@article {WAHEZI382, author = {DAWN M. WAHEZI and NORMAN T. ILOWITE and SWAPNIL RAJPATHAK and JACOB H. RAND}, title = {Prevalence of Annexin A5 Resistance in Children and Adolescents with Rheumatic Diseases}, volume = {39}, number = {2}, pages = {382--388}, year = {2012}, doi = {10.3899/jrheum.110768}, publisher = {The Journal of Rheumatology}, abstract = {Objective. The underlying mechanism(s) by which antiphospholipid antibodies (aPL) result in thrombosis remains poorly understood. A significant body of evidence has evolved to support the hypothesis that antibody-mediated disruption of an annexin A5 anticoagulant shield may play a role in the pathogenesis; this proposed mechanism has not been previously studied in children. Methods. We investigated the association between aPL and resistance to annexin A5 anticoagulant activity in 90 children with a variety of rheumatic diseases using a novel mechanistic assay, the annexin A5 resistance assay (A5R). Results. Patients with a diagnosis of primary aPL syndrome, systemic lupus erythematosus, and mixed connective tissue disease demonstrated lower mean A5R levels (p = 0.030), higher prevalence of positive aPL (p \< 0.001), and more thrombotic events (p = 0.014) compared to those with other diagnoses. Patients with persistently positive aPL had significantly lower mean A5R compared to patients with no aPL (mean A5R = 203\% {\textpm} 44\% vs 247\% {\textpm} 35\%; p \< 0.001), whereas patients with transient aPL did not. Patients with thrombosis had lower A5R levels compared to those without thrombosis (mean A5R = 207\% {\textpm} 36\% vs 237\% {\textpm} 46\%; p = 0.048). Conclusion. Children and adolescents with rheumatic diseases and persistent aPL have reduced annexin A5 anticoagulant activity, whereas transient, nonpathogenic aPL have less effect on annexin A5 activity.}, issn = {0315-162X}, URL = {https://www.jrheum.org/content/39/2/382}, eprint = {https://www.jrheum.org/content/39/2/382.full.pdf}, journal = {The Journal of Rheumatology} }