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Search Results: 1 - 10 of 118832 matches for " Helena Canh?o "
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Soluble receptor activator of nuclear factor κB ligand/osteoprotegerin ratio is increased in systemic lupus erythematosus patients
Diana Carmona-Fernandes, Maria Santos, Inês Perpétuo, Jo?o Fonseca, Helena Canho
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3500
Abstract: Our aim was to assess serum OPG and soluble RANKL (sRANKL) levels as well as sRANKL/OPG ratio in female SLE patients and compare it with female controls.We have evaluated 103 SLE patients and 114 healthy controls, all Caucasian females. All participants underwent a clinical and laboratory evaluation. sRANKL and OPG were quantified in serum by ELISA based methods. sRANKL, OPG and sRANKL/OPG ratio levels were compared between SLE patients and age, sex and race matched healthy controls. For SLE patients, a multivariate analysis was performed, to find the possible predictors of the changes in sRANKL, OPG and sRANKL/OPG ratio levels.Although sRANKL levels did not differ between the two groups, serum OPG was lower in SLE patients (P < 0.001). This led to an increased sRANKL/OPG ratio (P = 0.010) in the patients' group.The multivariate analysis was performed considering age and other clinical and laboratorial potential confounders for these variations in the SLE patients group. We have showed that age (P = 0.001) and levels of anti-Sm antibodies (P = 0.016) were independent predictors of sRANKL/OPG ratio variations in SLE patients. No relationship with therapy or disease activity measured by SLEDAI2K was found.These results are suggestive of increased osteoclastic stimuli driven by the SLE disease mechanisms.Systemic lupus erythematosus (SLE) is a chronic, multisystemic disease of unknown etiology characterized by chronic inflammation and damage to various organs and systems due to the production of autoreactive cells and antibodies [1-3].SLE patients have lower bone mineral density (BMD) when compared with healthy individuals and are at increased risk of fracture [4-7]. Although corticosteroid exposure is a major contributor to bone loss in SLE [4,5,8]. disease activity and associated co-morbidities may contribute to this process [5,8]. In addition, vitamin D deficiency is a common finding among SLE patients, further contributing to impaired bone health [5].Bone remodelin
Recomenda??es para diagnóstico e tratamento da tuberculose latente e activa nas doen?as inflamatórias articulares candidatas a tratamento com fármacos inibidores do factor de necrose tumoral alfa
Fonseca,Jo?o Eurico; Lucas,Helena; Canho,Helena; Duarte,Raquel; Santos,Maria José; Villar,Miguel; Faustino,Augusto; Raymundo,Elena;
Revista Portuguesa de Pneumologia , 2006,
Abstract: the portuguese society of rheumatology (spr) and the portuguese society of pulmonology (spp) have developed guidelines for the diagnosis and treatment of latent tuberculosis infection (ltbi) and active tuberculosis (at) in patients with inflammatory joint diseases (ijd), namely rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, treated with tumour necrosis factor alpha (tnf-á) antagonists. due to the high risk of tuberculosis (tb) in patients with ijd, ltbi and at screening should be performed as soon as possible, ideally at the moment of ijd diagnosis. even if tb screening was performed at the beginning of the disease, the evaluation should be repeated before starting anti-tnf-á therapy. when tb (ltbi or at) treatment is indicated, it should be performed before the beginning of anti-tnf-á therapy. if the ijd activity requires urgent anti-tnf-á therapy, these drugs can be started after two months of antituberculosis therapy in at cases, or after one month in ltbi cases. chest x-ray is mandatory for all patients. if abnormal, e.g. gohn complex, the patient should be treated as ltbi; residual lesions require the exclusion of at and patients with history of untreated or incomplete tb treatment should be treated as ltbi. in cases of suspected active lesions, at diagnosis should be confirmed and adequate therapy initiated. tuberculin skin test (tst), with two units of rt23, should be performed in all patients. if induration is less than 5 mm, the test should be repeated after 1 to 2 weeks, on the opposite forearm, and should be considered negative if the result is again inferior to 5 mm. positive tst implicates ltbi treatment. if tst is performed in immunosupressed ijd patients, ltbi treatment should be offered to the patient before starting anti-tnfá therapy, even in the presence of a negative test.
Recomenda??es para o diagnóstico e tratamento das tuberculoses latente e activa nas doen?as inflamatórias articulares candidatas a terapêutica com fármacos inibidores do factor de necrose tumoral alfa: Revis?o de Mar?o de 2008
Fonseca,Jo?o Eurico; Lucas,Helena; Canho,Helena; Duarte,Raquel; Santos,Maria José; Villar,Miguel; Faustino,Augusto; Raymundo,Elena;
Revista Portuguesa de Pneumologia , 2008,
Abstract: the portuguese society of rheumatology and the portuguese society of pulmonology have updated the guidelines for the diagnosis and treatment of latent tuberculosis infection (ltbi) and active tuberculosis (atb) in patients with inflammatory joint diseases (ijd) that are candidates to therapy with tumour necrosis factor alpha (tnfá) antagonists. in order to reduce the risk of tuberculosis (tb) reactivation and the incidence of new infections, tb screening is recommended to be done as soon as possible, ideally at the moment of ijd diagnosis, and patient assessment repeated before starting anti -tnfá therapy. treatment for atb and ltbi must be done under the care of a tb specialist. when tb treatment is indicated, it should be completed prior to starting anti-tnfá therapy. if the ijd activity justifies the need for immediate treatment, anti-tnfá therapy can be started two months after antituberculous therapy has been initiated, in the case of atb, and one month after in the case of ltbi. chest x -ray is mandatory for all patients. if gohn?s complex is present, the patient should be treated for ltbi; healed lesions require the exclusion of atb. in cases of suspected active lesions, atb should be excluded/confirmed and adequate therapy initiated. tuberculin skin test, with two units of rt23, should be performed in all patients. if the induration is <5 mm, the test should be repeated within 1 to 2 weeks, on the opposite forearm, and will be considered negative only if the result is again <5 mm. positive tst implicates ltbi treatment, unless previous proper treatment was provided. if tst is performed in immunossuppressed ijd patients, ltbi treatment should be offered to the patient before starting anti-tnf -á therapy, even in the presence of a negative test, after risk / benefit assessment.
Micro-computed tomography assessment of human femoral trabecular bone for two disease groups (fragility fracture and coxarthrosis): Age and gender related effects on the microstructure  [PDF]
Ana Catarina Vale, Manuel F. C. Pereira, António Maurício, Bruno Vidal, Ana Rodrigues, Joana Caetano-Lopes, Ara Nazarian, Jo?o E. Fonseca, Helena Canho, Maria Fátima Vaz
Journal of Biomedical Science and Engineering (JBiSE) , 2013, DOI: 10.4236/jbise.2013.62021
Abstract:

The aim of this study was to identify three-dimensional microstructural changes of trabecular bone with age and gender, using micro-computed tomography. Human trabecular bone from two disease groups, osteoporosis and osteoarthritis was analyzed. A prior analysis of the effects of some procedure variables on the micro-CT results was performed. Preliminary micro-CT scans were performed with three voxel resolutions and two acquisition conditions. On the reconstruction step, the image segmentation was performed with three different threshold values. Samples were collected from patients, with coxarthrosis (osteoarthritis) or fragility fracture (osteoporosis). The specimens of the coxarthrosis group include twenty females and fifteen males, while the fragility fracture group was composed by twenty three females and seven males. The mean age of the population was 69 ± 11 (females) and 67 ± 10 years (males), in the coxarthrosis group, while in the fragility fracture group was 81 ± 6 (females) and 78 ± 6 (males) years. The 30 μm voxel size provided lower percentage difference for the microarchitecture parameters. Acquisition conditions with 160 μA and 60 kV permit the evaluation of all the volume’s sample, with low average values of the coefficients of variation of the microstructural parameters. No statistically significant differences were found between the two diseases groups, neither between genders. However, with aging, there is a decrease of bone volume fraction, trabecular number and fractal dimension, and an increase of structural model index and trabecular separation, for both disease groups and genders. The parameters bone specific surface, trabecular thickness and degree of anisotropy have different behaviors with age, depending on the type of disease. While in coxarthrosis patients, trabecular thickness increases with age, in the fragility fracture group, there is a decrease of trabecular thickness with increasing age. Our findings indicate that disease, age and gender do not provide significant differences in trabecular microstructure. With aging, some parameters exhibit different trends which are possibly related to different mechanisms for

Early Vascular Alterations in SLE and RA Patients—A Step towards Understanding the Associated Cardiovascular Risk
Maria José Santos, Diana Carmona-Fernandes, Helena Canho, José Canas da Silva, Jo?o Eurico Fonseca, Victor Gil
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0044668
Abstract: Accelerated atherosclerosis represents a major problem in both systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients, and endothelial damage is a key feature of atherogenesis. We aimed to assess early endothelial changes in SLE and RA female patients (127 SLE and 107 RA) without previous CV events. Biomarkers of endothelial cell activation (intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), thrombomodulin (TM), and tissue factor (TF)) were measured and endothelial function was assessed using peripheral artery tonometry. Reactive hyperemia index (RHI), an indicator of microvascular reactivity, and augmentation index (AIx), a measure of arterial stiffness, were obtained. In addition, traditional CV risk factors, disease activity and medication were determined. Women with SLE displayed higher sICAM-1 and TM and lower TF levels than women with RA (p = 0.001, p<0.001 and p<0.001, respectively). These differences remained significant after controlling for CV risk factors and medication. Serum levels of vascular biomarkers were increased in active disease and a moderate correlation was observed between sVCAM-1 levels and lupus disease activity (rho = 0.246) and between TF levels and RA disease activity (rho = 0.301). Although RHI was similar across the groups, AIx was higher in lupus as compared to RA (p = 0.04). Also in active SLE, a trend towards poorer vasodilation was observed (p = 0.06). In conclusion, women with SLE and RA present with distinct patterns of endothelial cell activation biomarkers not explained by differences in traditional CV risk factors. Early vascular alterations are more pronounced in SLE which is in line with the higher CV risk of these patients.
Upregulation of Inflammatory Genes and Downregulation of Sclerostin Gene Expression Are Key Elements in the Early Phase of Fragility Fracture Healing
Joana Caetano-Lopes,Ana Lopes,Ana Rodrigues,Diana Fernandes,Inês P. Perpétuo,Teresa Monjardino,Raquel Lucas,Jacinto Monteiro,Yrj? T. Konttinen,Helena Canho,Jo?o E. Fonseca
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0016947
Abstract: Fracture healing is orchestrated by a specific set of events that culminates in the repair of bone and reachievement of its biomechanical properties. The aim of our work was to study the sequence of gene expression events involved in inflammation and bone remodeling occurring in the early phases of callus formation in osteoporotic patients.
Identification of a cytokine network sustaining neutrophil and Th17 activation in untreated early rheumatoid arthritis
Rita Casc?o, Rita A Moura, Inês Perpétuo, Helena Canho, Elsa Vieira-Sousa, Ana F Mour?o, Ana M Rodrigues, Joaquim Polido-Pereira, Mário V Queiroz, Henrique S Rosário, Maria M Souto-Carneiro, Luis Graca, Jo?o E Fonseca
Arthritis Research & Therapy , 2010, DOI: 10.1186/ar3168
Abstract: Cytokines related to neutrophil and Th17 activation were quantified in the serum of VERA and established RA patients and compared with other very early arthritis (VEA) and healthy controls. Synovial fluid (SF) from RA and osteoarthritis (OA) patients was also analyzed.VERA patients had increased serum levels of cytokines promoting Th17 polarization (IL-1β and IL-6), as well as IL-8 and Th17-derived cytokines (IL-17A and IL-22) known to induce neutrophil-mediated inflammation. In established RA this pattern is more evident within the SF. Early treatment with methotrexate or corticosteroids led to clinical improvement but without an impact on the cytokine pattern.VERA patients already display increased levels of cytokines related with Th17 polarization and neutrophil recruitment and activation, a dysregulation also found in SF of established RA. 0 Thus, our data suggest that a cytokine-milieu favoring Th17 and neutrophil activity is an early event in RA pathogenesis.Rheumatoid arthritis (RA), the most common chronic autoimmune disease, affects approximately 1% of the population worldwide. This disease comprises a syndrome of pain, stiffness, and symmetrical synovitis which leads to joint destruction, functional disability, and substantial comorbidity due to the involvement of multiple organs and systems. The migration of leukocytes toward the synovium is crucial for the establishment of a chronic inflammatory process in RA [1-3]. This multi-regulated mechanism involves interactions with endothelial cells through cell adhesion molecules and complex cytokine and chemokine pathways.Neutrophils specifically play an important role in the onset and perpetuation of RA, not only as interleukin (IL)-producing cells but also as cells responsible for the release of high amounts of reactive oxygen species and destructive enzymes, such as metalloproteases, contributing to joint erosions [4]. Neutrophils are among the first leukocytes to arrive at sites of inflammation. In fact, th
Chronic arthritis leads to disturbances in the bone collagen network
Joana Caetano-Lopes, Ana M Nery, Helena Canho, Joana Duarte, Rita Casc?o, Ana Rodrigues, Inês P Perpétuo, Saba Abdulghani, Pedro M Amaral, Shimon Sakaguchi, Yrj? T Konttinen, Luís Gra?a, Maria F Vaz, Jo?o E Fonseca
Arthritis Research & Therapy , 2010, DOI: 10.1186/ar2908
Abstract: Serum, vertebrae and femur bones were collected from eight-month-old polyarthritis SKG mice and controls. Strength of the femoral bones was evaluated using three-point bending tests and density was assessed with a pycnometer. Bone turnover markers carboxy-terminal collagen cross-linking telopeptides (CTX-I) and amino-terminal propeptide of type I procollagen (PINP) were measured in serum. The organization and density of bone collagen were analyzed in vertebrae using second-harmonic generation (SHG) imaging with a two-photon microscope and trabecular bone microstructure was assessed by scanning electron microscope (SEM).Femoral bones of SKG mice revealed increased fragility expressed by deterioration of mechanical properties, namely altered stiffness (P = 0.007) and reduced strength (P = 0.006), when compared to controls. Accordingly, inter-trabecular distance and trabecular thickness as observed by SEM were reduced in SKG mice. PINP was significantly higher in arthritic mice (9.18 ± 3.21 ng/ml) when compared to controls (1.71 ± 0.53 ng/ml, P < 0.001). Bone resorption marker CTX-I was 9.67 ± 3.18 ng/ml in arthritic SKG mice compared to 6.23 ± 4.11 ng/ml in controls (P = 0.176). The forward-to-backward signal ratio measured by SHG was higher in SKG animals, reflecting disorganized matrix and loose collagen structure, compared to controls.We have shown for the first time that chronic arthritis by itself impairs bone matrix architecture, probably due to disturbed bone remodeling and increased collagen turnover. This effect might predispose patients to bone fragility fractures.Bone is a dynamic tissue composed mainly of a type I collagen matrix that constitutes the scaffold for calcium hydroxyapatite crystal deposition. Remodeling is a continuous process in which osteoclast-mediated bone resorption is coupled with osteoblast-mediated bone matrix production. Biochemical markers of bone turnover are produced during this process and released into circulation [1], providing
Gender-Specific Effects of Genetic Variants within Th1 and Th17 Cell-Mediated Immune Response Genes on the Risk of Developing Rheumatoid Arthritis
Rafael Cáliz, Luz María Canet, Carmen Belén Lupia?ez, Helena Canho, Alejandro Escudero, Ileana Filipescu, Juana Segura-Catena, María José Soto-Pino, Manuela Expósito-Ruiz, Miguel ángel Ferrer, Antonio García, Lurdes Romani, Alfonso González-Utrilla, Teresa Vallejo, Eva Pérez-Pampin, Kari Hemminki, Asta F?rsti, Eduardo Collantes, Jo?o Eurico Fonseca, Juan Sainz
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072732
Abstract: The present study was conducted to explore whether single nucleotide polymorphisms (SNPs) in Th1 and Th17 cell-mediated immune response genes differentially influence the risk of rheumatoid arthritis (RA) in women and men. In phase one, 27 functional/tagging polymorphisms in C-type lectins and MCP-1/CCR2 axis were genotyped in 458 RA patients and 512 controls. Carriers of Dectin-2rs4264222T allele had an increased risk of RA (OR = 1.47, 95%CI 1.10–1.96) whereas patients harboring the DC-SIGNrs4804803G, MCP-1rs1024611G, MCP-1rs13900T and MCP-1rs4586C alleles had a decreased risk of developing the disease (OR = 0.66, 95%CI 0.49–0.88; OR = 0.66, 95%CI 0.50–0.89; OR = 0.73, 95%CI 0.55–0.97 and OR = 0.68, 95%CI 0.51–0.91). Interestingly, significant gender-specific differences were observed for Dectin-2rs4264222 and Dectin-2rs7134303: women carrying the Dectin-2rs4264222T and Dectin-2rs7134303G alleles had an increased risk of RA (OR = 1.93, 95%CI 1.34–2.79 and OR = 1.90, 95%CI 1.29–2.80). Also five other SNPs showed significant associations only with one gender: women carrying the MCP-1rs1024611G, MCP-1rs13900T and MCP-1rs4586C alleles had a decreased risk of RA (OR = 0.61, 95%CI 0.43–0.87; OR = 0.67, 95%CI 0.47–0.95 and OR = 0.60, 95%CI 0.42–0.86). In men, carriers of the DC-SIGNrs2287886A allele had an increased risk of RA (OR = 1.70, 95%CI 1.03–2.78), whereas carriers of the DC-SIGNrs4804803G had a decreased risk of developing the disease (OR = 0.53, 95%CI 0.32–0.89). In phase 2, we genotyped these SNPs in 754 RA patients and 519 controls, leading to consistent gender-specific associations for Dectin-2rs4264222, MCP-1rs1024611, MCP-1rs13900 and DC-SIGNrs4804803 polymorphisms in the pooled sample (OR = 1.38, 95%CI 1.08–1.77; OR = 0.74, 95%CI 0.58–0.94; OR = 0.76, 95%CI 0.59–0.97 and OR = 0.56, 95%CI 0.34–0.93). SNP-SNP interaction analysis of significant SNPs also showed a significant two-locus interaction model in women that was not seen in men. This model consisted of Dectin-2rs4264222 and Dectin-2rs7134303 SNPs and suggested a synergistic effect between the variants. These findings suggest that Dectin-2, MCP-1 and DC-SIGN polymorphisms may, at least in part, account for gender-associated differences in susceptibility to RA.
Contribution for new genetic markers of rheumatoid arthritis activity and severity: sequencing of the tumor necrosis factor-alpha gene promoter
Jo?o Fonseca, Jo?o Cavaleiro, José Teles, Elsa Sousa, Valeska L Andreozzi, Marília Antunes, Maria A Amaral-Turkman, Helena Canho, Ana F Mour?o, Joana Lopes, Joana Caetano-Lopes, Pamela Weinmann, Marta Sobral, Patrícia Nero, Maria J Saavedra, Armando Malcata, Margarida Cruz, Rui Melo, Araceli Bra?a, Luis Miranda, José V Patto, Anabela Barcelos, José da Silva, Luís M Santos, Guilherme Figueiredo, Mário Rodrigues, Herberto Jesus, Alberto Quintal, Teresa Carvalho, José da Silva, Jaime Branco, Mário Queiroz
Arthritis Research & Therapy , 2007, DOI: 10.1186/ar2173
Abstract: Tumor necrosis factor-alpha (TNF-α) has been shown to be relevant for the physiopathology of rheumatoid arthritis (RA), and its inhibition by anti-TNF-α antibodies or recombinant soluble receptors results in a major improvement of this disease [1]. On the other hand, TNF-α production shows a wide variation, with high- and low-producer phenotypes present in humans [2] but with a strong concordance in monozygotic twins [3], pointing to the influence of genetic variation on the regulation of TNF-α circulating levels. These arguments have favored the view that genetic factors controlling TNF-α could have a major impact on RA outcome. An extensive network of gene products is involved in the production, modulation, and decay of TNF-α, affecting the stabilization of the transcripts, full activation of membrane-bound TNF-α by proteases, and the interaction with its membrane receptors and with membrane-shedded receptors [4]. In addition, the gene itself and/or its promoter area could be the source of genetic variation. However, present knowledge suggests that the highest genetic variability is concentrated in the promoter area of the TNF-α gene, where at least eight different single-nucleotide polymorphisms (SNPs) are concentrated, with the potential to affect the binding of transcriptor factors and thus to control the activity of the promoter and resulting mRNA and protein levels [4].Several studies have addressed the issue of TNF-α gene promoter SNPs and RA outcome. Although some contradictory results have emerged, the data published so far indicate the possible existence of TNF-α gene promoter variants that act as markers for disease severity and response to treatment in RA [5-7]. Nevertheless, further investigation is necessary to determine whether the previously identified TNF-α gene promoter variants contribute directly to RA outcome or act as genetic markers of other polymorphisms in the TNF-α gene promoter area.In this study, we have analyzed the promoter region of t
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