The Presence of Multiple Prothrombotic Risk Factors Is Associated with a Higher Risk of Thrombosis in Individuals with Anticardiolipin Antibodies

MARIE HUDSON, ANDRÉE-LAURE HERR, JOYCE RAUCH, CAROLYN NEVILLE, ERIKA CHANG, REDA IBRAHIM, CHANTAL SÉGUIN, JEANNINE KASSIS, LAMBERT BUSQUE, and PAUL R. FORTIN

ABSTRACT.

Objective. To explore the effect of multiple prothrombotic risk factors in individuals with anticardiolipin antibodies (aCL), we evaluated immunologic, coagulation, and genetic prothrombotic abnormalities in a cohort of individuals with different aCL titers.

Methods. We recruited 87 individuals into 4 categories (normal, low, intermediate, or high) based on their baseline IgG aCL (aCL-IgG) titers. We measured at followup: repeat aCL-IgG, IgM aCL (aCL-IgM), antibodies to ß2-glycoprotein I (anti-ß₂-GPI), lupus anticoagulant (LAC) antibodies, protein C, protein S, activated protein C resistance, factor V⁵⁰⁶ Leiden mutation, methyl tetrahydrofolate reductase (MTHFR) C677T genotype, and prothrombin 20210A gene mutation. Thrombotic events were confirmed.

Results. At recruitment, 20 individuals were negative for aCL-IgG and 67 were positive (22 low, 20 intermediate, and 25 high titer). Twenty of the 87 participants had experienced a previous thrombotic event: 4 in the aCL-IgG negative group and 16 in the aCL-IgG positive group. Among the 87 individuals, the number of those with concomitant prothrombotic risk factors was as follows: 5 had no other prothrombotic risk factors, 32 had 1 risk factor, 24 had 2 risk factors, 10 had 3 risk factors, 10 had 4 risk factors, and 6 had 5 risk factors. Thrombotic events were observed in 20%, 13%, 33%, 10%, 30%, and 50% of these groups, respectively, and the odds ratio associated with a previous thrombotic event was 1.46 per each additional prothrombotic risk factor (95% confidence interval: 1.003-2.134).

Conclusion. In individuals with positive aCL-IgG, we observed an association between the number of prothrombotic risk factors and history of thrombotic events. (J Rheumatol 2003;30:2385-91)

Key Indexing Terms:

THROMBOSIS
ANTIBODIES
ANTICARDIOLIPIN
LUPUS COAGULATION INHIBITOR
THROMBOPHILIA
FACTOR V

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From the Divisions of Rheumatology, Internal Medicine, and Clinical Epidemiology, Department of Medicine, McGill University Health Centre, Montreal General Hospital; the Department of Hematology, Maisonneuve-Rosemont Hospital, Montreal, Quebec; and the Arthritis Centre of Excellence, Division of Rheumatology, Toronto Western Hospital of the University Health Network, Toronto, Ontario, Canada.

Supported by operating grants from The Arthritis Society. Dr. Busque is a Scholar of the Fonds de la Recherche en Santé du Québec. Dr. Fortin is a Senior Scholar of The Arthritis Society, and is supported in part by the Arthritis Centre of Excellence at the University of Toronto.

M. Hudson, MD, FRCPC, Division of Rheumatology; A-L. Herr, MD, Division of Internal Medicine; J. Rauch, PhD, Division of Rheumatology, Department of Medicine, McGill University Health Centre, Montreal General Hospital, and Associate Professor, McGill University; C. Neville, RN, BA, Clinical Epidemiology, Department of Medicine, Montreal General Hospital; E. Chang, MSc, Arthritis Centre of Excellence, Division of Rheumatology, Toronto Western Hospital of the University Health Network; R. Ibrahim, MD, FRCPC; C. Séguin, MD, FRCPC; J. Kassis, MD, FRCPC; L. Busque, MD, FRCPC, Department of Hematology, Maisonneuve-Rosemont Hospital; P.R. Fortin, MD, MPH, FRCPC, Arthritis Centre of Excellence, Division of Rheumatology, Toronto Western Hospital of the University Health Network.

Address reprint requests to Dr. P.R. Fortin, Division of Rheumatology, Room MP-10-304, Toronto Western Hospital, 399 Bathurst St, Toronto, ON, Canada, M5T 2S8. E-mail: paul.fortin@uhn.on.ca.

Submitted January 10, 2003; revision accepted April 15, 2003.

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