Occurrence of anti-prothrombin and anti-β2- glycoprotein I antibodies in patients with history of thrombosis

Which are the Best Biological Markers of the Antiphospholipid Syndrome?

“…Although it can be recognized in some patients, the frequency does not seem to be high [39,59,63,73,74,78,86]. Possible explanations for the antibody reactivity against human 2-GPI-but not to PL-based ELISAs may be the species specificity found in anti-2-GPI (specially IgM) [87] or that the epitope recognized by antibodies is not expressed when 2-GPI is bound to PLs.…”

Does the anti-prothrombin antibodies measurement provide additional information in patients with thrombosis?

“…A few previous studies reported the presence of IgG-anti-prothrombin antibodies in LA or aCL-negative patients with thrombosis (Barcat et al, 1999;Forastiero et al, 1999). However in these studies, the presence of anti-prothrombin antibodies was only investigated using an ELISA directed against human aPT.…”

“…It is worth noting that the majority of clinical studies were focused on the prevalence and the clinical significance of aPT and/or aPS/PT in systemic lupus erythematosus (Atsumi et al, 2000). Few studies reported the presence of anti-prothrombin antibodies in patients with previous thrombosis without aPL (Vaarala et al, 1996;Forastiero et al, 1999).…”

Anti-β2-glycoprotein I antibodies of IgM class are linked to thrombotic disorders in young women without autoimmune disease

“…Evidence suggesting a relationship between anti-b2GPI and the risk of arterial and venous thrombosis in these patients is not so abundant and uniform results have not been found. The predominance of isotype IgG, or IgM, or both, or none has been reported in different groups of patients with different localization of the thrombosis (Forastiero et al, 1999;Zanon et al, 1999;Farsi et al, 1999;Galli et al, 2000;Brey et al, 2001;Previtali et al, 2002). Evidently, additional data focused on strictly defined subgroups of patients are needed.…”

“…However, their exact prevalence and role in the pathogenesis of arterial and venous thromboses in the absence of autoimmune disease is still inconclusive (Hughes, 1998;Forastiero et al, 1999;Zanon et al, 1999;Petri, 2000;Brey et al, 2001;Previtali et al, 2002).…”