A multitude of laboratory and clinical interferences influence the utility of platelet-based diagnostic indices, including immature platelet fraction, in longitudinal monitoring and prognostication of patients with chronic liver disease (CLD). The complex yet highly regulated molecular basis of platelet production and clearance kinetics becomes dysregulated in liver pathogenesis. These underlying molecular mechanisms, including premature platelet clearance and bone marrow suppression in parallel with the progressive (e.g., treatment-naïve) or regressive (e.g., on-treatment and off-treatment) disease courses, involved in CLDs, may further confound the changes in platelet-liver correlations over time. Platelet count and function are commonly and secondarily altered in vivo in CLDs. However, the precise characterization of platelet functions during cirrhosis, including in vitro platelet aggregation, has proven challenging due to interferences such as thrombocytopenia. A flow cytometric approach may help monitor the unstably rebalanced hyper- and hypoaggregable states in patients with cirrhosis at risk of hyperaggregable, prothrombotic, or bleeding events. Studies have attempted to stratify patients with cirrhosis by substages and prognosis through the use of novel indices such as the ratio of in vitro endogenous platelet aggregation to platelet count. This review attempts to highlight clinical and laboratory precautions in the context of platelet-assisted CLD monitoring.
Keywords: elastography; flow cytometry; liver cirrhosis; monitoring; platelet aggregation; platelet count; risk assessment; thrombopoietin.