Rheumatoidarthritis (RA) is a chronic systemic inlammatory disease, characterised by polyarthritis and extra-articular organ disease, including rheumatoid nodules, ophthalmologic manifestations, cardiopulmonary disease, vasculitis, neuropathy, glomerulonephritis, Felty’s syndrome, and amyloidosis. Extra-articular manifestations of RA (ExRA) occur in 17.8–40.9% of RA patients, 1.5–21.5% of them presenting as severe forms and usually associated with increased morbidity and mortality. They can develop at any time during the course of the disease, even in the early stages, and are associated with certain predisposing factors, such as the presence of rheumatoid factor, smoking, and long-standing severe disease. Rheumatoid nodules, the most common ExRA, have been found to be associated with the development of severe features, such as vasculitis, rheumatoid lung disease, pericarditis, and pleuritis, especially in those patients who develop them within 2 years from RA diagnosis. There is no uniformity in the deinition of the term ExRA, which limits comparability between diferent studies. Several recent surveys suggest a lower frequency, probably due to a better control of disease activity. Diagnosis of ExRA is a challenge for clinicians, given its variable and complex presentation, and the lack of speciic diagnostic tests; it must be based on clinical recognition and exclusion of other causes of the signs and symptoms. Furthermore, management continues to be diicult with a bad prognosis in many conditions. This article reviews the clinical aspects of major ExRA, focusing on incidence, clinical features, and therapeutic approaches, and how modern immunosuppressive therapy can change the outcome.
Dendritic cells are main important APC’s .These cells on maturation combines with MHC molecules and co-receptors like CD-80, CD-40 activates T-cells and B-cells. This main action is regulated by IL-12gene in dendritic cells. Tolerogenic vaccination signifies exotic tool that is launched in to humans or domestic animals with an intention to enroot immunity and to generate immunological tolerance that is condition marked by stolidity to a specific antigen. Here in this critique we have cited applicability of RNA modified DC in treatment of Rheumatoidarthritis. By using the method of RNA interference using siRNA-IL12 treated DC we can treat RA by decreasing T- cell responses towards our own cells.
Abstract Rheumatoidarthritis (RA) is a chronic condition that affects about 1% of the adult pop- ulation. In a historical cohort of Minas Gerais State, 11,573 RA patients registered in the Out- patient Information System (SIA) between 2008 and 2013 were identified. For this study we ad- opted the public funding body’s perspective and the values were adjusted by the national inflation index (IPCA) of December 2015. Etanercept was the most expensive treatment. The mean cohort age was 52 years old and most of the patients were women. Multiple regression analysis indicated a negative association between higher expenditure and age, female sex, and diagnosis at entry in the cohort and positive association between high expenditure and the Human Development Index (HDI) of the municipality and use of tumor ne- crosis factor agents. This study identified the fac- tors that have an impact on RA drug treatment expenditure. Also, we showed that methods that enable extracting demographic and expenditure data of administrative information systems may represent important tools in the construction of economic studies to subsidize economic health evaluations, especially from the standpoint of the managers.
Bronchocentric granulomatosis (BcG) is characterized by granulomatous destruction of bronchial or bron- chiolar walls and adjacent parenchyma, with debris and exudates filling the airway lumen. Approximately 50% of total cases have been associated with asthma and al- lergic bronchopulmonary aspergillosis, while it has been rarely reported in the context of rheumatoidarthritis (RA). We describe the case of a 69-year-old fe- male RA patient with BcG presenting as a solitary cavi - tary pulmonary mass. In addition, we conducted a li - terature review about the clinical and imaging features of BcG in RA patients.
In our study, RA functional class was the main predictor of the indirect costs of the disease. Poor functional classes were associated with the highest indirect costs in our sample. This ﬁnding is in line with other studies [34,35]. Leardini et al. have found that direct and indirect costs increase as RA becomes more severe, with Class IV patients costing six times as much as Class I patients . Guillemin et al. have also found a signiﬁcant association between indirect costs and poor functional class, with similar costs for Class I and II patients that have two and three times lower costs than that associated with Class III and IV patients, respectively . Our data also show a sig- niﬁcant correlation between RA indirect costs and socioeconomic status and sex. RA-related disability to work has been associated with lower levels of educa- tion, jobs that demand higher physical strength, higher HAQ disability scores, longer disease duration, persis- tent erythrocyte sedimentation rate abnormalities, patient’s global assessment of the disease, pain and joints count . It is likely that all these factors contribute to increased incapacity to work among the lowest socioeconomic segments of the population. At same time, patients with the lowest socioeconomic status usually have less formal education and poor professional qualiﬁcation with the consequent lowest paying jobs, which accounts for the lower indirect costs observed for these patients. In contrast, patients with higher socioeconomic status tend to be more edu- cated, professionally qualiﬁed, and hold better paying jobs so that once their capability to work is compro- mised, the associated indirect costs are higher. In the Table 5 Sensitivity analysis of the indirect costs (in minimum wages) of rheumatoidarthritis in Brazil—comparison of estimates based on individual and population incomes
Rheumatoidarthritis (RA) is characterized by chronic inflammation of the synovial joints resulting from hyperplasia of synovial fibroblasts and infiltration of lymphocytes, macrophages and plasma cells, all of which manifest signs of activation. All these cells proliferate abnormally, invade bone and carti- lage, produce an elevated amount of pro-inflammatory cytokines, metalloproteinases and trigger osteo- clast formation and activation. Some of the pathophysiological consequences of the disease may be explained by the inadequate apoptosis, which may promote the survival of autoreactive T cells, mac- rophages or synovial fibroblasts. Although RA does not result from single genetic mutations, elucidation of the molecular mechanisms implicated in joint destruction has revealed novel targets for gene therapy. Gene transfer strategies include inhibition of pro-inflammatory cytokines, blockade of cartilage-de- grading metalloproteinases, inhibition of synovial cell activation and manipulation of the Th1-Th2 cytokine balance. Recent findings have iluminated the idea that induction of apoptosis in the rheumatoid joint can be also used to gain therapeutic advantage in the disease. In the present review we will discuss different strategies used for gene transfer in RA and chronic inflammation. Particularly, we will high- light the importance of programmed cell death as a novel target for gene therapy using endogenous biological mediators, such as galectin-1, a β -galactoside-binding protein that induces apoptosis of ac- tivated T cells and immature thymocytes.
Rheumatoidarthritis (RA), psoriatic arthritis (PsA) and axial spondyloarthritis (ax-SpA) are the most common inflammatory rheumatic diseases in ordinary outpatient clinics. In Norway the prevalence reported is 0.5% for RA , 0.2% for PsA  and 0.2% for ankylosing spondyli- tis (AS) . These inflammatory disorders are characterised by different clinical, laboratory and imaging hallmarks. RA is characterised by symmetric and erosive arthritis typically affect- ing small and medium-sized joints . PsA is a more heterogeneous inflammatory disease which may present as mild monoarthritis or severe polyarthritis and may also involve the axial skeleton and the entheses [5,6]. AS is a systemic inflammatory disorder that affects the sacroili- ac joints and the spine, and can also affect peripheral joints and entheses . Axial spondyloar- thritis (ax-SpA) is a common term for inflammatory joint disorders with inflammation in axial skeleton and may include AS, undifferentiated spondyloarthritis and PsA with axial involve- ment [8,9]. In RA, bone involvement is characterized by erosions, whereas in PsA and ax-SpA bone involvement also includes signs of bone new formation [4,10,11].
Rheumatoidarthritis (RA) is a chronic debilitating disease character- ized by distinct autoimmune, inflammatory and fibrovascular compo- nents which lead to synovial proliferation and joint destruction. However, existing treatments specifically target only autoimmune and inflammatory components despite the fact that neovascularization of the inflamed synovium is a hallmark of rheumatoidarthritis. Angio- genesis may contribute to synovial growth, leukocyte recruitment and tissue remodeling, thus potentiating disease progression. Although no therapies currently target angiogenesis, several existing therapies have anti-angiogenic activity. Recent advances in anti-angiogenic strate- gies in oncology, including the identification of integrin avß3 as a crucial effector of angiogenesis, suggest a means to assess the role of angiogenesis in rheumatoidarthritis. Synovial endothelial cells have been shown to express integrin avß3, suggesting that these cells may be targeted for angiogenesis inhibition. Prior studies in rat arthritis models have shown benefit after the addition of broad spectrum integrin antagonists. However, formal assessment of integrin-targeted anti-angiogenic activity is now underway. These controlled studies will be important in assessing the efficacy of therapies which target angiogenesis in RA.
Crohn’s disease (CD) is an chronic autoimmune inlammatory bowel disease (IBD) which may involve any part of the gastrointestinal system (GIS) (1). Although the rellationships among autoimmune diseases are known, association of rheumatoidarthritis (RA) and CD is an extremely rare condition (2,3).
Aim: Rheumatoidarthritis (RA) is a chronic autoim- mune disease, which affects many tissues and organs, but majorly attacks synovial joints. Beyond the major histocompatibility complex (MHC) genes, peptidyl arginine deiminase type IV (PADI4) has been sugges ted to be associated with RA susceptibility. Evidence re- garding the association of PADI4 single nucleotide poly- morphisms (SNPs) and RA is controversial, thus we conducted this large-scale case-control study to assess the association of rs874881 and rs11203367 PADI4 SNPs with susceptibility to RA.
Introduction: Features suggestive of neuropathic pain (NP) have been described in rheumatoidarthritis (RA) in addition to nociceptive pain. We aimed to determine the clinical predictors of NP in RA patients and study its association with radiographic structural damage. Methods: Cross-sectional study was performed with RA patients followed at our Rheumatology department. Patients with diagnosed neuropathy of other origin, non-RA related risk factors for NP (e.g. diabetes melli- tus) or fibromyalgia, according to expert opinion, were excluded. Demographic and clinical data were collec ted and disease activity/functional measures were evalua - ted. Two questionnaires were applied to assess NP: the Leeds Assessment of Neuropathic Symptoms (LANSS) and the painDETECT questionnaire (PDQ). Radio- graphs performed in up to 12 months before/after the evaluation were classified according to the modified van der Heijde Sharp’s method. Univariate and multi- variate logistic regression were performed to identify the predictors of NP.
Rheumatoidarthritis (RA) is a chronic multisystem autoimmune disease with yet unfolded pathogenesis (1,2). The prevalence of RA is globally estimated to be around 1% of the general population; however, in Asian Pacific countries, it is lower than this rate (3). In Iran, 0.37% of urban population is involved with RA (3). Women are affected approximately three times more often than men. The prevalence increases with age, and sex differences diminish in the older ages.
In the present study, we evaluated 42 wrists using the semi-quantitative scales power Doppler ultrasound (PDUS) and gray scale ultrasound (GSUS) with scores ranging from 0 to 3 and correlated the results with clinical, laboratory and radiographic data. Twenty-one patients (17 women and 4 men) with rheumatoidarthritis according to criteria of the American College of Rheuma- tology were enrolled in the study from September 2008 to July 2009 at Universidade Estadual de Campinas (UNICAMP). The average disease duration was 14 months. The patients were 66.6% Caucasians and 33.3% non-Caucasians, with a mean age of 42 and 41 years, respectively. A dorsal longitudinal scan was performed by ultrasound on the radiocarpal and midcarpal joints using GE LOGIQ XP-linear ultrasound and a high frequency (8-10 MHz) transducer. All patients were X-rayed, and the Larsen score was determined for the joints, with grades ranging from 0 to V. This study showed significant correlations between clini- cal, sonographic and laboratory data: GSUS and swollen right wrist (r = 0.546), GSUS of right wrist and swelling of left wrist (r = 0.511), PDUS of right wrist and pain in left wrist (r = 0.436), PDUS of right wrist and C-reactive protein (r = 0.466). Ultrasound can be considered a useful tool in the diagnosis of synovitis in early rheumatoidarthritis mainly when the anti-cyclic citrullinated peptide and rheumatoid factor are negative, and can lead to an early change in the therapeutic decision.
Objective: to describe the profile of patients with RheumatoidArthritis (RA) and their caregivers receiving care at the Rheumatology Outpatient Clinic of a teaching hospital, and evaluate the burden of the caregivers. Method: a cross-sectional study was performed with 41 patients with RA and their caregivers using a questionnaire to identify sociodemographic variables; the Burden Interview Scale and the Stanford Health Assessment Questionnaire. Descriptive analyzes and comparison between clinical-demographic variables and the functional status of patients were performed and the correlation between sociodemographic variables and levels of burden of caregivers was tested. Results: there was a prevalence of female patients (87.8%); a mean age of 64.4 years (±12.9); a mean time for the diagnosis of RA of 13.5 years (±8.5), a prevalence of moderate disability (39.0%); lower disability in the Hygiene domain (1.6; ±0.5) and greater disability in the Other Activities of Daily Life (2.1; ±0.6), Reach (2.0; ±0.7) and Grip (2.0; ±0.7) domains. The caregivers were women (73.2%); aged between 17 and 81 years (mean: 46.8; ±15.1); with a high school education (41.4%). The degree of kinship was 56.2% offspring and 36.6% spouses. Eighteen (44.0%) caregivers suffered burden, nine (22.0%) of whom had mild burden and nine (22.0%) of whom suffered intense burden. There was a higher incidence of intense burden among spouses (12.2%) and mild burden among children (12.2%). Conclusion: the low occurrence of burden among caregivers may be related to the profile of the patients, who presented good levels of independence for self-care. The profile of caregivers and the prevalence of overburdened spouses and offspring shows the need and importance of the implementation of caregiver training by health service professionals to improve care for RA patients.
The immune system is a complex organization of cells and antibodies designed normally to seek and destroy invaders of the body particularly infections. Rheumatoidarthritis is an auto immune disease that mistakenly attacks our own immune system and damage tissues around joints, tendons, ligaments and muscles by means of T-cell differentiation.
Rheumatoidarthritis (RA) and juvenile idiopathic/rheuma- toid arthritis (JIA) are chronic, inflammatory, systemic, auto- immune diseases characterized by chronic arthritis leading to progressive joint erosions. The individual functional and social impact of rheumatoidarthritis is of great importance. Disability and joint damage occur rapidly and early in the course of the disease. The remarkably improved outcomes have been achieved initiating biologic therapy with close monitor- ing of disease progression. Biologic agents are drugs, usually proteins, which can influence chronic immune dysregulation resulting in chronic arthritis. According to the mechanism of action these drugs include: 1) anti-TNF drugs (etanercept, infiximab, adalimumab); 2) IL-1 blocking drugs (anakinra); 3)
RheumatoidArthritis (RA) is a chronic autoimmune disease that primarily attacks synovial joints. In the RA joints, various inflammatory cells, including innate immune cells (e.g. mast cells, macrophages, dendritic cells, and NK cells), adaptive immune cells (T- and B-cells), and fibroblast-like synoviocytes (FLS), are activated. These cells interact with each other via an array of cytokines and/or cell-to-cell contacts, leading to prolonged inflammation, abnormal proliferation of FLS, and the destruction of cartilage and bone [1,2,3]. Despite incremental advances in the diagnosis and treatment of RA, novel molecular targets are still needed to improve the accuracy of diagnosis and the therapeutic outcomes. For example, two metrics widely used to assess RA activity, i.e., erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are not specific to RA because they also are elevated in non-RA conditions including infections and trauma. In addition, rheumatoid factor and anti-CCP antibody, well-known diagnostic markers for RA, represent B-cell hyperactivity to self- antigens, but are limited in reflecting the multi-cellular commu- nication networks occurring in the RA joints.
A 30-year-old woman who had been diagnosed rheumatoidarthritis many years ago and not treated since 2 years was referred to local the Department of Chest Diseases of State Hospital with a sudden onset of right lateral chest pain. The chest X-ray on admission showed pleural efusion on the right hemithorax. Thora- centesis was applied. Hemorrhagic pleural efusion was obtained. It was thought rheumatoid pleurisy with its clinical, radiological and laboratory indings. In this case report, we have presented the difuculties during diferential diagnosis of pleural efusion in rheumatoidarthritis patients and details accompanied by a literature review.