DANIELLE MARTINS DE MEDEIROS HISANO
Projetos de Pesquisa
Unidades Organizacionais
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.- Juvenile onset systemic lupus erythematosus: a possible role for vitamin D in disease status and bone health(2012) CASELLA, C. B.; SEGURO, L. P. C.; TAKAYAMA, L.; MEDEIROS, D.; BONFA, E.; PEREIRA, R. M. R.Purpose: In juvenile onset systemic lupus erythematosus (JoSLE), evidence for the association between vitamin D status, lupus activity, and bone health is very limited and not conclusive. The aim of this study was, therefore, to assess in JoSLE patients the possible relevance of vitamin D deficiency in disease and bone parameters. Methods: Fifty-seven JoSLE patients were initially compared to 37 age, race and body mass index (BMI) -matched healthy controls. The serum concentration of 25 hydroxyvitamin D (25OHD) was determined by radioimmunoassay. Patients with 25OHD deficiency (acurrency sign20 ng/mL) were compared to those with levels > 20 ng/mL. Disease activity was evaluated by SLE Disease Activity Index (SLEDAI). Bone mineral density (BMD) and body composition (BC) were measured using dual-energy X-ray absorptiometry (DXA). Results: 25OHD levels were similar in patients and controls (21.44 +/- 7.91 vs 22.54 +/- 8.25 ng/mL, p = 0.519), regardless of supplementation (65% of patients and none in controls). Thirty-one patients with 25OHD deficiency (acurrency sign20 ng/mL) were further compared to the 26 JoSLE patients with levels > 20 ng/mL. These two groups were well-balanced regarding vitamin D confounding variables: age (p = 0.100), ethnicity (p = 1.000), BMI (p = 0.911), season (p = 0.502), frequency of vitamin D supplementation (p = 0.587), creatinine (p = 0.751), renal involvement (p = 0.597), fat mass (p = 0.764), lean mass (p = 0.549), previous/current use of glucocorticoids(GC) (p = 1.0), immunosuppressors (p = 0.765), and mean current daily dose of GC (p = 0.345). Patients with vitamin D deficiency had higher SLEDAI (3.35 +/- 4.35 vs 1.00 +/- 2.48, p = 0.018), lower C4 levels (12.79 +/- 6.78 vs 18.38 +/- 12.24 mg/dL, p = 0.038), lower spine BMD (0.798 +/- 0.148 vs 0.880 +/- 0.127 g/cm2, p = 0.037) and whole body BMD (0.962 +/- 0.109 vs 1.027 +/- 0.098 g/cm2, p = 0.024). Conclusion: JoSLE vitamin D deficiency, in spite of conventional vitamin D supplementation, affects bone and disease activity status independent of therapy and fat mass reinforcing the recommendation to achieve adequate levels. Lupus (2012) 21, 1335-1342.
- Increased arterial stiffness assessed by pulse wave velocity in Behcet's disease and its association with the lipid profile(2013) CALDAS, C. A. M.; BORBA, E. F.; BORTOLOTTO, L. A.; MEDEIROS, D. M.; BONFA, E.; GONCALVES, C. R.Objective To evaluate the structural and functional properties of vessels in Behcet's Disease (BD) using carotid-femoral pulse wave velocity (PWV) and an echo-tracking system. Methods BD patients without traditional cardiovascular risk factors were selected. All BD patients performed PWV and carotid ultrasound. BD patients were divided into groups based on the presence of systemic (vascular and/or ocular and/or central nervous system involvement) and vascular involvement. Healthy controls age- and sex-matched with the same exclusion criteria were selected. Results A total of 23 BD patients (mean age 35.0 +/- 7.6years) had significantly higher PWV levels compared with controls (8.48 +/- 1.14 vs. 7.53 +/- 1.40m/s, P=0.017). Intima-media thickness (594.87 +/- 138.61 vs. 561.08 +/- 134.26m, P=0.371), diastolic diameter (6383.78 +/- 960.49 vs. 6447.65 +/- 1159.73m, P=0.840), distension (401.95 +/- 117.72 vs. 337.91 +/- 175.36m, P=0.225) and relative distension (6.26 +/- 2.83 vs. 5.42 +/- 2.46m, P=0.293) were similar in both groups. The systemic disease group had significantly higher levels of PWV (8.79 +/- 1.21 vs. 7.88 +/- 0.72m/s, P=0.036) compared to those with exclusive mucocutaneous manifestations. BD patients with vascular involvement had similar PWV and echo-tracking parameters compared to those without vascular involvement (0.05), but had higher total and LDL cholesterol levels (P=0.019 and P=0.012, respectively). The multivariate linear regression analysis identified triglycerides as the most important factor in increasing PWV levels (P=0.001) in BD. Conclusions PWV is more useful than carotid ultrasound in detecting structural and functional vascular damage in BD and emphasizes the role of the disease itself in promoting these alterations. Our findings also reinforce the need for rigorous control of all risk factors in BD, particularly lipoproteins.
- Pandemic influenza immunization in primary antiphospholipid syndrome (PAPS): a trigger to thrombosis and autoantibody production?(2014) MEDEIROS, D. Martins de; SILVA, C. A.; BUENO, C.; RIBEIRO, A. C. Medeiros; VIANA, V. dos Santos T.; CARVALHO, J. Freire; BONFA, E.Objective The objective of this report is to conduct short- and long-term evaluation of a large panel of antiphospholipid (aPL) autoantibodies following pandemic influenza A/H1N1 non-adjuvant vaccine in primary antiphospholipid syndrome (PAPS) patients and healthy controls. Methods Forty-five PAPS and 33 healthy controls were immunized with H1N1 vaccine. They were prospectively assessed at pre-vaccination, and three weeks and six months after vaccination. aPL autoantibodies were determined by an enzyme-linked immunosorbent assay (ELISA) and included IgG/IgM: anticardiolipin (aCL), anti-beta2glycoprotein I (anti-2GPI); anti-annexin V, anti-phosphatidyl serine and anti-prothrombin antibodies. Anti-Sm was determined by ELISA and anti-double-stranded DNA (anti-dsDNA) by indirect immunofluorescence. Arterial and venous thrombosis were also clinically assessed. Results Pre-vaccination frequency of at least one aPL antibody was significantly higher in PAPS patients versus controls (58% vs. 24%, p=0.0052). The overall frequencies of aPL antibody at pre-vaccination, and three weeks and six months after immunization remained unchanged in patients (p=0.89) and controls (p=0.83). The frequency of each antibody specificity for patients and controls remained stable in the three evaluated periods (p>0.05). At three weeks, two PAPS patients developed a new but transient aPL antibody (aCL IgG and IgM), whereas at six months new aPL antibodies were observed in six PAPS patients and none had high titer. Anti-Sm and anti-dsDNA autoantibodies were uniformly negative and no new arterial or venous thrombosis were observed throughout the study. Conclusions This is the first study to demonstrate that pandemic influenza vaccine in PAPS patients does not trigger short- and long-term thrombosis or a significant production of aPL-related antibodies (ClinicalTrials.gov, #NCT01151644).