Role of anti-annexin A5 in pathogenesis of hypercoagulable state in patients with antiphospholipid syndrome
Article first published online: 28 JAN 2013
© 2013 The Authors International Journal of Rheumatic Diseases © 2013 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd
International Journal of Rheumatic Diseases
Volume 16, Issue 3, pages 325–330, June 2013
How to Cite
Singh, N. K., Yadav, D. P., Gupta, A., Singh, U. and Godara, M. (2013), Role of anti-annexin A5 in pathogenesis of hypercoagulable state in patients with antiphospholipid syndrome. International Journal of Rheumatic Diseases, 16: 325–330. doi: 10.1111/1756-185X.12044
- Issue published online: 11 AUG 2013
- Article first published online: 28 JAN 2013
- anti-phospholipid antibody syndrome;
- disease aetiology and pathogenesis;
- human anti-phospholipid antibody syndrome
Despite several attempts made during the last decade, the exact pathogenesis of exceedingly high thrombotic events and bad obstetric outcome in antiphospholipid syndrome (APS) remains elusive. Anti-annexin A5 (aANX IgG) is thought to have a role in pathophysiology of APS. We studied role of aANX IgG in the pathogenesis of hypercoagulable state in APS patients.
We estimated levels of aANX IgG in 112 patients with APS (86 primary and 26 secondary). We also estimated aANX IgG levels in 40 age- and sex-matched healthy controls, 10 patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) each, without any history of thrombosis or pregnancy morbidity, 10 patients of non-APS thrombosis and 10 patients of pregnancy loss without APS.
Only three healthy controls, two SLE (P = 0.239), one RA patient (P = 0.794), three non-APS thrombosis patients (P = 0.086) and two patients with pregnancy loss without APS (P = 0.258) had marginally elevated values, whereas 53 primary APS (P < 0.001) and 16 secondary APS (P < 0.001) were positive. We also compared aANX IgG levels in different groups. Mean ± standard errors of the mean of healthy controls was 3.77 ± 0.49, in SLE patients it was 4.88 ± 1.17 (P = 1.000), in RA patients it was 4.67 ± 0.97 (P = 1.000), in non-APS thrombosis it was 7.93 ± 0.88 (P = 0.488) and in pregnancy loss without APS it was 6.80 ± 0.93 (P = 0.789). However, it was significantly elevated in primary APS (12.87 ± 1.07, P < 0.001), secondary APS (11.98 ± 1.41, P = 0.001) and total APS patients (12.68 ± 0.88, P < 0.001).
From the above observations it appears that aANX IgG plays a significant role in producing a hypercoagulable state in primary and secondary APS.