EDWIN ROGER PARRA CUENTAS

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Assunto: Rheumatology ×

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  • article 29 Citação(ões) na Scopus
    A long-term prospective randomized controlled study of non-specific interstitial pneumonia (NSIP) treatment in scleroderma
    (2011) DOMICIANO, Diogo S.; BONFA, Eloisa; BORGES, Claudia T. L.; KAIRALLA, Ronaldo A.; CAPELOZZI, Vera L.; PARRA, Edwin; CHRISTMANN, Romy Beatriz
    The association of cyclophosphamide (CYC) and prednisone (PRED) for the treatment of lung fibrosis in systemic sclerosis (SSc) was only evaluated in uncontrolled studies, although in idiopathic interstitial lung disease (ILD) this association seems to be beneficial in patients with non-specific interstitial pneumonia (NSIP). Objectives: To treat SSc-ILD in a prospective open-label controlled study based on lung pattern during 12 months of treatment. Methods: A 3-year analysis was also performed. Twenty-four consecutive patients with SSc and ILD were submitted to an open lung biopsy. Eighteen patients (NSIP) were randomized in two groups: CYC versus CYC + PRED during 12 months. Lung function tests (diffusion lung capacity of monoxide carbone corrected for hemoglobin concentration (DLCO-Hb), forced vital capacity (FVC), total lung capacity) and Modified Rodnan Skin Score (MRSS) were performed before, after one of treatment and after 3 years from the end of the treatment. Results: Pulmonary function tests were similar in both groups on baseline. After 1 year of treatment, FVC% was comparable between CYC groups (p = 0.72) and in CYC + PRED (p = 0.40). Three years after the end of treatment, FVC% values (p = 0.39 in group CYC and p = 0.61 in CYC + PRED and p = 0.22 in CYC + PRED) and DLCO-Hb (p = 0.54 in CYC and p = 0.28 in CYC + PRED) were similar compared to 1 year of treatment. We observed a reduction of the MRSS in the CYC + PRED group after 1 year of treatment (p = 0.02); although after 3 years, MRSS values remained stable in both groups. Conclusions: CYC was effective to stabilize lung function parameters in NSIP lung pattern of SSc disease for 3 years after the end of a 1-year therapy.
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    PULMONARY FIBROSIS INDUCED BY BLEOMYCIN IS DRIVEN BY HIGH COLLAGEN V AND TGF-< BETA > SYNTHESIS
    (2014) MARTINS, V.; LOPES, D. B.; ANTUNES, M.; VELOSA, A. P. P.; TEODORO, W. R.; PARRA, E. R.; CAPELOZZI, V. L.
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    INFLUENCE OF ALPHA 2 DO COLLAGEN V OVEREXPRESSION IN PHYSIOPHATOLOGY OF FIBROSIS SYSTEMIC SCLEROSIS PATIENTS
    (2014) MORAIS, J.; MARTIN, P.; VELOSA, A. P. P.; ANDRADE, P. C.; CRUZ, I. B.; MIRACCA, E. C.; FAC, F. A. C. Barrence; CARRASCO, S.; GOLDEINSTEIN-SCHAINBERG, C.; NAGAI, M. A.; PARRA, E. R.; CAPELOZZI, V. L.; TEODORO, W. R.
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    HLA-B27 PREVALENCE IN A COHORT OF BRAZILIAN PATIENTS WITH PSORIATIC ARTHRITIS AND ANKYLOSING SPONDYLITIS
    (2014) GOLDENSTEIN-SCHAINBERG, C.; CARRASCO, S.; SAAD, C. G.; MORAES, J. C. B.; GONCALVES, C. R.; SAMPAIO-BARROS, P.; PARRA, E. R.
  • article 87 Citação(ões) na Scopus
    miR-155 in the progression of lung fibrosis in systemic sclerosis
    (2016) CHRISTMANN, Romy B.; WOOTEN, Alicia; SAMPAIO-BARROS, Percival; BORGES, Claudia L.; CARVALHO, Carlos R. R.; KAIRALLA, Ronaldo A.; FEGHALI-BOSTWICK, Carol; ZIEMEK, Jessica; MEI, Yu; GOUMMIH, Salma; TAN, Jiangning; ALVAREZ, Diana; KASS, Daniel J.; ROJAS, Mauricio; MATTOS, Thiago Lemos de; PARRA, Edwin; STIFANO, Giuseppina; CAPELOZZI, Vera L.; SIMMS, Robert W.; LAFYATIS, Robert
    Background: MicroRNA (miRNA) control key elements of mRNA stability and likely contribute to the dysregulated lung gene expression observed in systemic sclerosis associated interstitial lung disease (SSc-ILD). We analyzed the miRNA gene expression of tissue and cells from patients with SSc-ILD. A chronic lung fibrotic murine model was used. Methods: RNA was isolated from lung tissue of 12 patients with SSc-ILD and 5 controls. High-resolution computed tomography (HRCT) was performed at baseline and 2-3 years after treatment. Lung fibroblasts and peripheral blood mononuclear cells (PBMC) were isolated from healthy controls and patients with SSc-ILD. miRNA and mRNA were analyzed by microarray, quantitative polymerase chain reaction, and/or Nanostring; pathway analysis was performed by DNA Intelligent Analysis (DIANA)-miRPath v2.0 software. Wild-type and miR-155 deficient (miR-155ko) mice were exposed to bleomycin. Results: Lung miRNA microarray data distinguished patients with SSc-ILD from healthy controls with 185 miRNA differentially expressed (q < 0.25). DIANA-miRPath revealed 57 Kyoto Encyclopedia of Genes and Genomes pathways related to the most dysregulated miRNA. miR-155 and miR-143 were strongly correlated with progression of the HRCT score. Lung fibroblasts only mildly expressed miR-155/miR-21 after several stimuli. miR-155 PBMC expression strongly correlated with lung function tests in SSc-ILD. miR-155ko mice developed milder lung fibrosis, survived longer, and weaker lung induction of several genes after bleomycin exposure compared to wild-type mice. Conclusions: miRNA are dysregulated in the lungs and PBMC of patients with SSc-ILD. Based on mRNA-miRNA interaction analysis and pathway tools, miRNA may play a role in the progression of the disease. Our findings suggest that targeting miR-155 might provide a novel therapeutic strategy for SSc-ILD.
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    DYNAMIC COLLAGEN V REMODELING IS RELATED TO SKIN THICKENING IN SSc
    (2012) MARTIN, P.; TEODORO, W. R.; VELOSA, A. P.; CARRASCO, S.; MORAIS, J. de; CHRISTMANN, R. B.; PARRAS, E. R.; CAPELOZZI, V. L.; YOSHINARI, N. H.
    Background. Normal physiological properties of skin, one of the primary organs affected in SSc, depends on collagen Types I (COL I), III (COLIII) and V (COLV) assembly forming heterotypic fibres. COLV regulates fibril diameter and loss of this function could result in tissue fibrosis. In this way, our aim was to evaluate the histological and molecular profiles of COLI, COLIII and COLV in SSc skin and its correlation with skin thickening and disease activity. Methods. Skin biopsies of 18 patients (5 at early and 13 at late disease stage) and 10 healthy controls were studied. Assessment of skin thickening was performed using the modified Rodnan skin score (MRSS) and disease activity was calculated by Valentini Disease Activity Index. Quantification of COLI, COLIII and COLV was evaluated by histomorphometry in dermis and quantitative RT–PCR in dermal fibroblast culture. Results. A higher expression of abnormal COLV was observed in dermis of patients with early disease when compared with control group and late disease. The COLIII content was also higher in early SSc when compared with healthy controls and late SSc. On the other hand, the amount of COLI was higher in late disease when compared with control and early SSc. A positive correlation between COLV and MRSS (r = 0.42, P = 0.04) as well as disease activity (r = 0.45, P = 0.03) was observed, but there was no correlation between COLI and COLIII expression and these parameters. COLV α-1 and COLV α-2, as well as COLI α-1 and COLIII α-1 mRNA expression were higher in SSc when compared with control group. Conclusion. We found increased COLIII and COLV deposition in early SSc and increased COLI expression in late SSc indicating that collagen remodelling in SSc is a dynamic process. The fact that abnormal COLV expression decreases in later disease stages could explain why skin thickening sometimes improves spontaneously with time. Besides, COLV is correlated to MRSS and disease activity. These findings include COLV as an important regulator of cutaneous thickness in SSc and may add this protein as a new target for future treatments.
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    HLA-B27 ANALYSIS BY FLOW CITOMETRY IN BRAZILIAN PATIENTS WITH ANKYLOSING SPONDYLITIS AND PSORIATIC ARTHRITIS
    (2013) GOLDENSTEIN-SCHAINBERG, C.; CARRASCO, S.; SAAD, C.; GONCALVES, C.; SAMPAIO-BARROS, P.; PARRA, E.
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    Abnormal Collagen Fibers Deposition In The Synovial Joints Is a Characteristic Of The Temporal Evolution Of The Diabetic rats' Model Induced By Streptozotocin
    (2013) ANDRADE, Priscila C.; VELOSA, Ana Paula P.; MORAIS, Jymenez; PARRA, Edwin R.; GOLDEINSTEIN-SCHAINBERG, Claudia; CAPELOZZI, Vera L.; TEODORO, Walcy R.
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    COLLAGEN V-INDUCED NASAL TOLERANCE PROMOTES DECREASE IN TOPO I PROTEIN SYNTHESIS AND PULMONARY FIBROSIS OF SSc MODEL
    (2012) VELOSA, A. P.; TEODORO, W. R.; CALLADO, M. R.; FILHO, A. S.; FERNEZLIAN, S. M.; KATAYAMA, M. L.; PARRA, E. R.; CAPELOZZI, V. L.; YOSHINARI, N. H.
    Background. Autoantibodies against topo I (anti-Scl-70) are found to be associated with increased mortality and correlate with the extent of pulmonary fibrosis in SSc. To evaluate anti-Scl-70 antibodies and topo I expression in lung and to correlate with pulmonary fibrosis in experimental SSc after collagen V (COL V)-induced nasal tolerance. Methods. Female New Zealand rabbits (n = 12) were immunized with 1 mg/ml of COL V in Freund's adjuvant (IM). After 150 days, six immunized animals were tolerated by nasal administration of type COL V (25 μg/day) (IM-TOL), daily during 60 days. Anti-Scl-70 antibodies were evaluated by ELISA. Immunohistochemistry, histomorphometry and RT–PCR evaluated pulmonary topo I expression, types I, III and V collagen and TGF-β expression in pulmonary parenchyma. Results. A significant decrease in topo I expression by pulmonary endothelial cells was found comparing IM-TOL vs IM [29.86 (10.48) vs 76.11 (20.91), P = 0.019]. No difference was found for the anti-Scl-70 frequency after tolerance. Type V collagen content around the small vessels [0.371 (0.118) vs 0.874 (0.282), P < 0.001] and bronchioles [0.294 (0.139) vs 0.646 (0.172), P < 0.001], beyond mRNA expression to types I [0.10 (0.07) vs 1.0 (0.528), P = 0,002] and V [1.12 (0.42) vs 4.74 (2.25), P = 0,009] collagen decreased in IM-TOL, when compared with IM TGF-β expression decreased in endothelial [10.77 (4.3) vs 43.5 (5.7), P < 0,0001] and smooth muscle cells [9.93 (3.77) vs 53.68 (4.06), P < 0,0001] from pulmonary vessels, epithelial cells [6.03 (1.47) vs 13.65 (1.39), P < 0,0001] and interstitial fibroblasts [11.55 (1.88) vs 20.13 (1.60), P < 0,0001] in IM-TOL compared with IM. Conclusions. The results showed that a direct link between nasal type V collagen tolerance and a decline in topo I expression may reduce pulmonary fibrosis, suggesting that strategies aimed at preventing the increase of the type V collagen synthesis, or the local responses to increased topo I expression, may have a greater impact in SSc.