DANIELLE MARTINS DE MEDEIROS HISANO
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LIM/17 - Laboratório de Investigação em Reumatologia, Hospital das Clínicas, Faculdade de Medicina
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conferenceObject Pandemic Influenza Immunization in Primary Antiphospholipid Syndrome (PAPS): A Trigger to Autoantibody Production?(2012) MEDEIROS, Danielle M.; BUENO, Cleonice; RIBEIRO, Ana Cristina M.; CALICH, Ana L. G.; BONFIGLIOLI, Karina Rossi; VIANA, Vilma S.; CARVALHO, Jozelio F.; SILVA, Clovis Artur; BONFA, EloisaBackground/Purpose: There are scarce data suggesting that pan-demic influenza vaccination may induce antiphospholipid (APL) autoan- tibodies in inflammatory rheumatic diseases, particularly in systemic lupus erythematosus patients. However, there is no study evaluating the APL autoantibodies induction in primary antiphospholipid syndrome (PAPS) patients. The objective was to perform short and long-term evaluations of a large panel of APL autoantibodies following pandemic influenza A/H1N1 non-adjuvant vaccine in PAPS patients and healthy controls. Lupus specific antibodies were also investigated in these patients. Methods: Forty-five PAPS patients (Sapporo criteria) and 33 healthy controls were vaccinated with monovalent, inactivated H1N1 vaccine (Butantan Institute/Sanofi Pasteur, São Paulo, Brazil). They were prospec-tively assessed at pre-vaccination, 3 weeks and 6 months after vaccination. APL autoantibodies were determined by an enzyme-linked immunosor-bent assay (ELISA) and included: anti-cardiolipin (aCL) IgG/IgM and anti-β2GPI IgG/IgM antibodies (Inova Diagnostics, USA); anti-annexin V IgG/IgM, anti-phosphatidyl serine IgG/IgM and anti-prothrombin IgG/IgM (Orgentec Diagnostica, Germany). Anti-Sm was determined by ELISA (Inova Diagnostics, USA) and anti-dsDNA by indirect immun-fluorescence. Arterial and venous thromboses were also clinically assessed. The statistical analyses were carried out with qui square test, McNemar s test and one-way repeated measures analysis of variance (ANOVA). Results: Pre-vaccination frequency of at least one APL antibody was significantly higher in PAPS patients compared to controls (58% vs. 21%, p=0.003). The overall frequencies of APL antibody at pre-vaccination, 3 weeks and 6 months after immunization remained unchanged in patients (p=0.89) and controls (p=0.83). Further analysis of each evaluated antibody in PAPS revealed that their percentages at pre-vaccination and after 3 weeks and 6 months were also comparable (p>0.05): aCL IgG (42%, 38% and 42%), aCL IgM (22%, 20% and 24%), anti-β2GPI IgG (22%, 22% and 20%), anti-β2GPI IgM (15%, 15% and 18%), anti- annexin V IgG (4.5%, 4.5% and 2.5%), anti-annexin V IgM (uniformly negative), anti-phosphatidyl serine IgG (38%, 35% and 38%), anti- phosphatidyl serine IgM (15%, 13% and 13%), anti-prothrombin IgG (20%, 15% and 18%) and anti-prothrombin IgM (2.5%, 2.5% and 2.5%). The same pattern was observed for the control group (p>0.05). At 3 weeks, 2 PAPS patients developed a new but transient APL anti-body (moderate titer aCL IgG and IgM) whereas at 6 months, new APL antibodies were observed in 6 PAPS patients: 3 moderate titer aCL IgM, 1 moderate anti-β2GPI IgM, 1 low anti-phosphatidyl serine IgG and 1 low anti-prothrombin IgG. Fluctuations of antibody levels were not detected for any evaluated antibody (p>0.05). Of note, anti-Sm and anti-dsDNA autoantibodies were consistently negative during all evaluations. No new arterial or venous thrombosis events occurred during the study period. Conclusion: This was the first study to demonstrate that pandemic non-adjuvant influenza A/H1N1 in PAPS patients does not trigger a change in APL antibody profile or induce lupus specific autoantibodies.