EDUARDO FERREIRA BORBA NETO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina - Docente
LIM/17 - Laboratório de Investigação em Reumatologia, Hospital das Clínicas, Faculdade de Medicina
LIM/17 - Laboratório de Investigação em Reumatologia, Hospital das Clínicas, Faculdade de Medicina
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conferenceObject Dyslipidemia in Juvenile Dermatomyositis: The Role of Disease Activity(2012) KOZU, Katia T.; SILVA, Clovis Artur; BONFA, Eloisa; SALLUM, Adriana M.; PEREIRA, Rosa M. R.; VIANA, Vilma S.; BORBA, Eduardo F.; CAMPOS, Lucia M. A.conferenceObject Peripheral Neuropathy Due to Systemic Lupus Erythematosus (SLE) Itself: Incidence, Disease Risk Factors and Outcome(2012) FARGETTI, Simone; SHINJO, Samuel K.; PASOTO, Sandra G.; CALICH, Ana L.; BONFA, Eloisa; BORBA, Eduardo F.Background/Purpose: Peripheral neuropathy (PN) solely attributable to SLE itself is difficult to define since most of these patients are exposed to several other conditions that may cause this manifestation. The aim is to determine characteristics and outcome of PN attributed exclusively to SLE and its possible association with clinical/laboratorial features in a large cohort. Methods: SLE patients (ACR 1997) with PN were identified from our Lupus Outpatient Clinic computerized database of 1038 patients. Only patients with definitive PN proved by electroneuromyography were included. Exclusion criteria were conditions related to PN: diabetes mellitus, alcohol consumption, use of any drug related to neuropathy (thalidomide, statins, etc.), thyroid disease, infection, cancer, vitamin B12 deficiency, renal or hepatic failure, and other autoimmune disease (antiphospholipid syndrome, Sjogren’s syndrome, etc.). Medical records were extensively reviewed and included clinical/laboratorial data, treatment, and evolution. Each SLE patient with PN [n 22] was compared with 2 SLE patients without PN (controls) [n 44] that were age- and sex-matched and had similar disease duration. Results: PN exclusively attributed to SLE was identified in 22 patients (2.1%). The mean age (34.4 11.6 vs. 33.9 9.6 years, p 0.85) and disease duration (9.2 7.7 vs. 9.9 6.8 years, p 0.73) of PN were similar to controls. The interval between SLE onset and PN diagnosis was 4.9 5.7 years and the mean SLEDAI scores was higher in PN patients (5.4 7.6 vs. 1.8 2.9,p 0.001). The most common pattern on electroneuromyography was sensorimotor polyneuropathy of lower limbs (50%), followed by monon-europathy (26.9%), and polyradiculoneuropathy (15.3%). PN was associated to hematological involvement (72.7% vs. 43.2%,p 0.036), leukopenia (50% vs. 20.5%,p 0.022), lymphopenia (68.2% vs. 29.5%,p 0.004), cutaneous vasculitis (54.5% vs. 22.7%,p 0.014), and anti-Sm (50% vs. 15.9%,p 0.007). Multivariate analysis revealed that PN was related to anti-Sm (OR 5.36; 95%CI 1.37–20.99) and cutaneous vasculitis (OR 4.97; 95%CI 1.23–20.08). All SLE patients received corticosteroids, most of them associated with immunosuppressive drug (59% cyclophosphamide; 31.8% azathioprine). After immunosuppressive therapy, 63.6% improved of neurological symptoms and 31.8% remained stable. Conclusion: Our study suggested that PN attributed to SLE itself is rare in the absence of other conditions and seems to be strongly associated to anti-Sm antibodies and cutaneous vasculitis. A favorable outcome with immunosuppressive therapy is observed in most of SLE patients with this neurological manifestation.conferenceObject The Influence Of Socioeconomic and Race In Damage Score In Patients With Systemic Lupus Erythematosus(2013) TEIXEIRA, Roberto; BORBA, Eduardo F.; SR., Georges Christopoulos; SATO, EmiliaconferenceObject Anti-Ribosomal P Antibodies in a Large Cohort of Autoimmune Hepatitis with No Evidence of Lupus: A Common Underlying Mechanism Targeting Liver?(2012) CALICH, Ana Luisa; VIANA, Vilma S. T.; CANCADO, Eduardo L.; TERRABUIO, Debora R.; TUSTUMI, Francisco; LEON, Elaine P.; SILVA, Clovis Artur; BORBA NETO, Eduardo F.; BONFA, EloisaconferenceObject Inactive Systemic Lupus Erythematosus: Cytokines and Soluble Tumor Necrosis Factor Receptors Response To Moderate/Intense Exercise(2013) PERANDINI, Luiz A.; SALES-DE-OLIVEIRA, Diego; MELLO, Suzana B. V.; CAMARA, Niels O.; LIMA, Fernanda R.; BORBA, Eduardo F.; BONFA, Eloisa; SA-PINTO, Ana Lucia; ROSCHEL, Hamilton; GUALANO, BrunoconferenceObject Active Systemic Lupus Erythematosus: Cytokines and Soluble Tumor Necrosis Factor Receptors Response To Moderate/Intense Exercise(2013) PERANDINI, Luiz A.; SALES-DE-OLIVEIRA, Diego; MELLO, Suzana B. V.; CAMARA, Niels O.; LIMA, Fernanda R.; BORBA, Eduardo F.; BONFA, Eloisa; SA-PINTO, Ana Lucia; ROSCHEL, Hamilton; GUALANO, BrunoconferenceObject Podocyte Injury in Membranous and Proliferative Lupus Nephritis: Distinct Underlying Mechanisms?(2012) REZENDE, Gabriela M.; VIANA, Vilma S. T.; MALHEIROS, Denise M.; LEON, Elaine P.; BORBA, Eduardo F.; SILVA, Neila A. S.; NORONHA, Irene L.; SILVA, Cleonice; BONFA, EloisaBackground/Purpose: Lupus nephritis (LN) is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE) with proteinuria being the predominant common manifestation and may therefore reflect podocyte injury. Podocytes are highly specialized cells that have a relevant role in the glomerular filtration barrier and alteration in the expression of their biomarkers has been shown to be associated with podocyte dysfunction in some glomerulopathies. A systematic analysis of podocyte-associated molecules encom-passing different subcellular compartments was performed in a large series of LN biopsies. Expression of Wilms tumor protein (WT1), Synaptopodin (Synpo) and glomerular epithelial protein 1 (GLEPP1) with nuclear, cytoplasmic and membrane distribution respectively, were evaluated attempting to identify if podocyte phenotype is distinct in proliferative and membranous nephritis. Possible association of molecular expression alterations with long term proteinuria severity and outcome in lupus was also investigated. Methods: Immunohistochemistry analysis was performed using monoclonal antibodies to WT1, Synpo and GLEPP1 proteins in 52 biopsies from patients with lupus nephritis fulfilling the revised ACR criteria for SLE. Demographic, clinical and laboratorial data at the time of biopsy were analyzed. Results: Thirty-nine (75%) biopsies were classified as proliferative LN and thirteen (25%) as pure membranous class V. Immunohistochemistry analysis in normal kidney revealed preserved staining of WT1, Synpo and GLEPP1 podocyte biomarkers along the capillary walls. Preserved and concomitant WT1 and Synpo staining was observed in a significant higher frequency in pure class V biopsies than in proliferative LN (69.23 vs. 2.56%, p 0.0001). Likewise, preserved GLEPP1 expression was also more frequent in pure class V LN (53.85 vs. 2.86%, p 0.0002). Proteinuria and serum albumin levels at the time of biopsy did not statistically differ in the two groups (p 0.87 and p 0.41) whereas in the mean long-term follow-up of four years a tendency of lower proteinuria (p 0.050) was observed in those patients with biopsies expressing preserved WT1/Synpo staining. Conclusion: This is the first study comparing proliferative and membranous lupus nephritis which evaluated simultaneously the expression of proteins in different subcellular podocyte compartments and provided novel evidence of preserved podocyte structural architecture predominantly in membranous lesions which may account for a better long term outcome of patients with this LN histological class. These findings suggest possible different underlying mechanisms for proteinuria in both conditions.conferenceObject Ovarian Dysfunction In Adult Childhood-Onset Systemic Lupus Erythematosus Patients: A Possible Role Of Methotrexate?(2013) ARAUJO, Daniel B.; YAMAKAMI, Lucas; BONFA, Eloisa; VIANA, Vilma S. T.; PASOTO, Sandra G.; PEREIRA, Rosa M.; SERAFIN, Paulo C.; BORBA, Eduardo F.; SILVA, Clovis A.conferenceObject Altered Circulating Follicular Helper T Cell Phenotype and Subset Composition Are Associated with Disease Activity in Patients with Systemic Lupus Erythematosus(2012) HO, Hsi-en; CHOI, Jin Young; BUNIN, Viviane M.; PASOTO, Sandra G.; CARRASCO, Solange; BORBA, Eduardo F.; GONCALVES, Celio R.; COSTA, Priscila R.; KALLAS, Esper G.; BONFA, Eloisa; CRAFT, Joseph E.Background/Purpose: Autoreactive B cells in SLE undergo autoantigen selection, suggesting a requirement for germinal center follicular helper T (Tfh) cells in their maturation. However, evidence for dysregulation of Tfh cells in SLE and their potential contribution to disease remains unclear. Recently, blood CXCR5 CD4 T cells, a heterogeneous pool consisting of functionally distinct Th1-, Th2-, and Th17-like subsets, have been proposed to be the circulating counterpart of Tfh (cTfh) cells. We now ask if changes in cTfh markers or subset composition within blood CXCR5 cells are found in SLE patients, and the extent to which such alterations are associated with B cell and disease activity. Methods: Blood samples from 49 clinically well-characterized SLE patients, 28 Behc ̧et’s disease (BD) patients, and 16 healthy controls were included. Expression of Tfh surface markers (CXCR5; ICOS, inducible T-cell costimulator; PD-1, programmed cell death protein-1), composition of blood CXCR5 subsets, and frequency of plasmablasts were enumerated by flow cytometry. The phenotype of blood CXCR5 subsets was correlated with disease activity, clinical history, and plasmablast expansion. Results: SLE patients had significant expansion of CXCR5 ICOS PD-1 CD4 T cells compared to controls (p 0.001). PD-1, but not ICOS or CXCR5, expression was markedly elevated in CD4 T cells of SLE patients compared to BD patients and healthy controls (p 0.001). PD-1 MFI in CXCR5 cells correlated with SLE disease activity index (SLEDAI; Spearman r 0.43, p 0.03). PD-1 MFI also correlated with expansion of plasmablasts (Spearman r 0.34, p 0.02). In SLE patients with high anti-dsDNA antibody titers, PD-1 expression in CXCR5cells was also significantly elevated compared to patients with no detectable titers (p 0.004). Enhanced PD-1 expression was neither a function of disease duration nor past activity; rather, it reflected current disease activity. Compared to BD patients, SLE patients also had an increase in the CXCR5 Th2 (p 0.05) and a decrease in the Th17 (p 0.001) subsets. Concurrently, PD-1 expression in SLE patients was significantly higher in CXCR5 Th2 cells compared to Th17 cells (p 0.01). The expansion of the CXCR5 Th2 subset was also positively associated with SLEDAI scores. Conclusion: Our results demonstrate that dysregulation of cTfh cells is strongly correlated with disease activity in SLE, supporting a potential causal relationship. The altered composition of blood CXCR5 cells also appeared to be a fundamental cellular defect in SLE, with our results revealing a novel dimension of Tfh dysregulation that may be central to disease pathogenesis.