known to have acquired platelet hypofunction; however, HCV-induced inflammatory and immunological phenomena are thought to be responsible for in-vivo platelet activation. This study aimed to evaluate the platelet function in patients with HCV-induced liver cirrhosis and also to study the relationship of platelet function to disease severity and various clinical/laboratory findings in cirrhotic patients.

Materials and methods

Evaluation of platelet function was carried out on 50 patients with HCV-induced liver cirrhosis using the platelet function analyzer-100 (PFA-100), compared with 30 healthy volunteers.


The study demonstrated the presence of platelet hypofunction reflected by the prolonged PFA-100 closure time in patients of Child–Pugh stage B compared with those of stage A and C, in moderate compared with negative/mild and severe ascites, and in grade II esophageal varices compared with other grades. Patients with Child–Pugh stage B and C, severe ascites, and stage III/IV esophageal varices had significantly lower platelet count/spleen size ratios.


Chronic HCV-induced liver cirrhosis is implicated in alterations of primary hemostasis, with platelet hypofunction being more evident during relatively earlier disease stages compared with the later ones. PFA-100 closure time and platelet count/spleen size ratio could be used as noninvasive predictors of the grades of esophageal varices in cirrhotic patients. The simplicity of the PFA-100 could facilitate its use as a convenient primary screening test to detect platelet dysfunction in HCV-induced liver cirrhosis.

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