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ID PMID Title PublicationDate abstract
25692134 Lunasin inhibits cell proliferation via apoptosis and reduces the production of proinflamm 2015 Lunasin, a peptide with 43 amino acid residues and initially isolated and identified in soybean cotyledon, has gained extensive attention due to its anti-inflammatory and anticancer properties. However, its treatment efficacy on rheumatoid arthritis (RA) and corresponding mechanisms have not been reported. Herein, the synovial fibroblasts harvested and isolated from patients with RA were treated with lunasin at various concentrations to examine the proliferation, apoptosis status, and corresponding cell cycle of cultured RA synovial fibroblasts. Meanwhile, the underlying mechanisms of lunasin for RA treatment are explored through Western blot, real-time PCR, ELISA, and luciferase reporter assays. Lunasin significantly inhibited the proliferation and induced the apoptosis of cultured RA synovial fibroblasts. In addition, lunasin reduced the production of interleukin-6 (IL-6), IL-8, and matrix metalloproteinase-3 (MMP-3) and suppressed the activation of NF-κB in cultured RA synovial fibroblasts but did not reveal obvious modulation on the secretion and gene expression of MMP-1. Therefore, lunasin will have promising potential as a novel nutritional supplement or drug candidate for RA due to its potency of suppressing synovial cell proliferation and decreasing the production of proinflammatory cytokines and MMPs in synovial cells.
27459267 Association of inflammatory bowel disease with ankylosing spondylitis and rheumatoid arthr 2017 May OBJECTIVES: Tantalizing connections between autoimmune rheumatic diseases (ARDs) and inflammatory bowel disease (IBD) have become evident with regard to their genetic and immunologic background. However, the association between these two disease entities remains unclear. The aim of this study is to investigate the association between each ARD and IBD. METHODS: A nationwide population-based cross-sectional study was performed using the Korean National Health Insurance Claims database. The data of patients with IBD and age- and sex-matched controls between 2009 and 2013 were collected from the database. The prevalence of ARDs, including systemic lupus erythematosus (SLE), inflammatory myositis (polymyositis and dermatomyositis), systemic sclerosis (SSc), Sjögren's syndrome (SjS), ankylosing spondylitis (AS), and rheumatoid arthritis (RA), was determined. The associations between each ARD and IBD were analyzed using multivariate logistic regression models. RESULTS: A total of 40,843 IBD patients (28,197 patients with ulcerative colitis and 12,646 with Crohn's disease) and 122,529 controls were enrolled. The nonstratified analysis revealed that patients with IBD had significant risk of being concomitantly affected by AS (odds ratio [OR] 5.140, 95% confidence interval [95% CI] 4.069-6.492) and RA (OR: 3.474, 95% CI: 2.671-4.519) after adjusting for age and sex. No significant association was observed between IBD and other ARDs including SLE, inflammatory myositis, SSc, and SjS. CONCLUSION: IBD is significantly associated with AS and RA in the large-scaled population-based study. This result suggests that etiopathogenesis of IBD might be shared with AS and RA.
27243098 Evaluation of [(89)Zr]-Oxalate as a PET Tracer in Inflammation, Tumor, and Rheumatoid Arth 2016 Jul 5 To obtain an additional pharmacological agent for the diagnosis of inflammation, we investigated the medical use of (89)Zr-oxalate as a positron emission tomography (PET) probe for the in vivo imaging of inflammation and compared its efficacy to that of 2-deoxy-2-[(18)F]fluoro-d-glucose ([(18)F]FDG) and sodium [(18)F]fluoride. (89)Zr-oxalate exhibited observable higher uptake in a macrophage cell line than in tumor cells. The inflammatory lesions and tumors were clearly visualized by PET imaging and autoradiography using (89)Zr-oxalate. Compared to [(18)F]FDG and sodium [(18)F]fluoride, (89)Zr-oxalate demonstrated a high selectivity index to the tumor at an early time point after injection and to inflammation at a delayed time point after injection (24 h). Through histological examination, large numbers of macrophages and neutrophils were observed in the tumor lesions with the highest (89)Zr-oxalate uptake. In a rheumatoid arthritis (RA) mouse model, (89)Zr-oxalate demonstrated a high level of accumulation in inflammatory lesions. (89)Zr-oxalate is a new strategic tool for tumor imaging and inflammatory processes.
26885899 Integrative analysis of genome-wide association studies and gene expression analysis ident 2016 Feb 23 Rheumatoid arthritis (RA) is a complex and systematic autoimmune disease, which is usually influenced by both genetic and environmental factors. Pathway analyses based on a single data type such as microarray data or SNP data have successfully revealed some biology pathways associated with RA. However, we found that the pathway analysis based on a single data type only provide limited understanding about the pathogenesis of RA. Gene-disease association is usually caused by many ways, such as genotype, gene expression and so on. Therefore, the integrative analysis method combining multiple levels of evidence can more precisely and comprehensively identify the pathway associations. In this study, we performed a pathway analysis by integrating GWAS and gene expression analysis to detect the RA-related pathways. The integrative analysis identified 28 pathways associated with RA. Among these pathways, 18 pathways were also found by both GWAS and gene expression analysis, 7 pathways are novel RA-related pathways, such as B cell receptor signaling pathway, Toll-like receptor signaling pathway, Fc gamma R-mediated phagocytosis and so on. Compared with pathway analyses using only one type genomic data, we found integrative analysis can increase the power to identify the real associations and provided more stable and accurate results. We believe these results will contribute to perform future genetic studies in RA pathogenesis and may promote the development of new therapeutic strategies by targeting these pathways.
27221115 Mathematical modeling of the circadian dynamics of the neuroendocrine-immune network in ex 2016 Aug 1 The circadian dynamics of important neuroendocrine-immune mediators have been implicated in progression of rheumatoid arthritis pathophysiology, both clinically as well as in animal models. We present a mathematical model that describes the circadian interactions between mediators of the hypothalamic-pituitary-adrenal (HPA) axis and the proinflammatory cytokines. Model predictions demonstrate that chronically elevated cytokine expression results in the development of adrenal insufficiency and circadian variability in paw edema. Notably, our model also predicts that an increase in mean secretion of corticosterone (CST) after the induction of the disease is accompanied by a decrease in the amplitude of the CST oscillation. Furthermore, alterations in the phase of circadian oscillation of both cytokines and HPA axis mediators are observed. Therefore, by incorporating the circadian interactions between the neuroendocrine-immune mediators, our model is able to simulate important features of rheumatoid arthritis pathophysiology.
25019600 Cost-effectiveness of a one-year coaching program for healthy physical activity in early r 2015 PURPOSE: To describe cost-effectiveness of the Physical Activity in Rheumatoid Arthritis (PARA) study intervention. METHOD: Costs were collected and estimated retrospectively. Cost-effectiveness was calculated based on the intervention cost per patient with respect to change in health status (EuroQol global visual analog scale--EQ-VAS and EuroQol--EQ-5D) and activity limitation (Health assessment questionnaire - HAQ) using cost-effectiveness- and cost-minimization analyses. RESULTS: Total cost of the one-year intervention program was estimated to be €67 317 or €716 per participant. Estimated difference in total societal cost between the intervention (IG) and control (CG) was €580 per participant. Incremental cost-effectiveness ratio (ICER) for one point (1/100) of improvement in EQ-VAS was estimated to be €116. By offering the intervention to more affected participants in the IG compared to less affected participants, 15.5 extra points of improvement in EQ-VAS and 0.13 points of improvement on HAQ were gained at the same cost. "Ordinary physiotherapy" was most cost-effective with regard to EQ-5D. CONCLUSIONS: The intervention resulted in improved effect in health status for the IG with a cost of €116 per extra point in VAS. The intervention was cost-effective if targeted towards a subgroup of more affected patients when evaluating the effect using VAS and HAQ. IMPLICATIONS FOR REHABILITATION: The physical activity coaching intervention resulted in an improved effect on VAS for the intervention group, to a higher cost. In order to maximize cost-effectiveness, this type of physical activity coaching intervention should be targeted towards patients largely affected by their RA. The intervention is cost-effective from the patients' point of view, but not from that of the general population.
25773658 Increased detection of latent tuberculosis by tuberculin skin test and booster phenomenon 2015 Sep The incidence of tuberculosis (TB) in rheumatoid arthritis (RA) patients is up to four times higher when compared to the general population, but their risk increases with the use of TNF-a drugs. Appropriate screening of latent tuberculosis infection (LTBI) and proper management of such cases substantially reduce the incidence of active TB. Tuberculin skin test (TST) is a widely used method for the detection of LTBI. The time of diagnosis of RA as well as the age of the patient might modify the TST performance. We did an observational, comparative study of RA patients with early and established disease, with the objective to know the prevalence of LTBI using the TST and booster test; an induration ≥5 mm was considered reactive. We evaluated 143 patients (83 [58 %] early RA patients). We found 31.3 and 21.7 % TST positivity in early and established RA patients, respectively. With the use of booster test, the positivity increased to 46.5 and 28.8 %, respectively (p = 0.048, OR 1.33, 95 % CI 1.01-1.75). In conclusion, we found that TST and booster test increased LTBI detection in early RA patients, which may suggest that time of RA diagnosis might affect cellular immunity and therefore the TST response.
25178741 Contribution of ethnic group and socioeconomic status to degree of disability in rheumatoi 2015 Apr The aim of this study was to estimate the contributions of ethnic group and socioeconomic status as social determinants related to disability and disease activity in Chilean Mapuche and non-Mapuche patients with rheumatoid arthritis (RA). Descriptive cross-sectional study with a stratified hospital-based sample of 189 patients in treatment with disease-modifying anti-rheumatic drugs. We assessed disability as categorical variable with the Health Assessment Questionnaire, disease activity with the Disease Activity Score instrument, and socioeconomic status with a standard questionnaire used by the Chilean government. Measures of association, stratified analyses and a multiple logistic regression model were used to analyze the data using the Stata 12.1 software package. Low socioeconomic status (annual income below US$ 7,200) is associated with disability (OR 3.87 CI 1.68-9.20) and Mapuche ethnic identity also contributes to disability (OR 2.48, CI 1.09-5.89). Relevant but not statistically significant in multivariable models were variables such as age, gender and place of residence. RA patients with a low socioeconomic status have almost three times the odds of having a moderate to high disability, independent of their ethnic group, gender or place of residence. Therefore, healthcare efforts should be aimed at promoting early diagnosis and prompt treatment among populations with high levels of poverty, which in the region of the Araucanía means primarily indigenous rural areas.
27430622 Collagen triple helix repeat containing 1 is a new promigratory marker of arthritic pannus 2016 Jul 19 BACKGROUND: The formation of destructive hypercellular pannus is critical to joint damage in rheumatoid arthritis (RA). The collagen triple helix repeat containing 1 (CTHRC1) protein expressed by activated stromal cells of diverse origin has previously been implicated in tissue remodeling and carcinogenesis. We recently discovered that the synovial Cthrc1 mRNA directly correlates with arthritis severity in mice. This study characterizes the role of CTHRC1 in arthritic pannus formation. METHODS: Synovial joints of mice with collagen antibody-induced arthritis (CAIA) and human RA-fibroblast-like synoviocytes (FLS) were immunostained for CTHRC1, FLS and macrophage-specific markers. CTHRC1 levels in plasma from patients with RA were measured using sandwich ELISA. The migratory response of fibroblasts was studied with a transwell migration assay and time-lapse microscopy. Velocity and directness of cell migration was analyzed by recording the trajectories of cells treated with rhCTHRC1. RESULTS: Immunohistochemical analysis of normal and inflamed synovium revealed highly inducible expression of CTHRC1 in arthritis (10.9-fold). At the tissue level, CTHRC1-expressing cells occupied the same niche as large fibroblast-like cells positive for α-smooth muscle actin (α-SMA) and cadherin 11 (CDH11). CTHRC1 was produced by activated FLS predominantly located at the synovial intimal lining and at the bone-pannus interface. Cultured RA-FLS expressed CDH11, α-SMA, and CTHRC1. Upon treatment with exogenous rhCTHRC1, embryonic fibroblasts and RA-FLS significantly increased migration velocity, directness, and cell length along the front-tail axis (1.4-fold, p < 0.01). CONCLUSION: CTHRC1 was established as a novel marker of activated synoviocytes in murine experimental arthritis and RA. The pro-migratory effect of CTHRC1 on synoviocytes is considered one of the mechanisms promoting hypercellularity of the arthritic pannus.
27830969 Plasmapheresis therapy in combination with TNF-α inhibitor and DMARDs: A multitarget meth 2017 Jul OBJECTIVE: To evaluate the effects of a multitarget method involving plasmapheresis therapy combined with tumor necrosis factor (TNF)-α inhibitor and disease-modifying antirheumatic drugs (DMARDs) on disease activity parameters in the treatment of active rheumatoid arthritis (RA). METHODS: Sixty-five patients with active RA were divided into two groups according to the treatment administered: the plasmapheresis combination therapy group (Plasmapheresis combination group; 38 cases), in which patients received plasmapheresis therapy along with a TNF-α inhibitor (recombinant human tumor necrosis factor-Fc; rhTNFR:Fc; Etanercept biosimilars) and DMARDs, and a TNF-α inhibitor therapy group (biological agent group; 27 cases), in which patients received a TNF-α inhibitor and DMARDs. Clinical parameters were measured before and at 4 and 24 weeks after treatment. RESULTS: ACR20, ACR50, and ACR70 responses at week 4 were achieved in 84.2%, 78.9%, and 60.5% of the patients in the plasmapheresis combination group, respectively, and 74.1%, 55.6%, and 29.6% of the patients in the biological agent group, respectively. The ACR50 and ACR70 response rates were superior in the former than the latter group (p < 0.05). Similar patterns of statistical significance were observed for ACR20, ACR50, and ACR70 responses at week 24 after the treatment. ACR50 responses were achieved in 84.2% patients and ACR70 responses were achieved in 76.3% patients in the plasmapheresis combination group, and these proportions were better than those in the biological agent group (p < 0.05). CONCLUSIONS: The multitarget method combining plasmapheresis, TNF-α inhibitor, and DMARDs for RA therapy was superior to the combination of TNF-α inhibitor for reducing disease activity parameters in patients with active RA.
27665099 Cost-effectiveness of drug monitoring of anti-TNF therapy in inflammatory bowel disease an 2017 Jan BACKGROUND: Therapeutic drug monitoring (TDM) of anti-TNF is increasingly used to manage inflammatory bowel diseases (IBD) and rheumatoid arthritis (RA). The cost-effectiveness of this strategy is debated. METHODS: All studies comparing the cost-effectiveness of a TDM-based strategy and an empirical dose management of anti-TNF in IBD or RA were screened. Studies were identified through the MEDLINE electronic database (up to July 2016), and annual international meeting abstracts were also manually reviewed. RESULTS: Seven studies were included: two randomized controlled trials (RCTs) enrolling 332 patients [247 Crohn's disease (CD) and 85 ulcerative colitis (UC)] and five modeling approaches. Four studies included only CD patients, one included both CD and UC patients, and two included only RA patients. Three studies compared the cost-effectiveness of the two strategies in patients with secondary infliximab (IFX) failure (dose-escalation strategy), one in patients in remission on optimized IFX (de-escalation strategy), one in patients starting adalimumab, and two in patients with clinical response to maintenance anti-TNF therapy. The two RCTs demonstrated that a TDM strategy led to major cost savings, ranging from 28 to 34 %. The three modeling approaches with regard to CD patients demonstrated cost savings ranging from $5396 over a 1-year period to €13,130 per patient at 5 years of follow-up. A TDM strategy also led to major cost savings in the two modeling approaches in RA patients. CONCLUSIONS: Available evidence indicates that a TDM strategy leads to major cost savings related to anti-TNF therapy in both IBD and RA patients, with no negative impact on efficacy.
26819099 Anti-TNFα agents curb platelet activation in patients with rheumatoid arthritis. 2016 Aug BACKGROUND: Cardiovascular disease is important in rheumatoid arthritis (RA). Tissue factor (TF) is expressed upon platelet activation and initiates coagulation. Anti-tumour necrosis factor-α (TNFα) agents seem to decrease RA-associated cardiovascular events. We investigated whether (1) TNFα activates human platelets and (2) TNFα pharmacological blockade modulates the platelet-leucocyte reciprocal activation in RA. DESIGN: The expression of platelet TNFα receptors has been assessed by flow cytometry and immunogold electron microscopy. Platelet and leucocyte activation has been assessed also in the presence of antibodies against the TNFα receptors 1 and 2 and of infliximab. TF expression, binding to fibrinogen and phosphatidylserine exposure, has been assessed by flow cytometry, TF activity by coagulation time and by endogenous thrombin generation. Markers of platelet and leucocyte activation have been assessed in 161 subjects: 42 patients with RA, 12 with osteoarthritis, 37 age-matched and sex-matched patients with chronic stable angina and 70 age-matched and sex-matched healthy subjects. RESULTS: TNFα elicited the platelet activation and the expression of TF, which in turn prompted thrombin generation and clot formation. Inhibition of the TNFα-induced activation restricted platelet ability to activate leucocytes and to induce leucocyte TF. TNFα inhibition did not influence platelet activation induced by collagen, ADP or thrombin receptor activating peptide-6. Platelets of patients with RA were more activated than those of controls. Activation was reduced in patients treated with TNFα inhibitors. CONCLUSIONS: TNFα-dependent pathways control platelet activation and TF expression in RA. Further studies will verify whether the protective effect of TNFα inhibitors on cardiovascular events involves their ability to modulate platelet function.
23594471 Introduction to statistical modelling: linear regression. 2015 Jul In many studies we wish to assess how a range of variables are associated with a particular outcome and also determine the strength of such relationships so that we can begin to understand how these factors relate to each other at a population level. Ultimately, we may also be interested in predicting the outcome from a series of predictive factors available at, say, a routine clinic visit. In a recent article in Rheumatology, Desai et al. did precisely that when they studied the prediction of hip and spine BMD from hand BMD and various demographic, lifestyle, disease and therapy variables in patients with RA. This article aims to introduce the statistical methodology that can be used in such a situation and explain the meaning of some of the terms employed. It will also outline some common pitfalls encountered when performing such analyses.
26148843 Marginal genetic effects estimation in family and twin studies using random-effects models 2015 Dec Random-effects models are often used in family-based genetic association studies to properly capture the within families relationships. In such models, the regression parameters have a conditional on the random effects interpretation and they measure, e.g., genetic effects for each family. Estimating parameters that can be used to make inferences at the population level is often more relevant than the family-specific effects, but not straightforward. This is mainly for two reasons: First the analysis of family data often requires high-dimensional random-effects vectors to properly model the familial relationships, for instance when members with a different degree of relationship are considered, such as trios, mix of monozygotic and dizygotic twins, etc. The second complication is the biased sampling design, such as the multiple cases families design, which is often employed to enrich the sample with genetic information. For these reasons deriving parameters with the desired marginal interpretation can be challenging. In this work we consider the marginalized mixed-effects models, we discuss challenges in applying them in ascertained family data and propose penalized maximum likelihood methodology to stabilize the parameter estimation by using external information on the disease prevalence or heritability. The performance of our methodology is evaluated via simulation and is illustrated on data from Rheumatoid Arthritis patients, where we estimate the marginal effect of HLA-DRB1*13 and shared epitope alleles across three different study designs and combine them using meta-analysis.
25443993 Eosinophilic myositis as first manifestation in a patient with type 2 myotonic dystrophy C 2015 Feb Eosinophilic myositis is characterized by eosinophilic infiltration of skeletal muscles. In the absence of an identifiable causative factor or source (including parasitic infection, intake of drugs or L-tryptophan, certain systemic disorders as well as malignant diseases), the diagnosis of idiopathic eosinophilic myositis is usually retained. However, some muscular dystrophies have been recently identified in this subset of eosinophilic myositis. Here, we report a patient with an 8 kb CCTG expansion in intron 1 of the CNBP gene, a mutation characteristic of myotonic dystrophy type 2 (DM2), whose first manifestation was "idiopathic" eosinophilic myositis. This report suggests that in "idiopathic" eosinophilic myositis, clinicians should consider muscular dystrophies, including DM2.
27405874 Metabolomics profiling of the free and total oxidised lipids in urine by LC-MS/MS: applica 2016 Sep Oxidised lipids, covering enzymatic and auto-oxidation-synthesised mediators, are important signalling metabolites in inflammation while also providing a readout for oxidative stress, both of which are prominent physiological processes in a plethora of diseases. Excretion of these metabolites via urine is enhanced through the phase-II conjugation with glucuronic acid, resulting in increased hydrophilicity of these lipid mediators. Here, we developed a bovine liver-β-glucuronidase hydrolysing sample preparation method, using liquid chromatography coupled to tandem mass spectrometry to analyse the total urinary oxidised lipid profile including the prostaglandins, isoprostanes, dihydroxy-fatty acids, hydroxy-fatty acids and the nitro-fatty acids. Our method detected more than 70 oxidised lipids biosynthesised from two non-enzymatic and three enzymatic pathways in urine samples. The total oxidised lipid profiling method was developed and validated for human urine and was demonstrated for urine samples from patients with rheumatoid arthritis. Pro-inflammatory mediators PGF2α and PGF3α and oxidative stress markers iPF2α- IV, 11-HETE and 14-HDoHE were positively associated with improvement of disease activity score. Furthermore, the anti-inflammatory nitro-fatty acids were negatively associated with baseline disease activity. In conclusion, the developed methodology expands the current metabolic profiling of oxidised lipids in urine, and its application will enhance our understanding of the role these bioactive metabolites play in health and disease.
26077125 Genetic Determinants of Methotrexate Toxicity in Tunisian Patients with Rheumatoid Arthrit 2016 Aug BACKGROUND AND OBJECTIVE: Methotrexate (MTX) is a disease-modifying anti-rheumatic drug used in the treatment of rheumatoid arthritis (RA). It is the first line drug in the treatment of this disease. However, MTX-related adverse drug reactions (ADRs) are seen in 40 % of the patients. The aim of this study was to determine the impact of six genetic polymorphisms located in five genes encoding proteins involved in the MTX metabolic pathway in Tunisian RA patients and evaluate its association with MTX toxicity. METHODS: Genotyping of 5,10 methylenetetrahydrofolate reductase (MTHFR C677T and A1298C), dihydrofolate reductase (DHFR 19-base pair deletion allele), thymidylate synthase (TYMS 2R/3R), methionine synthase (MTR A2756G) and methionine synthase reductase (MTRR A66G) was performed using PCR and PCR-RFLP method in 141 RA patients treated with MTX. Demographic and clinical characteristics were obtained and ADRs were recorded. Association analyses with regard to MTX toxicity were performed using the χ (2) test, the toxicogenetic risk index (TRI) and the Mann-Whitney U-test. RESULTS: The analysis highlighted a significant association of the T/T genotype of MTHFR C677T polymorphism with increased MTX toxicity. However, the MTHFR A1298C, DHFR 19-base pair deletion allele, MTR A2756G and MTRR A66G polymorphisms were not associated with increased MTX toxicity. The TYMS 2R/3R polymorphism had a protective effect against MTX toxicity. CONCLUSION: The results demonstrated that the C677T polymorphism in the MTHFR gene is associated with MTX toxicity in Tunisian RA patients. In contrast, the TYMS 2R/3R polymorphism is associated with a protective effect against overall MTX toxicity.
27175698 Decline of Pulmonary Function Is Associated With the Presence of Rheumatoid Factor in Kore 2016 May Although higher-than-normal levels of rheumatoid factor (RF) are often observed in subjects without specific medical problems, little is known about the influence of RF on pulmonary function in health screening subjects. This study aimed to determine the association between the presence of RF and decreased pulmonary function in Korean health screening subjects without any history of joint disease or clinically apparent lung disease.A total of 115,641 study subjects (age range, 18-88 years) participated in the health checkup program. We excluded subjects who did not have pulmonary function test, as well as those with abnormal chest radiographs. Subjects with medical history of arthritis including rheumatoid arthritis, and lung disease based on the self-reported questionnaire. Final analysis was performed on 94,438 Koreans (41,261 women).RF-positive subjects had a lower forced vital capacity (FVC) predicted value and forced expiratory volume in 1 s (FEV1) predicted value than RF-negative subjects (82.8 ± 11.5% vs 83.8 ± 11.4% for FVC% predicted and 83.5 ± 13.0% vs 85.1 ± 12.9% for FEV1% predicted, P < 0.001 for both). RF positivity was significantly associated with the decline of FEV1% predicted regardless of smoking history (adjusted odds ratio [OR] = 1.289 [95% confidence interval [CI] 1.163-1.429], P < 0.001 for nonsmokers and adjusted OR = 1.138 [95% CI 1.004-1.289], P < 0.001 for smokers) while the decline of FVC% predicted only in nonsmokers (adjusted OR = 1.251 [95% CI 1.133-1.382], P < 0.001). Our results suggest that the presence of RF could impact pulmonary function in apparently healthy subjects. A follow-up study to investigate serial changes in pulmonary function may reveal the actual influence of raised RF titers.
27622415 Concepts in diagnosing, scoring, and monitoring tenosynovitis and other tendon abnormaliti 2016 Sep In the last years, important advancements have been made in implementing high resolution imaging related information inside the global management algorithm in RA patients. Musculoskeletal ultrasound has already proven its utility in visualizing directly the joint synovial tissue, the synovial vascularization and in monitoring the response to therapy. Recently, much attention has been given to the presence of tenosynovitis, as a constant, complementary but different facet of the inflammatory involvement in RA. Tenosynovitis identification in early RA stages may allow adequate treatment adjustment in early and established disease in order to prevent and/ or slow down the development of structural damage at tendon and joint level.
26608848 [Mechanism of bone and cartilage damage in rheumatoid arthritis]. 2015 Dec Rheumatoid arthritis(RA)is an autoimmune diseases characterized by inflammation and destruction of bone and cartilage. Bone destruction in RA is triggered by abnormal activation of immune system and osteoclasts induced by RANKL. Advances in osteoimmunology clarified that immune-factors such as inflammatory cytokines and antibodies promote not only inflammation but also bone destruction in RA. Importantly, a newly identified Th17 subset induces osteoclastogenesis potently by upregulating RANKL on synovial fibroblasts, indicating a synergy between T-synovial fibroblast plays a primary role in the inflammatory bone destruction. Recently, novel bone-regulating factors are identified and can be attractive therapeutic targets for destruct ion of bone and cartilage in RA.