The activation of factor XII complexes could be potential biomarkers for the risk for thrombotic events in patients with systemic lupus erythematosus, according to recent study results.
Researchers in Sweden incubated fibrin clots with whole blood or purified factor XII (FXII), a contact system component and plasma protease cascade that initiates coagulation when activated. Plasma was collected from 69 systemic lupus erythematosus (SLE) patients with previous vascular disease (VD; n=31) or without (n=38) and from 68 age- and sex-matched healthy controls with no history of VD. All were studied for activation and regulation of FXII, and researchers analyzed and evaluated samples for complexes formed between contact system enzymes and antithrombin [AT] or C1 inhibitor [C1INH]. Eight years was the median time between sampling and the last VD event.
Fibrin clots created significant FXII generation and were cofactors for AT. FXIIa-AT levels increased, and FXIIa-C1INH levels decreased in clotting plasma, with SLE patients displaying a similar reciprocal relationship. In SLE patients with VD history, FXIIa-AT was elevated while there was a significant decrease in the corresponding levels of factor FXIIa-C1INH. Platelet parameters were strongly correlated with FXIIa-AT.
Among SLE patients, odds ratios for VD were 8.9 (95% CI, 2.8-28.5) for those with low levels of FXIIa-C1INH, OR=6.1 (95% CI, 1.7-21.6) for patients with high levels of FXIIa-AT and OR=23.4 (95% CI, 2.8-194) for patients who combined both complexes.
“This study shows that activation of the contact system is involved in the pathophysiology of the SLE and that the activation of the contact system is likely to be triggered by fibrin,” the researchers concluded. “We show that the formation of FXIIa-AT complexes is associated with thrombotic events and that generation of these complexes represents a promising potential biomarker for evaluation of the risk of thrombotic events in SLE.”
Disclosure: The researchers report no relevant financial disclosures.