Obesity is a known risk factor for venous and arterial
thrombosis but the mechanisms are still unclear. In women,
obesity is correlated with low-grade
inflammation and recent data show that BMI is positively associated with
thrombin generation. We explored the correlations between
obesity,
inflammation and
thrombin generation in women with increased thrombotic risk by looking at a cohort of women with prior
venous thrombosis. One hundred and fifty-six women age 18-65 years were enrolled at diagnosis of first
venous thromboembolism (VTE). Plasma samples were obtained at least 3 weeks after cessation of
anticoagulant treatment.
Thrombin generation was determined with the calibrated automated thrombography (CAT) assay and the Innovance ETP assay.
Thrombin generation started later but was more pronounced with higher endogenous
thrombin generation potential (ETP) determined with CAT in patients with
obesity. The Innovance ETP assay showed results consistent with CAT. Furthermore, patients with
obesity had significantly higher levels of
fibrinogen,
C-reactive protein and
plasminogen activator inhibitor-I (PAI-I) than patients without
obesity. Increased levels of
fibrinogen were the main determinant of the prolonged lag-time in patients with
obesity whereas higher levels of
prothrombin could account for the difference in the ETP between the groups. We found an association between BMI and ETP values using two different methods to measure
thrombin generation.
Obesity correlated with increased
thrombin generation in women with VTE and the main determinants of this hypercoagulable state were increased levels of
fibrinogen and
prothrombin. This shows a possible link between
obesity, low-grade
inflammation and increased
thrombin generation in women at increased risk for future
thrombosis.