Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
---|---|---|---|---|
21261967 | Can vagus nerve stimulation halt or ameliorate rheumatoid arthritis and lupus? | 2011 Jan 24 | Acetylcholine, the principal vagus neurotransmitter, inhibits inflammation by suppressing the production of pro-inflammatory cytokines through a mechanism dependent on the α7 nicotinic acetylcholine receptor subunit (alpha7nAChR) that explains why vagus nerve stimulation is anti-inflammatory in nature. Strong expression of alpha7nAChR in the synovium of rheumatoid arthritis and psoriatic arthritis patients was detected. Peripheral macrophages and synovial fibroblasts respond in vitro to specific alpha7nAChR cholinergic stimulation with potent inhibition of proinflammatory cytokines. Fibroblasts balance inflammatory mechanisms and arthritis development through feedback cholinergic stimulation by nearby immune cells. Collagen induced arthritis in alpha7nAChR(-/-) mice was significantly severe and showed increased synovial inflammation and joint destruction compared to the wild-type mice. Similar to vagal nerve stimulation and alpha7nAChR agonists, polyunsaturated fatty acids: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) also suppress inflammation. In view of their similar anti-inflammatory actions, it is proposed that vagal nerve stimulation, alpha7nAChR agonists and EPA and DHA may augment the formation of anti-inflammatory lipid molecules: lipoxins, resolvins, protectins and maresins. This implies that therapies directed at regulation of the cholinergic and alpha7nAChR mediated mechanisms and enhancing the formation of lipoxins, resolvins, protectins and maresins may halt and/or ameliorate rheumatoid arthritis, lupus and other rheumatological conditions. | |
22094193 | Chronic widespread pain in the spectrum of rheumatological diseases. | 2011 Apr | Fibromyalgia (FM) is a rheumatic disease characterised by musculoskeletal pain, chronic diffuse tension and/or stiffness in joints and muscles, fatigue, sleep and emotional disturbances and pressure pain sensitivity in at least 11 of 18 tender points. There are currently no instrumental tests or specific diagnostic markers, and the characteristic symptoms of the disease overlap those of many other conditions classified in a different manner. FM is often associated with other diseases that act as confounding and aggravating factors, including primary Sjögren's syndrome (pSS), systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). It has been reported to coexist in 25% of patients with RA, 30% of patients with SLE and 50% of patients with pSS. Its clinical diagnosis is not easy because FM-like symptoms are frequent, and its differential diagnosis with other causes of chronic diffuse pain is difficult. This is even more true in the case of patients who are positive for antinuclear antibodies (ANAs) because, although sensitive, ANA positivity is not specific for SLE or connective tissue diseases, and can also be found in 10-15% of FM patients. Furthermore, composite indices such as the disease activity score (DAS)-28, which are widely used in everyday clinical practice and clinical trials, may be insufficient to evaluate real inflammatory activity in patients with RA associated with chronic pain syndromes such as FM, and can lead to an overestimate of disease activity in RA. The presence of diffuse pain in autoimmune rheumatic diseases compromises the quality of life of the patients, although overall mortality is not increased. A misdiagnosis harms the patients and the community. Rheumatologists should be able to recognise and distinguish primary and secondary FM, and need new guidelines and instruments to avoid making mistakes. | |
21816017 | Glycolysis and rheumatoid arthritis. | 2011 Aug | Glucose metabolism not only provides energy for physical activity but also mediates a variety of physiological processes through the formation of complex signalling networks. Recent studies have indicated that glucose metabolism plays an important role in the pathogenesis of rheumatoid arthritis (RA), an autoimmune disease involving the inflammation of joints. Herein, we review recent progress in this area. Evidence indicates that RA synovial tissues have increased glycolytic activity, which leads to an acidic microenvironment that further induced the transformation of normal synovial cells. Enhanced glycolysis activity is related to hypoxia in RA synovial membranes. Glucose phosphate isomerase, enolase and aldolase and key enzymes of the glycolysis pathway promote RA autoimmunity by acting as autoantigens. Lactate and pyruvate, substrates of RA synovium metabolism, stimulate abnormal cell proliferation, angiogenesis and pannus formation. | |
21345813 | Effects of interleukin (IL)-17A and IL-17F in human rheumatoid arthritis synoviocytes. | 2011 May | Rheumatoid arthritis (RA) is a chronic inflammatory disease where the contribution of T cells is now supported by clinical results. Among the cytokines produced by T cells, interleukin (IL)-17A (previously known as IL-17) and IL-17F constitute the signature cytokines of the newly described Th17 T helper cell subset. While the effects of IL-17A on RA synoviocytes been well described, those of IL-17F remain less studied. The present review describes the effects of IL-17A and IL-17F on synoviocytes and their contribution to RA pathogenesis. Although IL-17F is less active than IL-17A when used alone, IL-17A and IL-17F induce in synoviocytes a rather similar expression pattern in the presence of tumour necrosis factor α. They enhance their response by stabilising mRNA of cytokines and enhancing receptor expression. They increase the migration, chemokine gene expression and invasiveness of synoviocytes. They contribute to disease chronicity by inhibiting synoviocyte apoptosis. Finally, they enhance metalloprotease secretion leading to cartilage damage. These properties support the combined inhibition of IL-17A and -F to control RA inflammation and joint destruction. | |
23253237 | Associations of HLA-DRB1 alleles with anti-citrullinated protein antibody-positive and ant | 2012 Dec | AIM: The aim of this study was to investigate the associations between human leukocyte antigen (HLA)-DRB1 alleles with genetic susceptibility to rheumatoid arthritis (RA) and production of antibodies against cyclic citrullinated peptide (anti-CCP antibody) and rheumatoid factor (RF) in Turkish RA patients. METHODS: We studied 291 RA patients and 253 controls. Genotyping was performed by polymerase chain reaction with sequence-specific oligonucleotide probes hybridization method. Serum levels of anti-CCP antibody, IgM-RF and high sensitive C-reactive protein titers were measured by commercial kits using immunological methods. RESULTS: We found that HLA-DRB1*04 and *09 alleles were associated in anti-CCP+ and anti-CCP+ RA patients (P < 0.0001 and P < 0.001, respectively), while DRB1*01 and *04 were determined to be higher in RF+ RA patients (P < 0.001 and P < 0.0001, respectively). Moreover, DRB1*11 and DRB1*13 alleles were determined to be lower in RF and anti-CCP/RF+ RA patients (P < 0.001 for both). HLA-DRB1*04 was identified as a common responsible allele for susceptibility to the disease in anti-CCP, RF and anti-CCP/RF- RA patients (P = 0.0018, P = 0.0004 and P = 0.0023, respectively). HLA-DRB1*13 allele alone was found to be protective against to anti-CCP+ and RF- RA (P = 0.0003 and P = 0.006, respectively). On the contrary, there was no protective allele in anti-CCP/RF- RA as well as anti-CCP- RA patients. CONCLUSION: This study indicates that associate and protective HLA-DRB1 allele distributions are different in autoantibody (anti-CCP or RF or anti-CCP/RF)+ RA and autoantibody- RA patients, with exceptions of DRB1*04 and DRB1*13. | |
22214811 | [Tuberculous peritonitis during etanercept therapy for rheumatoid arthritis]. | 2011 | In August 2010, a 73-year-old woman with rheumatoid arthritis receiving etanercept (ETN) therapy for two years, developed high-fever and abdominal fullness. Though she had not been exposed to tuberculosis, isoniazid prophylaxis was administrated. Antibiotics were not effective. CT images revealed the massive ascites and peritonitis, and Ga scintigraphy demonstrated notable uptake in the peritoneum. Ascites analysis showed an elevated adenosine deaminase activity value (104.9 IU/l) without malignant cells. Moreover, PCR and culture for Mycobacterium tuberculosis were positive. Finally, a diagnosis of tuberculous peritonitis was established. After initiating a standard anti-tuberculosis regimen with four drugs, her clinical condition ameliorated and ascites promptly regressed. Although the tuberculous peritonitis during ETN therapy is rare, this report emphasized the importance of initial suspicion of tuberculosis in these patients with tumor necrosis factor inhibitors such as ETN. | |
21997404 | Lack of association between CAG repeat polymorphism in the androgen receptor gene and the | 2012 Apr | PURPOSE: Leflunomide (LEF) is a disease-modifying antirheumatic drug used for treating rheumatoid arthritis (RA) and the action of which may be modified by sex hormones. The aim of this study was to examine the association between CAG repeat polymorphism in the androgen receptor (AR) gene and the response to treatment with LEF in women with RA. METHODS: We studied 114 women diagnosed with RA and treated with LEF (20Â mg daily). Follow-up was 12Â months. CAG repeat polymorphism was determined using polymerase chain reaction (PCR) and subsequent fragment analysis by capillary electrophoresis. RESULTS: Analysis revealed no statistically significant associations between CAG repeat polymorphism in the AR gene and improvement of disease activity parameters: erythrocyte sedimentation rate, serum C-reactive protein, patient's global assessment of disease activity on a visual analog scale (VAS), disease activity score of 28 joints (DAS28), and swollen and tender joint count. CONCLUSION: Our results suggest no correlation between CAG repeat polymorphism in the AR gene and response to treatment with LEF in women with RA. | |
21314928 | Expression of K2P5.1 potassium channels on CD4+ T lymphocytes correlates with disease acti | 2011 Feb 11 | INTRODUCTION: CD4+ T cells express K(2P)5.1 (TWIK-related acid-sensitive potassium channel 2 (TASK2); KCNK5), a member of the two-pore domain potassium channel family, which has been shown to influence T cell effector functions. Recently, it was shown that K(2P)5.1 is upregulated upon (autoimmune) T cell stimulation. The aim of this study was to correlate expression levels of K(2P)5.1 on T cells from patients with rheumatoid arthritis (RA) to disease activity in these patients. METHODS: Expression levels of K(2P)5.1 were measured by RT-PCR in the peripheral blood of 58 patients with RA and correlated with disease activity parameters (C-reactive protein levels, erythrocyte sedimentation rates, disease activity score (DAS28) scores). Twenty patients undergoing therapy change were followed-up for six months. Additionally, synovial fluid and synovial biopsies were investigated for T lymphocytes expressing K(2P)5.1. RESULTS: K(2P)5.1 expression levels in CD4+ T cells show a strong correlation to DAS28 scores in RA patients. Similar correlations were found for serological inflammatory parameters (erythrocyte sedimentation rate, C-reactive protein). In addition, K(2P)5.1 expression levels of synovial fluid-derived T cells are higher compared to peripheral blood T cells. Prospective data in individual patients show a parallel behaviour of K(2P)5.1 expression to disease activity parameters during a longitudinal follow-up for six months. CONCLUSIONS: Disease activity in RA patients correlates strongly with K(2P)5.1 expression levels in CD4+ T lymphocytes in the peripheral blood in cross-sectional as well as in longitudinal observations. Further studies are needed to investigate the exact pathophysiological mechanisms and to evaluate the possible use of K(2P)5.1 as a potential biomarker for disease activity and differential diagnosis. | |
21644044 | The role of human xanthine oxidoreductase (HXOR), anti-HXOR antibodies, and microorganisms | 2012 Aug | This work is to investigate the levels of human xanthine oxidoreductase (HXOR), its antibodies, and microorganisms in synovial fluid of patients with untreated rheumatoid joint diseases. Synovial fluids were collected from sixty-four patients with rheumatoid joint diseases. Sixty-four age-matched individuals were included as control. Xanthine oxidoreductase (XOR) proteins level and anti-XOR antibodies were determined in the blood and synovial fluid, using human XOR as antigen, by enzyme-linked immunosorbent (ELISA) assay. Synovial fluids were cultured for bacteria and fungi. The titers of XOR protein in the synovial fluid of patients with rheumatoid arthritis were 90.43 ± 23.37 μg/ml (mean ± SD, n = 29) and up to 62.42 ± 8.74 μg/ml (mean ± SD, n = 35) in other joint inflammation. Anti-HXOR antibodies titers in patients were 167.72 ± 23.64 μg/ml, n = 64, which was significantly higher in rheumatoid arthritis patients. The results indicated that anti-HXOR antibodies in synovial fluids have a protective role as high concentrations against XOR were detected in inflammatory arthritis. These antibodies play a role in eliminating XOR from synovial fluids. However, immune complex formation could activate complement and participate in propagating the inflammatory cycle. Synovial aspirate ordinary microbial cultures were negative for any bacteria or fungi, but that does not exclude organisms of special culture requirements. | |
21687922 | Strategies for assessment and outcome measurement in physical and rehabilitation medicine: | 2011 Jul | The aim of this educational review, which is based upon expert opinion, is to describe to clinicians training in Physical and Rehabilitation Medicine and research students training to work in the field, the appropriate attributes and standards required for assessment and outcome measurement. "What to assess" is discussed in the context of the conceptual framework provided by the International Classification of Functioning, Disability and Health, supplemented with quality of life as an additional construct. The reasons for making the assessment, and the context in which the assessment will be used, are then considered. Examples of recommendations of some international organizations regarding what and how to assess are presented. Suggestions are made about the selection of assessment tools, including examples from two diagnostic groups: stroke and rheumatoid arthritis. Finally, the basic psychometric standards required for any assessment tool, and additional requirements for outcome assessment, are explained. | |
21556028 | Role of GILZ in immune regulation, glucocorticoid actions and rheumatoid arthritis. | 2011 Jun | Glucocorticoids have been exploited therapeutically for more than six decades through the use of synthetic glucocorticoids as anti-inflammatory agents, and are still used in as many as 50% of patients suffering from inflammatory diseases such as rheumatoid arthritis (RA). Better understanding of the mechanisms of action of glucocorticoids could enable the development of therapies that dissociate the broad-spectrum benefits of glucocorticoids from their adverse metabolic effects. The glucocorticoid-induced leucine zipper protein (GILZ; also known as TSC22 domain family protein 3) is a glucocorticoid-responsive molecule whose interactions with signal transduction pathways, many of which are operative in RA and other inflammatory diseases, suggest that it is a key endogenous regulator of the immune response. The overlap between the observed effects of GILZ on the immune system and those of glucocorticoids strongly suggest GILZ as a critical mediator of the therapeutic effects of glucocorticoids. Observations of the immunomodulatory effects of GILZ in human RA synovial cells, and in an in vivo model of RA, support the hypothesis that GILZ is a key glucocorticoid-induced regulator of inflammation in RA. Moreover, evidence that the effect of GILZ on bone loss might be in contrast to those of glucocorticoids suggests manipulation of GILZ as a potential means of dissociating the beneficial anti-inflammatory effects of glucocorticoids from their negative metabolic repercussions. | |
21263416 | Adenosine deaminase and C-reactive protein in diagnosing and monitoring of rheumatoid arth | 2011 Feb | AIM: To determine of catalytic activities of adenosine deaminase (ADA) and values of C-reactive protein (CRP) concentration in serums of patients with rheumatoid arthritis (RA), who were and were not treated with Methotrexate (MTX), and identifying the possibilities of using these biochemical parameters in diagnosing and monitoring of treatment effects in RA. METHODS: The study involved 120 subjects (60 healthy ones, who are in accordance with examined groups concerning age and sex, 30 suffering from RA who were not treated with MTX and 30 suffering from RA who were treated by MTX). Catalytic activities of ADA in serum were determined by spectrophotometric method using adenosine as a substrate. CRP concentrations in serum were determined immunoturbidimetrically. RESULTS: A statistically significant correlation between values of ADA catalytic activities and values of CRP concentrations (r = 0.55, p < 0.01) in serums of subjects with RA without MTX treatment. At subjects with RA treated by MTX, correlation between values of ADA catalytic activities and values of CRP concentrations in serums was not statistically significant (r = 0.33, p > 0.01). CONCLUSION: Study results have shown that ADA catalytic activity in serum can be a useful biochemical marker of inflammatory process in RA. | |
22956589 | Elevated rheumatoid factor and long term risk of rheumatoid arthritis: a prospective cohor | 2012 Sep 6 | OBJECTIVE: To test whether elevated concentration of rheumatoid factor is associated with long term development of rheumatoid arthritis. DESIGN: A prospective cohort study, the Copenhagen City Heart Study. Blood was drawn in 1981-83, and participants were followed until 10 August 2010. SETTING: Copenhagen general population. PARTICIPANTS: 9712 white Danish individuals from the general population aged 20-100 years without rheumatoid arthritis at study entry. MAIN OUTCOME MEASURES: Rheumatoid arthritis according to baseline plasma IgM rheumatoid factor level categories of 25-50, 50.1-100, and >100, versus <25 IU/mL. RESULTS: Rheumatoid factor levels were similar from age 20 to 100 years. During 187,659 person years, 183 individuals developed rheumatoid arthritis. In healthy individuals, a doubling in levels of rheumatoid factor was associated with a 3.3-fold (95% confidence interval 2.7 to 4.0) increased risk of developing rheumatoid arthritis, with a similar trend for most other autoimmune rheumatic diseases. The cumulative incidence of rheumatoid arthritis increased with increasing rheumatoid factor category (P(trend)<0.0001). Multivariable adjusted hazard ratios for rheumatoid arthritis were 3.6 (95% confidence interval 1.7 to 7.3) for rheumatoid factor levels of 25-50 IU/mL, 6.0 (3.4 to 10) for 50.1-100 IU/mL, and 26 (15 to 46) for >100 IU/mL, compared with <25 IU/mL (P(trend)<0.0001). The highest absolute 10 year risk of rheumatoid arthritis of 32% was observed in 50-69 years old women who smoked with rheumatoid factor levels >100 IU/mL. CONCLUSION: Individuals in the general population with elevated rheumatoid factor have up to 26-fold greater long term risk of rheumatoid arthritis, and up to 32% 10 year absolute risk of rheumatoid arthritis. These novel findings may lead to revision of guidelines for early referral to a rheumatologist and early arthritis clinics based on rheumatoid factor testing. | |
21596198 | [Anesthesia and rheumatoid arthritis]. | 2011 May | BACKGROUND AND OBJECTIVES: Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown etiology. It is known that RA patients have a reduced life expectancy when compared with the general population. Rheumatic diseases are numerous and occur with high variability; some of them develop very rapidly while others occur chronically provoking disability throughout life. Anesthetic risks in osteoarticular disorders involve not only the mechanical deformations caused by the disease, but also the cardiovascular, respiratory, renal, and digestive systems. CONTENTS: The purpose of this review was to stress the importance of stages in disease process that may affect anesthesia control before, during, and after surgery, highlighting the authors' experience in a retrospective review of patients with juvenile rheumatoid arthritis (JRA) undergoing placement of orthopedic prosthesis with emphasis on intubation techniques. CONCLUSIONS: Rheumatoid arthritis patients can present a number of complex problems for the anesthesiologist. This requires careful preoperative evaluation; anesthesia requires experience with the technique; and postoperative care should be judiciously chosen to meet the specific needs of the patient. The procedure requires effective communication among surgeon, rheumatologist and anesthesiologist so each member of the multidisciplinary team can contribute with his/her expertise in order to better benefit the patient. | |
23020882 | Mechanisms of premature atherosclerosis in rheumatoid arthritis and lupus. | 2013 | Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), the two most common systemic autoimmune disorders, have both unique and overlapping manifestations. One feature they share is a significantly enhanced risk of atherosclerotic cardiovascular (CV) disease that significantly contributes to morbidity and mortality. The primary mechanisms that drive CV damage in these diseases remain to be fully characterized, but recent discoveries indicate that distinct inflammatory pathways and immune dysregulation characteristic of RA and SLE likely play prominent roles. This review focuses on analyzing the major mechanisms and pathways potentially implicated in the acceleration of atherothrombosis and CV risk in SLE and RA, as well as in the identification of putative preventive strategies that may mitigate vascular complications in systemic autoimmunity. | |
22593670 | Satisfaction with access to health services: the perspective of Estonian patients with rhe | 2012 | In this cross-sectional study we explained the possible determinants of satisfaction with access to health services in patients with rheumatoid arthritis (RA). Of the 2000 randomly selected Estonian adult patients with RA, a total 1259 completed the survey. Regression analysis was used to analyse the predictors of patients' satisfaction with access to health services. Half of the respondents were satisfied with their access to health services. Factors that had a negative impact on satisfaction included pain intensity, longer waiting times to see the doctors, as well as low satisfaction with the doctors. Transportation costs to visit a rheumatologist and higher rehabilitation expenses also affected the degree of satisfaction. Patients who could choose the date and time at which they could visit the rheumatologist or who could visit their "own" doctor were more likely to be satisfied than patients whose appointment times were appointed by a healthcare provider. | |
22073933 | Core management principles in rheumatoid arthritis to help guide managed care professional | 2011 Nov | BACKGROUND: Rheumatoid arthritis (RA) is a chronic, systemic autoimmune inflammatory disease that affects approximately 1% of the population. Initial symptoms include joint swelling, stiffness, and tenderness, which are all causes of disability. The diagnosis of RA is based on patient history of joint pain and stiffness, the documentation of symmetric polyarticular joint synovitis, and laboratory measures including radiographs, inflammatory markers, and autoantibodies. As the disease progresses, synovial inflammation leads to cartilage damage, bone erosions, and joint destruction, the major causes of long-term disability. RA is associated with many comorbidities and complications, including cardiovascular disease, which is responsible for higher rates of mortality among patients compared with the general population. Over the past 2 decades, advances in the development of synthetic disease-modifying antirheumatic drugs (DMARDs) and biologic agents for RA have markedly changed treatment goals and management strategies. OBJECTIVES: To review recent updates in the diagnosis and treatment of RA, as well as the importance of early and aggressive treatment and management strategies. SUMMARY: Borrowing from other medical fields, a paradigm of "tight control" of RA has been supported by evidence and is gaining wide acceptance in rheumatology. In 2010, the American College of Rheumatology and the European League Against Rheumatism (EULAR) published revised classification criteria for RA, which will assist in the diagnosis of early RA and facilitate appropriate treatment intervention. Over the last decade, many patients on biologic agents have demonstrated that early and aggressive treatment of RA is beneficial in treating synovial inflammation, delaying joint damage, and improving patient outcomes. Contemporary management strategies based on early diagnosis, aggressive treatment, and regular monitoring have helped a significant number of patients with RA achieve current treatment goals of low levels of disease activity and, in some cases, clinical remission. | |
22642916 | Does periodontopathic bacterial infection contribute to the etiopathogenesis of the autoim | 2012 May | There is a significant association between rheumatoid arthritis (RA) and periodontal disease (PD). Patients with longstanding active RA have been found to have a substantially increased frequency of PD compared with healthy subjects. Further, patients with PD have been shown to have a higher prevalence of RA than patients without periodontitis. Antibodies to Gram-negative, anaerobic periodontal pathogens such as Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, and Tannerella forsythia have been detected in the serum and synovial fluid of RA patients. These pathogens have also been identified in the synovial fluid of RA patients, with higher levels of bacterial DNA in RA patients than in controls. This review examines the association between periodontopathic bacteria and the etiology of RA. | |
22378716 | Treatment decisions and related costs differ significantly depending on the choice of a di | 2012 Jul | OBJECTIVE: To evaluate the therapeutic and economic consequences of various disease activity indices (DAIs) in RA according to 1987 and 2010 criteria. METHODS: Data on disease activity states from all sustained visits were assessed from all patients who participate in the treatment in the Rotterdam Early Arthritis Cohort (tREACH) study, a stratified randomized trial to evaluate different treatment strategies in patients with a symptom duration of <1 year. Frequencies of treatment adaptations, based upon exclusive thresholds of various DAIs, were visualized in reclassification tables. The Stuart-Maxwell test was applied to analyse any significant differences between treatment decisions according to the different DAIs. Simulated annual median medication costs were estimated using the tREACH medication protocol with standard national costs. RESULTS: DAIs perform similar in RA according to 1987 and 2010 criteria. A total of 1104 DASs per DAI were available from 296 patients. DAIs differ significantly, compared with DASs, in classifying a patient's disease state. Consequently, treatment intensifications occur more frequently with SDAI, CDAI and DAS-28 usage, compared with DAS. Tapering treatment occurs less frequently with SDAI and CDAI and more frequently with DAS-28 usage. Simulated annual median medication costs are significantly higher if DAS-28, SDAI and CDAI are used compared with DAS usage. CONCLUSION: Usage of various DAIs in a single patient leads to inconsistent disease state categorizations. Consequently, these inconsistencies significantly influence therapeutic decisions and accompanying costs. As DAI usage is imperative to uphold current European League Against Rheumatology (EULAR) treatment recommendations, physicians should consider these therapeutic and economic consequences before choosing a particular DAI. | |
21608214 | [The objectivity research on 322 rheumatoid arthritis patients of dampness-heat impeding a | 2011 Apr | OBJECTIVE: To analyze the Chinese medical syndrome typing laws in rheumatoid arthritis (RA) patients of the dampness-heat impeding syndrome and the cold-dampness impeding syndrome. METHODS: Clinical data and serum of 322 inpatients and outpatients were collected to perform DAS28 score. Laboratory indices including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), albumin (ALB), globulin (GLB), and blood routines (white blood cell, red blood cell, and platelet) were tested by conventional methods, and the serum levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta were detected by ELISA. The difference of each index was analyzed between RA patients of the dampness-heat impeding syndrome and the cold-dampness impeding syndrome. RESULTS: The levels of DAS28 scores, ESR, CRP, white blood cell count, and platelet of RA patients of the dampness-heat impeding syndrome were significantly higher than those of the cold-dampness impeding syndrome (P <0.01). The serum level of GLB of RA patients of the dampness-heat impeding syndrome was obviously higher than that of the cold-dampness impeding syndrome (P <0.01), while the serum ALB level of RA patients of the dampness-heat impeding syndrome was obviously lower than that of the cold-dampness impeding syndrome (P<0.01). Compared with the dampness-heat impeding syndrome, ROC curve results showed the area under the curve (AUC) were ranked from large to small as DAS28 score > ESR >CRP >GLB > PLT >WBC (P<0.01). Compared with the cold-dampness impeding syndrome, only ALB was of diagnostic value for cold-dampness impeding syndrome and the AUC was 0.636 (P = 0.000). CONCLUSION: DAS28 score, ESR, CRP, PLT, WBC, GLB, and ALB could be used as objective index in identifying the differences between the dampness-heat impeding syndrome and the cold-dampness impeding syndrome in RA patients. |