Search for: rheumatoid arthritis    methotrexate    autoimmune disease    biomarker    gene expression    GWAS    HLA genes    non-HLA genes   

ID PMID Title PublicationDate abstract
14561205 Oral tolerance in the treatment of rheumatoid arthritis. 2002 Mar Oral tolerance (OT) consists of the oral administration of antigens (Ag) that could alter the response of the immune system. This is a form of peripheral immune tolerance in which mature lymphocytes in the peripheral lymphoid tissues are rendered non functional or hyporesponsive by prior oral administration of Ag. It was first described in 1911 in animal models of anaphylaxis. This therapeutic approach requires the orally administration of Ag and the active participation of the gut-associated lymphoid tissue (GALT), a tissue comprising Peyer's patches, intraepitelial cells and villi containing epithelials cells which is a well organized immune network. The mechanisms by which OT is mediated included deletion or anergy and active cellular suppression. The primary factor determining which form of tolerance will be developed after oral administration of Ag is the Ag dosage. Thus, it is thought that low doses of Ag induce the generation of active suppression, via regulatory T cells in the GALT, which then migrate to the systemic immune system. These regulatory T cells produce down-regulatory cytokines such as IL4, IL10 and TGFbeta, a Th2 / Th3 cytokine pattern. Conversely, high dose of Ag favors anergy or clonal deletion. The phenomenon in which regulatory cells, as generated by oral tolerization, are primed in an Ag specific manner, but act in the respective microenvironment in a non-Ag specific manner is called bystander suppression. This phenomenon is of particular interest and explained the use of OT in T cell mediated autoimmune diseases such as rheumatoid arthritis (RA), multiple sclerosis (MS) and type I diabetes, some diseases in which the autoAg remains unknown or where there are reactivities to multiple autoAgs. There were several studies demonstrating the effectiveness of orally administered Ag in different animal models of autoimmune diseases, such as experimental allergic encephalomyelitis, collagen induced arthritis, diabetes, but also uveitis, myastenia gravis and transplantation. These mouse or rat models of autoimmune diseases gave the rationale for the therapeutic use of OT in human and this therapeutic approach has been tried in MS and RA, using oral myelin or oral collagen, respectively. In RA, 4 trials of oral type II collagen (CII) in RA have been published. Taken together, these studies suggested that oral CII in RA gave a trend toward clinical improvement, with significance in only 2 studies. Bacterial extract from Escherichia coli containing heat shock proteins has been tried in oral treatment for RA. Two placebo controlled trials and 2 comparative studies gave favorable results for this bacterial extract with no or mild adverse events. Although oral/mucosal tolerance has given successful results in animal models of autoimmune diseases, the enthusiasm for this therapeutic approach in human diseases must be tempered. The discrepancies between the effectiveness of OT in animal models and the results in human trials raise some questions, the identification of the subgroup of patients who might respond to this treatment and the source (or nature) of the administered Ag (homologous versus heterologous), for instance.
12027497 The effect of activity and type of rheumatoid arthritis on the flexible implant arthroplas 2002 Apr A retrospective study was performed on 184 Swanson flexible implant arthroplasties of the metacarpophalangeal joint in 75 hands of 64 patients with rheumatoid arthritis, to investigate the influence of systemic factors on the clinical and radiological results. The mean follow-up period was 6 years. The postoperative serum C-reactive protein level was found to affect postoperative pain, and there was a larger extension lag and more subsidence of the implant in those with the mutilating type of the disease.
11915973 Health-related quality of life in early rheumatoid arthritis: impact of disease and treatm 2002 Mar OBJECTIVE: To document the burden of early rheumatoid arthritis (RA) on health-related quality of life (HQL) and compare changes in HQL across 2 treatments. STUDY DESIGN: Analysis of HQL scores among patients enrolled in a multicenter, double-blind, randomized control trial of early RA treatment. PATIENTS AND METHODS: A total of 424 patients with early RA were randomized to 1 of 2 treatment groups: etanercept or methotrexate. Patients were treated and followed for 52 weeks. Health-related quality of life was assessed before and throughout treatment using the Medical Outcomes Study Short Form 36 Health Survey (SF-36) and the Health Assessment Questionnaire (HAQ). The HQL burden of RA was established by comparing SF-36 scale scores to general US population norms. The impact of treatment on HQL was determined by comparing scores on both SF-36 and HAQ scales. RESULTS: Before treatment, RA patients showed significant decrements in scores on all SF-36 scales and summary measures in comparison with age- and sex-matched general US population norms, multivariate analysis of variance (MANOVA) F(8,2815) = 204.6, P < .0001. After 52 weeks of treatment, 7 of 8 SF-36 scales and the physical summary measure remained significantly below the general US population norm, MANOVA F(8,2815) = 41.9, P < .0001. Patients randomized to etanercept showed significantly better HQL improvement earlier in treatment than patients randomized to methotrexate on the SF-36 physical summary, MANOVA F(10,4230) = 6.1, P< .0001, the SF-36 arthritis-specific health index, MANOVA F(10,4230) = 8.5, P < .0001, and the HAQ, MANOVA F(10,4230) = 14.7, P < .0001. At 52 weeks, there were no significant differences between treatment groups. CONCLUSIONS: Rheumatoid arthritis places tremendous disease burden on patients' HQL. Successful treatment of early RA improved HQL. Etanercept showed a rapid HQL response.
12810200 Antibody therapy for rheumatoid arthritis. 2003 Jun High-quality monoclonal antibodies (mAbs) with specificity for relevant disease molecules can now be produced in abundance. Anti-tumour necrosis factor-alpha therapies have set a new standard for symptom control in rheumatoid arthritis, and blockade of tumour necrosis factor has the potential to protect joints from structural damage. Other targets for therapeutic antibodies include the cytokines interleukin (IL)-1, IL-6, IL-8, IL-15, IL-17 and IL-18. In addition, there is preliminary evidence for the clinical efficacy of both keliximab, a mAb targeting the T cell antigen CD4, and rituximab, a chimeric mAb against the B cell antigen CD20 and CTLA4-Ig, which blocks the CD28/B7 interaction. Phase III studies have yet to be undertaken for these novel biological agents, and it is unclear whether any of these agents will have true disease-modifying capabilities.
12915158 Treatment of early rheumatoid arthritis. 2003 Oct Increasing attention has focused on the early treatment of rheumatoid arthritis (RA) because of the short time lag that can exist between the onset of synovitis and the development of joint damage and loss of function. For optimal benefit, treatment may need to begin in a theoretical 'window of opportunity' that exists within the first few weeks or months of disease onset. Current evidence suggests that early introduction of therapy with disease-modifying antirheumatic drugs (DMARDs) can slow the progression of joint damage and improve long-term outcomes. Moreover, results of several studies suggest that early treatment with two- and three-DMARD combinations can produce superior benefits compared with DMARD monotherapy. Although early DMARD therapy has proven ability to slow the pace of joint destruction, individual treatment decisions are problematic because of the difficulty in accurately predicting individual prognosis and differential responses to therapy. Controlled trials are needed in early disease to investigate these questions and to identify treatment strategies that can effectively induce sustained remission and prevent joint damage.
14658004 Articular, B-cell, non-Hodgkin's lymphoma mimicking rheumatoid arthritis: synovial involve 2004 May Polyarticular joint manifestations as the predominant symptom of non-Hodgkin's lymphoma (NHL) are quite rare. In the absence of peripheral lymph node and visceral involvement, lymphomas presenting as polyarthritis create a problem for the patients as another rheumatic disease. We present a case that had been diagnosed with rheumatoid arthritis because of symmetrical articular symptoms. The patient later developed severe pain and marked swelling in her right fourth finger, and a diagnosis of septic arthritis and osteomyelitis complicating rheumatoid arthritis was assumed. The final diagnosis of NHL with synovial involvement could be made only after histopathologic examination of a biopsy specimen obtained from the amputated finger. This is the first case report demonstrating direct synovial involvement of a small joint in a patient with NHL presenting with polyarthritis. Articular and periarticular involvement of multiple joints shown by MRI in this patient suggests that direct synovial involvement may be responsible for the polyarticular symptoms in such patients.
11896391 How antibodies to a ubiquitous cytoplasmic enzyme may provoke joint-specific autoimmune di 2002 Apr Arthritis in the K/BxN mouse model results from pathogenic immunoglobulins (Igs) that recognize the ubiquitous cytoplasmic enzyme glucose-6-phosphate isomerase (GPI). But how is a joint-specific disease of autoimmune and inflammatory nature induced by systemic self-reactivity? No unusual amounts or sequence, splice or modification variants of GPI expression were found in joints. Instead, immunohistological examination revealed the accumulation of extracellular GPI on the lining of the normal articular cavity, most visibly along the cartilage surface. In arthritic mice, these GPI deposits were amplified and localized with IgG and C3 complement. Similar deposits were found in human arthritic joints. We propose that GPI-anti-GPI complexes on articular surfaces initiate an inflammatory cascade via the alternative complement pathway, which is unbridled because the cartilage surface lacks the usual cellular inhibitors. This may constitute a generic scenario of arthritogenesis, in which extra-articular proteins coat the cartilage or joint extracellular matrix.
11968222 Extracorporeal immunoadsorption treatment for rheumatoid arthritis. 2002 Jan Immunoadsorption treatment is a non-drug therapy for rheumatoid arthritis. The treatment is based on filtering the patient's plasma through a column containing staphylococcal protein A. The treatment is effective in alleviating the symptoms of severe rheumatoid arthritis in some patients. Data on long-term outcomes are not available. The mechanism of action of this treatment is unclear. Most adverse effects are associated with the apheresis procedure. The cost per 12 week course of treatment is likely to be more than C $20,000. The cost-effectiveness of the technology is not yet established.
15188350 The safety of anakinra in high-risk patients with active rheumatoid arthritis: six-month o 2004 Jun OBJECTIVE: To determine in a placebo-controlled, double-blind trial the safety profile of daily anakinra (Kineret) use in patients with active rheumatoid arthritis (RA) and concurrent comorbid conditions. METHODS: In 169 centers in 9 countries, 1,414 patients with active RA were randomly assigned to receive either anakinra (100 mg) or placebo treatment (4:1 anakinra-to-placebo allocation ratio), with study drug administered by daily subcutaneous injection for 6 months. The current post hoc analysis assessed baseline comorbid conditions, and patients were considered at high risk for the occurrence of adverse events if they had a history of at least one of the following: cardiovascular event, pulmonary event, central nervous system-related event, infection, diabetes, malignancy, or renal impairment. Within each treatment group (anakinra or placebo), incidence rates were summarized for serious adverse events, infectious events, and serious infectious events in high-risk patients and compared with these incidence rates in patients without comorbid conditions. RESULTS: The majority of patients in the trial had one or more comorbid conditions. In these high-risk patients, there were no differences in the incidence of serious adverse events or infectious events between treatment groups. The incidence of serious infectious events with anakinra use was similar between high-risk patients (2.5%) and the entire study population (2.1%) and was not attributable to any single comorbidity. CONCLUSION: Results of the analysis of adverse events in patients with active RA and coexisting comorbidities suggest that the favorable safety profile of anakinra is maintained in a high-risk patient population.
11856640 Involvement of receptor activator of NFkappaB ligand and tumor necrosis factor-alpha in bo 2002 Feb Bone loss represents a major unsolved problem in rheumatoid arthritis (RA). The skeletal complications of RA consist of focal bone erosions and periarticular osteoporosis at sites of active inflammation, and generalized bone loss with reduced bone mass. New evidence indicates that osteoclasts are key mediators of all forms of bone loss in RA. TNF-alpha is one of the most potent osteoclastogenic cytokines produced in inflammation and is pivotal in the pathogenesis of RA. Production of tumor necrosis factor-alpha (TNF-alpha) and other proinflammatory cytokines in RA is largely CD4(+) T-cell dependent and mostly a result of interferon-gamma (IFN-gamma) secretion. Synovial T cells contribute to synovitis by secreting IFN-gamma and interleukin (IL)-17 as well as directly interacting with macrophages and fibroblasts through cell-to-cell contact mechanisms. Activated synovial T cells express both membrane-bound and soluble forms of receptor activator of NF-kappaB ligand (RANKL). In rheumatoid synovium, fibroblasts also provide an abundant source of RANKL. Furthermore, TNF-alpha and IL-1 target stromal-osteoblastic cells to increase IL-6, IL-11, and parathyroid hormone-related protein (PTHrP) production as well as expression of RANKL. In the presence of permissive levels of RANKL, TNF-alpha acts directly to stimulate osteoclast differentiation of macrophages and myeloid progenitor cells. In addition, TNF-alpha induces IL-1 release by synovial fibroblasts and macrophages, and IL-1, together with RANKL, is a major survival and activation signal for nascent osteoclasts. Consequently, TNF-alpha and IL-1, acting in concert with RANKL, can powerfully promote osteoclast recruitment, activation, and osteolysis in RA. The most convincing support for this hypothesis has come from in vivo studies of animal models. Protection of bone in the presence of continued inflammation in arthritic rats treated with osteoprotegerin (OPG) supports the concept that osteoclasts mediate bone loss, providing further evidence that OPG protects bone integrity by downregulating osteoclastogenesis and promoting osteoclast apoptosis. Modulation of the RANKL/OPG equilibrium in arthritis may provide additional skeletal benefits, such as chondroprotection. The nexus between T-cell activation, TNF-alpha overproduction, and the RANKL/OPG/RANK ligand-receptor system points to a unifying paradigm for the entire spectrum of skeletal pathology in RA. Strategies that address osteoclastic bone resorption will represent an important new facet of therapy for RA.
12635939 Rheumatoid arthritis: proposal for the use of anti-microbial therapy in early cases. 2003 Rheumatoid arthritis (RA) is a chronic disease, affecting women more than men, especially in those possessing the "shared epitope" (EQK/RRAA) amino acid sequences present in HLA-DR1/4 molecules. Proteus mirabilis carries sequences showing molecular mimicry to the "shared epitope" and to type XI collagen of hyaline cartilage. Elevated levels of antibodies to P. mirabilis have been reported from 14 different countries involving 1375 RA patients and the microbe has been isolated from urine cultures of such patients. Our working hypothesis is that the disease develops as a result of repeated episodes of Proteus upper urinary tract infections. Prospective studies involving the trial of anti-Proteus measures in RA patients should be evaluated in the management of this disease. Antibiotics, high fluid intake, and fruit extracts, such as cranberry juice, have all been found to be effective in the treatment of urinary tract infections. Such measures could be used as possible additional adjuncts to the standard therapy with NSAIDs and DMARDs.
15205911 Human immunodeficiency virus vector-mediated intra-articular expression of angiostatin inh 2005 Sep We examined the feasibility of the human immunodeficiency virus (HIV) vector-mediated local expression of angiostatin in the treatment of murine collagen-induced arthritis in a mouse model generated by immunization with bovine type II collagen and Freund's complete adjuvant. The HIV vector containing the murine angiostatin expression unit (HIV-angiostatin) was injected into right knee joints after arthritis development; the HIV vector containing the enhanced green fluorescein protein (EGFP) marker gene (HIV-EGFP) was injected into the left joints. Quantitative histological evaluation demonstrated that synovial cell hyperplasia and pannus formation were significantly reduced in the right knee joints as determined by this protocol. Suppression of radiographical changes in the ipsilateral paws was also observed. These results indicate that the HIV vector-mediated expression of angiostatin efficiently inhibits the progression of collagen-induced arthritis. Angiostatic gene therapy may provide a new approach to the effective treatment of rheumatoid arthritis.
14996870 Primary Souter-Strathclyde total elbow prosthesis in rheumatoid arthritis. 2004 Mar BACKGROUND: Total elbow arthroplasty is a well-established treatment for the painful elbow joint in patients with rheumatoid arthritis. We present the results of what we believe to be the first prospective study of the Souter-Strathclyde total elbow prosthesis. METHODS: Between June 1982 and December 2000, 204 primary total elbow prostheses were inserted in 166 patients who had rheumatoid arthritis. No patient was lost to follow-up. The mean duration of follow-up was 6.4 years. All patients were examined preoperatively, at one and two years postoperatively, and at regular intervals thereafter. RESULTS: Six of the 204 elbows had pain at rest at the time of the latest follow-up. Ten patients (ten elbows) without previous neurological symptoms had development of paresthesias in the distribution of the ulnar nerve postoperatively. Patients who had pain at rest or at night and those who had ulnar nerve symptoms preoperatively were found to have a significant chance of having the same complaints postoperatively. Pain at rest or at night and a decrease in function during the follow-up period were associated with humeral loosening. Twenty-four elbows had revision of the total elbow prosthesis because of loosening of the humeral component (ten), loosening after fracture (six), dislocation (four), infection (two), restricted range of motion (one), or fracture of the middle part of the humeral shaft, proximal to the prosthesis (one). One prosthesis was removed because of humeral loosening, and eight were removed because of deep infection. Another five prostheses were radiographically loose at the time of the latest follow-up. The rate of implant survival, according to the method of Kaplan-Meier, was 77.4% after ten years and 65.2% after eighteen years. CONCLUSIONS: Total elbow replacement is associated with a high complication rate and therefore may be warranted only for seriously disabled patients. Currently, the results associated with the Souter-Strathclyde total elbow prosthesis are comparable with the results associated with other prostheses, but loosening of the humeral component remains a concern. LEVEL OF EVIDENCE: Therapeutic study, Level IV (case series [no, or historical, control group]). See Instructions to Authors for a complete description of levels of evidence.
12707578 Abandoned therapies and unpublished trials in rheumatoid arthritis. 2003 May The capability of selectively targeting pathogenic elements of disease with biologic therapies has created a new therapeutic repertoire. Although a substantial number of biologic agents have been developed for treatment of rheumatoid arthritis, few have been approved for use. Most of the agents have failed to reach the approval stage because of inadequate clinical benefit. Despite this, studies of these agents have provided extremely valuable lessons in study design, immunobiology, pharmacodynamic evaluation, and the utility of animal models in the development of biologic agents. These insights have laid the groundwork for future development of other novel therapeutic agents in the treatment of rheumatoid arthritis.
17564304 Antirheumatic effect of pirfenidone in a double blind clinical pilot trial in humans. 2004 The antirheumatic effect of pirfenidone was compared with a positive control drug, oxyphenbutazone which is used in patients suffering from rheumatoid arthritis, in a double blind clinical trial in humans. The data collected in this pilot project revealed that pirfenidone was more effective (p < 0.025) than oxyphenbutazone in providing relief from arthritic pain. In addition, a greater number (p < 0.025) of patients reported favorable response to oral pirfenidone than oral oxyphenbutazone. However, there were no significant differences in the number of patients who dropped out from the trial and the number of patients who tolerated the drugs for 21 days of the trial between the pirfenidone and oxyphenbutazone groups. It was concluded from this pilot study that pirfenidone potentially offers a novel therapeutic modality for the management of rheumatoid arthritis with little or no adverse effects unlike steroidal and non-steroidal anti-inflammatory drugs which are frequently used for this chronic debilitating disease.
12598856 Intense immunosuppression and stem-cell transplantation for patients with severe rheumatic 2003 Jan BACKGROUND: Intense immunosuppression plus stem-cell transplantation (SCT) has emerged as a new treatment modality for patients with refractory, severe rheumatic autoimmune disease. Its rationale is based on eliminating autoaggressive lymphocytes by lympho- or myeloablative conditioning followed by stem-cell rescue. Preclinical studies in animal models of autoimmune disease and observations in patients with rheumatoid arthritis (RA) who were cured after allogeneic bone marrow transplantation for concomitant hematologic malignancy have provided support for the concept. METHODS: The authors reviewed the results of recent phase I/II studies and data from the EBMT/EULAR Registry on more than 400 patients with autoimmune diseases including RA, systemic lupus erythematosus (SLE), systemic sclerosis (SSc), and juvenile idiopathic arthritis (JIA). RESULTS: Toxicity resulting from stem-cell grafting depended on underlying disease and the intensity of the conditioning regimen. Treatment-related mortality was low in RA (1.4%) but relatively high (>10%) in patients with JIA, SLE, and SSc, possibly related to visceral involvement in these patients. With the application of uniform and strict criteria, safety has improved. Long-term remissions up to 4 years have been observed in SSc and JIA, while relatively more relapses have occurred in patients with SLE and RA. Sensitivity to antirheumatic drugs was restored in RA and SLE patients, however, resulting in improved disease control. CONCLUSIONS: Intense immunosuppression and SCT may be an effective therapy for selected patients with severe rheumatic autoimmune disease. Its merits need to be proven via multicenter phase III studies by comparing efficacy and safety with conventional therapy.
11925906 [How Japanese clinicians treat rheumatoid arthritis (RA): a survey at the 44th annual meet 2002 Feb OBJECTIVE AND METHODS: To gain insight into the current management of RA in Japan, a survey was done at the 44th annual meeting of Japan Rheumatism Association in 2000. RESULTS: Four hundred and ninety clinicians responded to our survey, including 212 internists and 252 orthopedists, respectively. In the management of RA, there was a wide difference between their present behaviors and the ideal way they believe. In particular, an appropriate communication between internists and orthopedists was lacking. There was a wide variation in their evaluations and prescribing behaviors. The treatment of RA in Japan turned out to be unique compared with those in the US and Europe. Prescriptions with little evidence were not unusual. CONCLUSIONS: There was a great variation among Japanese clinicians in the management of RA. These results might be associated with poor outcomes of RA patients in Japan. Dissemination of information concerning the management of RA, such as guidelines, as well as the establishment of a better health care system is necessary.
12860725 Chemokine blockade and chronic inflammatory disease: proof of concept in patients with rhe 2003 Aug BACKGROUND: Chemokines and their receptors are considered important contributors in cell migration and inflammation in chronic inflammatory disorders. Chemokines affecting monocytes/macrophages are considered potential therapeutic targets, but no studies of the effects of blocking the chemokine repertoire in humans with a chronic inflammatory disease have been reported. OBJECTIVE: To carry out a double blind, placebo controlled, phase Ib clinical trial with a specific, oral CCR1 antagonist. METHODS: 16 patients with active rheumatoid arthritis (RA) were randomised 3:1 to active:placebo treatment for 14 days. Synovial biopsy specimens were obtained on days 1 and 15. Immunohistochemistry was used to detect the presence of various cell types before and after treatment and the results measured by digital image analysis. Results before and after treatment were compared by paired t test, and a two sample t test was used to compare the changes from baseline in the two groups. RESULTS: All patients completed the study. A significant reduction in the number of macrophages (p=0.016), intimal macrophages (p=0.026), and CCR1+cells (p=0.049) in patients treated with the chemokine antagonist compared with the placebo group occurred in the synovium. Significant decreases in overall cellularity, intimal lining layer cellularity, CD4+ T cells, and CD8+ T cells also occurred in treated patients. Cells lacking CCR1 were not affected. Trends towards clinical improvement were seen in the treated patients but not in the placebo group. Severe side effects were not reported. CONCLUSION: Specific chemokine receptor blockade can result in relevant biological effects in patients with active RA.
14658102 15-year follow-up study of total knee arthroplasty in patients with rheumatoid arthritis. 2003 Dec In 25 patients with rheumatoid arthritis, 36 cases of cemented Kinematic total knee arthroplasty were reviewed clinically and radiographically at 13 to 19 years after surgery. The mean age at the time of surgery was 51.6 +/- 8.9 years. According to the follow-up results evaluated with the Hospital for Special Surgery knee scoring system, 28 knees (77.7%) were classified as good or excellent. The mean flexion angle at follow-up evaluation was 99 degrees +/- 24 degrees (10 degrees -140 degrees ). At the tibial or femoral bone-cement interfaces, a radiolucent line was seen in 10 of 36 knees (27.8%) at follow-up evaluation. The survival rate of prostheses with revision as the endpoint was estimated to be 93.7% at 15 years. Kinematic total knee arthroplasty in rheumatoid arthritis patients provided a good long-term outcome.
12658918 [Effect of bizhongxiao decoction on the expression of VEGF in the synovial membrane of C I 2002 Dec 28 OBJECTIVE: To observe the effect of bizhongxiao (BZX) decoction on the expression of VEGF in the synovial membrane of C II-induced arthritis(CIA) in rats and to explore the mechanism of BZX decoction in the treatment of rheumatoid arthritis RA. METHODS: Seventy-five SD rats were randomly divided into four groups. The rat experimental arthritis model was established by subcutaneous injection of II collogen. The expression of VEGF was detected with immunohistochemistry in different times. RESULTS: The incidence of arthritis in the rats immunized with C II was approximately 88.57%. The arthritis index of the model group was rising, but that of the BZX decoction group and the methotrexate (MTX) group were decreasing on the 30th day. No expression of VEGF was found in the synovial membrane of the normal group. The expression of VEGF of the model group was notably higher than that of the BZX decoction group and the MTX group in different times (P < 0.01). The expression of VEGF of the model group rose step by step, but that of the BZX decoction group and the MTX group decreased and was significantly lower than that of the model group (P < 0.01). The expression of VEGF of the BZX decoction group was significantly lower than that of the MTX group(P < 0.05). CONCLUSION: The expression of VEGF is relative to the synovial pannus formation in RA. BZX decoction and MTX could decrease the expression of VEGF, but the curative effect of BZX decoction is significantly better than that of MTX. BZX decoction could inhibit the formation of the synovial pannus or bone in RA by decreasing the expression of VEGF.