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Abstract
Aim: Non-alcoholic fatty liver disease (NAFLD) represents the most common liver disease worldwide. Patients with NAFLD are at high risk for cardiovascular diseases that represents the major cause of morbidity and mortality in this setting. Platelets play a key role in precipitating atherosclerotic complications as indicated by interventional studies with aspirin, which significantly reduces cardiovascular events by impairing platelet Thromboxane B2 (TxB2) biosynthesis. We investigated the behaviour of platelet activation in patients with NAFLD.
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