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Antiphospholipid Antibodies and Incidence of Venous Thrombosis in a Cohort of Patients with Systemic Lupus Erythematosus
EMILY SOMERS, LAURENCE S. MAGDER, and MICHELLE PETRI
ABSTRACT. Methods. The study population consisted of 678 patients with SLE enrolled in the Hopkins Lupus Cohort. Medical records were reviewed to identify the occurrence of VT prior to cohort entry. During cohort participation, VT was diagnosed by ultrasound or venography. Lupus anticoagulant [LAC, Russell viper venom time (RVVT) assay] and anticardiolipin (aCL, polyclonal assay) status of each subject was determined on a quarterly basis. The Kaplan-Meier approach was used to estimate probability of having a VT over time since SLE diagnosis. The association between the most recently measured values of LAC and aCL on the subsequent risk of VT was estimated using Cox proportional hazards models. Results. Counting only first occurrences, the rate of VT was 5.1 cases per 1000 person-years. Of those with a mean RVVT greater than 37 s during followup, an estimated 42% will develop a VT within 20 years of SLE diagnosis [95% confidence interval (CI) 21% to 63%, p < 0.0001 compared to those with lower RVVT]. The immediate risk (hazard) of deep venous thrombosis increased 34% with each 5 second prolongation of the RVVT test, based on the most recent assessment of RVVT, controlling for gender and cholesterol [p = 0.0022, 95% CI 11% to 61%]. Of those with a mean polyclonal aCL greater than 2.3 units, 34% developed a VT within 20 years of SLE diagnosis (95% CI 11% to 57%, p = 0.0097 compared to those with lower aCL). The immediate risk (hazard) of deep venous thrombosis was not significantly associated with the most recent assessment of aCL. Conclusion. This large prospective study indicates that patients with SLE are at substantial risk for VT over time. Both the presence of a LAC and of polyclonal aCL are associated with the risk of VT, but LAC is a better predictor of risk than is aCL. (J Rheumatol 2002:29:2531-6) Key Indexing Terms:
ANTIPHOSPHOLIPID ANTIBODIES
From Johns Hopkins University, School of Medicine and the University of Maryland, School of Medicine, Baltimore, MD, USA. Supported by grant NIH RO-1 AR 43727, the Johns Hopkins University Outpatient Clinical Research Center Grant # M01RR00052, and the Sally Nyborg Foundation. E. Somers, ScM, School of Medicine, Johns Hopkins University; L.S. Magder, PhD, MPH, School of Medicine, University of Maryland; M. Petri, MD, MPH, School of Medicine, Johns Hopkins University. Address reprint requests to Dr. M. Petri, Johns Hopkins University, 1830 E. Monument St., Suite 7500, Baltimore, MD 21205. E-mail: mpetri@welch.jhu.edu Submitted October 10, 2001; revision accepted June 21, 2002. |