Hyperfibrinogenemia and Increased Stiffness of Plasma Clots in the Active Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease associated with an increased risk of thrombosis. We hypothesized that inflammation-associated hyperfibrinogenemia can contribute to the prothrombotic phenotype of fibrin clots by changing their mechanical properties. Twenty-eight SLE patients were categorized based on their disease activity scores (SLEDAI) into the groups with inactive (SLEDAI 4, n = 14) forms of the disease. Clots from individual platelet-free plasma samples were probed using shear rheometry and viscoelastic properties of the fibrin gels were determined as the storage ( G′ ) and loss ( G ″) moduli. A significant increase of G ′ was revealed in the clots from the plasma of active SLE patients over inactive SLE, which correlated with elevated fibrinogen levels. Clots from the plasma of inactive SLE patients had the elasticity and fibrinogen levels indistinguishable from those in control plasma from healthy subjects. Thus, inflammatory hyperfibrinogenemia in the active SLE form makes fibrin clots stiffer which has been previously shown to be associated with a higher incidence of thrombotic disorders.