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Blood, 1 November 2004, Vol. 104, No. 9, pp. 2783-2790.
Prepublished online as a Blood First Edition Paper on July 8, 2004; DOI 10.1182/blood-2004-01-0203.
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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Detection of antibody-mediated reduction of annexin A5 anticoagulant activity in plasmas of patients with the antiphospholipid syndrome
Jacob H. Rand,
Xiao-Xuan Wu,
Robert Lapinski,
Waander L. van Heerde,
Chris P. Reutelingsperger,
Pojen P. Chen, and
Thomas L. Ortel
From the Department of Pathology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY; the Department of Community and Preventive Medicine, Mount Sinai School of Medicine, New York, NY; the Central Hematology Laboratory, University Medical Center St Radboud, Nijmegen, the Netherlands; the Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, the Netherlands; the Division of Rheumatology, University of California at Los Angeles, Los Angeles, CA; and the Departments of Medicine and Pathology, Duke University Medical Center, Durham, NC.
Annexin A5 (A5) forms 2-dimensional crystals over phospholipid bilayers, blocking their availability for coagulation reactions. Recently, human antiphospholipid (aPL) monoclonal antibodies (mAbs) have been demonstrated by atomic force microscopy (AFM) to disrupt this crystallization and accelerate coagulation. We therefore performed a study with small, well-defined groups of patients to investigate whether these effects on A5 binding and activity are also detectable in plasmas from patients with the aPL syndrome. A5 binding to phospholipid was significantly reduced by plasmas of patients with the aPL syndrome and thromboembolism compared with healthy controls (mean ± SD, 26.7 ± 4.3 ng/well [n = 25] vs 30.5 ± 3.1 ng/well [n = 20], P < .01) and the non-aPL thromboembolism group (29.9 ± 3.2 ng/well [n = 15], P < .05). A5 anticoagulant activity was reduced by plasmas of patients with aPL syndrome and thromboembolism compared with aPL antibodies without thrombosis (182 ± 31% [n = 25] vs 210 ± 35% [n = 26], P < .01), non-aPL thromboembolism (229 ± 16% [n = 15], P < .001), and healthy controls (231 ± 14% [n = 30], P < .001). In conclusion, in accordance with recent AFM data with monoclonal human aPL antibodies, plasmas from patients with aPL antibodies with thromboembolism reduce both A5 binding to phospholipid and A5 anticoagulant activity. This "annexin A5 resistance" identifies a novel mechanism for thrombosis in the aPL syndrome. (Blood. 2004;104: 2783-2790)
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