Background Although accumulating evidence suggests that the
hemostatic balance is impaired in patients with
hypertriglyceridemia,
hyperbilirubinemia or hemolytic
anemias, little is known on the underlying biological mechanisms. This experimental study was aimed at exploring whether increasing values of
triglycerides,
bilirubin or cell-free
hemoglobin promote
thrombin generation in plasma. Methods Three different pools were prepared from three different sets of 20 normal routine plasma
citrate samples. The native pools were spiked with increasing amounts of exogenous
triglycerides (up to 8.8 mmol/L),
bilirubin (up to 350 μmol/L) or autologous hemolyzed blood (up to 3.5 g/L cell-free
hemoglobin). Using the fully-automated
thrombin generation analyzer ST Genesia, we measured the following parameters: lag time (LT), time to peak (TP), peak height (PH) and endogenous
thrombin potential (ETP). Results A sustained increase of PH and ETP was found in parallel with increasing
triglyceride concentrations, peaking in the aliquot with 8.8 mmol/L. Conversely, LT and TP displayed an opposite trend, reaching a maximum decrease in the 8.8 mmol/L aliquot. Increasing
bilirubin concentrations promoted remarkable increases of PH and ETP and decreases of TP and LT, up to 211 μmol/L. After this threshold, all parameters tended to return towards baseline values. A constant increase of PH and ETP was also noted in hemolyzed samples, peaking in the 3.5 g/L cell-free
hemoglobin aliquot, whereas the TP and LT remained unchanged in all hemolyzed aliquots. Conclusions Our findings suggest that
hypertriglyceridemia,
hyperbilirubinemia and
hemolysis may promote a hypercoagulable state in human plasma.