Tissue factor pathway inhibitor and thrombin-activatable carboxypeptidase B for prediction of early atherosclerosis in gouty arthritis.

Gouty arthritis (GA) is a chronic inflammatory arthritis in which both clinical and subclinical atherosclerosis are more frequent. The dynamic equilibrium between coagulation and fibrinolysis is impaired in inflammatory diseases. We determined TFPI and TAFI antigen levels in GA patients and evaluated their association with subclinical atherosclerosis. We included 45 GA patients (41 males, 4 females; mean age: 51.6years) and 25 asymptomatic hyperuricemic (AHU) subjects (19 males, 6 females; mean age: 48.1years). Cardiovascular risk factors were determined. TAFI and TFPI levels were determined by ELISA. B-mode ultrasonography was used to detect subclinical atherosclerosis. Cardiovascular risk factors were similar in both groups. The carotid IMT was significantly higher in GA group than in AHU group (0.74±0.23mm vs. 0.61±0.13mm, p=0.009). TFPI level was significantly higher in GA group than in AHU group (86.2±48.9ng/mL vs. 25.8±21.4ng/mL, p<0.001); TAFI antigen was significantly higher in AHU group (22.6±3.6ng/mL vs. 25.7±5.3ng/mL, p=0.006) than in GA patients. Atherosclerotic plaque formation was more frequent in GA group (p=0.041). When GA patients with and without plaques were compared, the first group had significantly higher mean age (p=0.01) and TFPI level (p=0.028). TFPI level correlated with carotid IMT (r=0.302; p=0.028). Logistic regression analysis showed that age (OR: 1.236, 95%CI: 1.059-1.443, p=0.007) and TFPI (OR: 1.031, 95%CI: 1.008-1.054, p=0.008) were independent risk factors for the presence of plaques. GA patients had more frequent subclinical atherosclerosis than subjects with AHU. Higher TFPI levels in GA patients -probably associated with enhanced endothelial damage- were related to subclinical atherosclerosis. Lower TAFI levels in GA pointed to impaired fibrinolysis.