Preserved hemostatic status in patients with non-alcoholic fatty liver disease

Platelet‐leucocyte aggregation is augmented in cirrhosis and further increased by platelet transfusion

“…In plasma samples, markers of primary haemostasis (platelet count, von Willebrand factor [VWF], ADAMTS13), coagulation (factor VIII, prothrombin time [PT], international normalised ratio [INR], activated partial thromboplastin time [APTT], antithrombin and fibrinogen) and thrombin generation (F1 + 2, thrombin‐anti‐thrombin complexes [TAT]) were quantified as previously described . Plasma fibrinolytic capacity was measured utilising a plasma‐based clot lysis time assay, also described previously . Plasma thrombin generating potential was measured in vitro in the presence and absence of thrombomodulin by calibrated automated thrombography.…”

Biology of portal hypertension

“…Initially, the assessment of the cirrhotic platelet was that it was dysfunctional and predisposed the patient to a bleeding tendency [89,90]. More recently, however, investigators have found that the activity of cirrhotic platelets in hemostasis and thrombosis is potentially preserved [91] or even increased [92], although there are conflicting data [93]. As recently reviewed [94], the function of platelets in various types of liver injury is quite complex, with multiple situation-specific factors determining whether platelets will play a profibrotic role versus an antifibrotic, pro-regenerative role.…”

The cirrhotic platelet: Shedding light on an enigma

“…In addition to issues with the platelet aggregation test, the interpretation of markers of in vivo platelet activation is complex, because these markers are cleared by the liver such that elevated levels may not reflect in vivo platelet activation, but rather reflect accumulation of these markers due to a lack of clearance . Reliable approaches to study platelet functionality in cirrhosis thus appear restricted to studies on platelets themselves, such as by platelet count–adjusted aggregometry, platelet count–adjusted studies of platelet adhesion and aggregation under conditions of flow, or flow cytometric analyses …”

“…(6) Reliable approaches to study platelet functionality in cirrhosis thus appear restricted to studies on platelets themselves, such as by platelet count-adjusted aggregometry, (1) platelet count-adjusted studies of platelet adhesion and aggregation under conditions of flow, (11) or flow cytometric analyses. (7) Flow cytometry can both identify the in vivo platelet activation status (for example, by measurements of platelet-monocyte aggregates as performed in the study by Raparelli et al, or by assessment of markers of platelet activation on the platelet itself) and platelet function after stimulation, which is (in contrast to aggregometry) independent of the platelet count within the sample. However, an analysis of the literature on unequivocal assays of platelet function reveals that there is no consensus ( Table 1).…”