Inflammation in patients with lupus anticoagulant and implications for thrombosis

The underlying mechanism of the prothrombotic state associated with the lupus anticoagulant (LAC) has not been fully elucidated. Evidence suggests involvement of inflammation in arterial and venous thrombosis, and it may be hypothesized that subclinical inflammation aggravates the tendency to thrombosis in patients with LAC.

Levels of high sensitivity C-reactive protein (hs-CRP), fibrinogen, and factor VIII (VIII) were measured in 38 patients with LAC and a history of thrombosis, 27 with LAC and no history of thrombosis, and 33 healthy controls.

Hs-CRP, fibrinogen, and factor VIII levels were significantly higher in patients with LAC with thrombosis (hs-CRP median = 0.3 mg/dl, interquartile range, IQR, 0.11-0.62, p < 0.001 vs controls; fibrinogen mean = 395 +/- 90 SD mg/dl, p < 0.001; factor VIII mean = 181 +/- 50%, p = 0.005) as well as in those without thrombosis (median = 0.21, IQR 0.10-0.12, p < 0.001; mean = 378 +/- 91, p = 0.003; mean = 179 +/- 39, p = 0.015) compared to controls (median = 0.07, IQR 0.03-0.12; mean = 308 +/- 48; mean = 137 +/- 39). After adjustment for age, body mass index, smoking status, and blood group (only for factor VIII) the differences between LAC groups and controls remained significant, except for the comparison of fibrinogen between patients without thrombosis and controls. The association between LAC and markers of inflammation was confirmed using linear regression analysis. Markers of systemic inflammation did not differentiate between LAC patients with and without thrombosis (p = 0.829 for hs-CRP, p = 0.649 for fibrinogen, p = 0.996 for factor VIII).

Our results show that LAC is associated with an inflammatory state. However, there was no evidence for an association between inflammatory markers and thromboembolism in patients with LAC.