Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement
Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.
Influenza Vaccination Can Induce New Onset Anticardiolipins but Not 2-Glycoprotein-I Antibodies among Patients with Systemic Lupus Erythematosus.
Vista3, Evan Glenn, Crowe3, Sherry R., Dedeke3, Amy B., Anderson2, Jourdan R., Thompson3, Linda F., Air4, Gillian, James1, Judith A.
Oklahoma Med Research Foundation, Oklahoma City, OK
Oklahoma Medical Research Foundation
Oklahoma Medical Research Foundation, Oklahoma City, OK
University of Oklahoma Health Science Center, Oklahoma City, OK
Antiphospholipid syndrome is characterized by pathogenic autoantibodies against anticardiolipins (aCLs), lupus anticoagulant, and Independent b2-glycoprotein (b2GPI). The factors causing production of these antiphospholipid antibodies (aPLs) remain unidentified but have been documented in a large number of infectious diseases. Controversy exists as to whether vaccination triggers the same autoimmune reactions as infections in systemic lupus erythematosus (SLE) patients. Among the aPLs, b2GPI has been described as the actual target antigen for autoimmune aPLs, but conflicting reports still exist.
A total of 102 patients fulfilling the ACR criteria for SLE and 104 age, race and gender matched healthy controls enrolled in our lupus flu cohort from 2005 to 2009 and received regular seasonal influenza vaccinations. Sera were tested by ELISA for aCL IgG at the time of vaccination and 2, 6 and 12 weeks after vaccination. The international standardized ratios for aCL reactivity were calculated for each and manufacture cut-offs were used to define low, moderate, and high levels of aCL. Logistic regression was used to account randomly for those enrolled in multiple years to select the unique 206 individuals. Vaccine responses were ranked either as high or low according to an overall anti-influenza antibody response index (which includes hemagglutination inhibition, relative avidity and maximum native antibody responses). Those who have new onset reactivity to aCL IgG were further tested for b2GPI IgG antibodies. Paired t-testing for all patients with aCL reactivity was used to determine changes after vaccination at 2, 6, and 12 weeks compared to baseline.
More SLE patients compared to healthy controls developed new low aCL reactivity (14/102 cases and 4/104 controls; OR 4.1, p 0.02) and new moderate aCL reactivity (13/102 cases and 3/104 controls; OR 5.1, p 0.01) after influenza vaccination. From specific timepoints after vaccination, new low aCL reactivity were significant for SLE patients after 6 weeks (11/102 cases and 1/104 control) and 12 weeks (10/102 cases and 2/104 control) (OR 12.8, p 0.02 and OR 5.7, p 0.03 respectively) and for new moderate aCL reactivity only after 6 weeks (10/102 cases and 1/104 controls; OR 11.5, p 0.02). High aCL reactivity was only seen among 2 patients with low and moderate aCL reactivity pre-vaccination. Overall, vaccine response was significantly higher among patients with new onset aCL reactivity compared to controls (p 0.02). No new b2GPI antibodies were detected post-vaccination among patients with new aCL reactivity. The normalized optical density measurements for patients with recorded aCL reactivity at any time points were significantly higher after 2 weeks (0.43±0.24, p 0.0013), 6 weeks (0.49±0.37, p 0.004), and 12 weeks (0.47±0.44, p 0.03) after vaccination compared to the baseline (0.30±0.15).
This study shows transient increases in aCLs, but not anti-b2GPI responses, after influenza vaccination supporting the possibility that these changes in autoantibody levels may not be clinically important for increased thrombosis risk post-vaccination.
To cite this abstract, please use the following information:
Vista, Evan Glenn, Crowe, Sherry R., Dedeke, Amy B., Anderson, Jourdan R., Thompson, Linda F., Air, Gillian, et al; Influenza Vaccination Can Induce New Onset Anticardiolipins but Not 2-Glycoprotein-I Antibodies among Patients with Systemic Lupus Erythematosus. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :9