Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
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16393765 | Work disability in rheumatoid arthritis is predicted by physical and psychological health | 2005 Nov | OBJECTIVE: To explore the prevalence of work disability (WD) and to identify bio-psychological factors that predicts future WD in rheumatoid arthritis (RA) over a 7-year period. METHODS: Patients were selected from the Oslo RA register. The prevalence of WD was studied cross-sectionally among respondents <67 years (n = 526) in a postal survey. Mean age (SD) was 51.1 (11.9) years, mean disease duration 11.3 (9.4) years, and 49% of patients were RF-positive. The patients studied for predictive factors for WD were respondents in postal surveys both at baseline and at the 7-year follow-up, in work at baseline and still in working age (<67 years) at follow-up (n = 159). Mean age at baseline (SD) was 44.5 (9.7) years, mean disease duration 8.4 (6.6) years, mean years of formal education 12.7 (3.1) years, 48% were RF-positive. Assessments included socio-demographic variables and health status measures (MHAQ, AIMS2, SF-36, fatigue and pain on VAS 0-100 mm, self efficacy, and RAI as a measure for helplessness). RESULTS: Among the 526 respondents at baseline <67 years, the prevalence of WD was 40%. A high level of education was a predictor of reduced risk of work disability [odds ratio (OR) = 0.4, 95% confidence interval (CI) 0.1; 0.9], while female gender (OR 3.0, 95% CI 1.1; 8.0), physical disability (MHAQ-score) (OR = 3.9, 95% CI 1.2; 12.5) and helplessness over median RAI-score (OR = 3.0, 95% CI 1.4; 6.7) were independent predictors of increased risk for new work disability over 7 years. CONCLUSION: Physical disability, increased helplessness, low formal education, and female gender were found to be independent risk factors for new work disability over the 7-year study period. | |
17121034 | [Correlations between diagnostic information and therapeutic efficacy in rheumatoid arthri | 2006 Oct | OBJECTIVE: To explore the correlations between diagnostic information and therapeutic efficacy in rheumatoid arthritis (RA) with decision tree model analysis. METHODS: Three hundred and ninety seven patients came from 9 clinical centers were randomly divided into the Western medicine (WM) group (n=194) treated with non-steroidal anti-inflammatory drugs and slow-acting antirheumatic drug and the Chinese medicine (CM) group (n=203) with basic therapy and syndrome-differentiation dependant TCM treatment. TCM and WM diagnostic information were collected. The ACR 20 was used for efficacy evaluation and the information of patients before treatment was analyzed by SAS 8.2 statistical package. Through single-factor exploratory analysis, odds ratio of efficacy and variable was calculated taken P < 0.2 as the including criteria for data mining analysis with decision tree model. All data were classified into the training set (75%) and verifying set (25%) with efficacy as the variable for layering to make further verification of the data-mining analysis. RESULTS: Twenty variables were included in the CM group and 26 in the WM group in the data-mining model. In the former, 9 variables were positively correlated to the efficacy, including degree of arthralgia, tenderness and morning stiffness, number of swollen joint, and joint with tenderness, levels of IgM, rheumatoid factor (RF), C-reactive protein (CRP), and total assessment from doctor; and disease duration and degree of nocturnal polyuria were negatively correlated to that. While in the latter, 8 were positively correlated to the efficacy, including erythrocyte sedimentation rate (ESR), sour and weak waist and knees, white fur in tongue, joint ache and stiffness, swollen joint, and total assessment from doctor and patient, and red tongue with yellow fur and leucocyte count negatively correlated to it. Data mining with decision tree analysis revealed that different combinations of morning stiffness, slight red tongue, joint tenderness and nocturnal polyuria in the CM group, and those of white fur in tongue, CRP level, leucocyte count and morning stiffness in the WM group showed different efficacy, which were also verified in the randomly chosen verifying set. CONCLUSION: To analyze the correlations between diagnostic information and therapeutic efficacy with decision tree analysis is conformed to the theory of TCM in applying treatment according to syndrome differentiation individually, thus it would contribute to elevate the accuracy of therapy. | |
16766362 | Risk factors for the development of rheumatoid arthritis. | 2006 May | There is increasing interest in attempting to understand what the risk factors are that lead to the development of rheumatoid arthritis (RA). Twin studies have proved a genetic role but also quantified the non-genetic risk. There is thus scope for identifying environmental predictors that might offer a strategy to prevent the disease. Changes in the female hormonal environment such as in pregnancy, breastfeeding and the use of the oral contraceptive (OC) pill appear to have a role. Of the traditional lifestyle exposures, cigarette smoking has been associated with a consistently increased risk that might also apply to the passive inhalation of smoke. Occupation probably has a minor influence, although exposure to silica dust is of aetiological importance. Recent studies have highlighted a role for diet, with suggestions that diets high in caffeine, low in antioxidants and high in red meat may contribute to an increased risk. The most plausible environmental exposure is infection and although several decades of study have produced few definitive candidate organisms, Epstein-Barr virus (EBV) remains an interesting target. | |
15818688 | Familial aggregation of systemic lupus erythematosus, rheumatoid arthritis, and other auto | 2005 Apr | OBJECTIVE: To determine whether there is familial aggregation of systemic lupus erythematosus (SLE) and/or other autoimmune diseases in SLE patients and to identify clinical differences between patients with and those without familial autoimmunity. METHODS: We interviewed members of the Grupo Latinoamericano de Estudio del Lupus Eritematoso (GLADEL) inception cohort of 1,214 SLE patients to ascertain whether they had relatives with SLE and/or other autoimmune diseases. Identified relatives were studied. Familial aggregation was tested using reported highest and intermediate population prevalence data for SLE, rheumatoid arthritis (RA), or all autoimmune diseases, and studies were performed to identify the genetic model applicable for SLE. RESULTS: We identified 116 first-, second-, or third-degree relatives with SLE, 79 with RA, 23 with autoimmune thyroiditis, 3 with scleroderma, 1 with polymyositis, and 16 with other autoimmune diseases, related to 166 of the 1,177 SLE patients in the GLADEL cohort who agreed to participate. Forty-two SLE patients had 2 or more relatives with an autoimmune disease. We found a lambda(sibling) of 5.8 and 29.0 for SLE and of 3.2-5.3 for RA, when comparing with their reported high or intermediate population prevalence, respectively. We also found familial aggregation for autoimmune disease in general (lambda(sibling) = 1.5) and determined that for SLE, a polygenic additive genetic model, rather than a multiplicative one, is applicable. CONCLUSION: In SLE there is familial aggregation of SLE, RA, and autoimmune disease in general. A polygenic additive model applies for SLE. American Indian-white Mestizo SLE patients and those with higher socioeconomic level were more likely to have familial autoimmunity. | |
16447061 | Vitamin D receptor gene polymorphism in rheumatoid arthritis and associated osteoporosis. | 2006 Sep | Rheumatoid arthritis (RA) is commonly associated with decreased bone mineral density (BMD) due to numerous factors. BsmI polymorphism of the vitamin D receptor (VDR) gene has been implicated in the pathogenesis of osteoporosis. Vitamin D has several immunomodulatory effects and thus may play a role in the course of arthritis. However, little data is available on the possible relationship between RA and VDR gene polymorphisms. In this study, the frequency of BsmI polymorphism genotypes were compared with that found in other countries. In this study, 64 RA patients and 40 healthy controls were tested for VDR gene BsmI polymorphism genotypes. Frequencies of B and b alleles were associated with markers of bone metabolism and RA. Among control subjects, the frequency of the BB genotype is relatively high (27.5%). In RA with secondary osteopenia/osteoporosis the BB genotype was more rare, the bb was more common than in control subjects. Markers of bone metabolism were associated with the B allele. RA patients carrying the B allele had lower BMD and increased bone loss over 1 year. The B allele was also correlated with increased osteoclast and osteoblast function, as determined by the assessment of biochemical markers of bone metabolism. Rheumatoid factor titer, which is an independent marker for disease progression in RA, was higher in bb patients. Our data suggest, that the imbalance in B and b allele expression may be involved in the pathogenesis of RA-associated osteoporosis. The possible involvement of vitamin D and VDR gene polymorphisms in the development and progression of RA needs further elucidation. | |
16646979 | Osteogenic protein 1 in synovial fluid from patients with rheumatoid arthritis or osteoart | 2006 | The measurement of body fluid levels of biochemical markers in joint tissues has begun to provide clinically useful information. Synovial fluid (SF) plays an important role in articular joint lubrication, nutrition, and metabolism of cartilage and other connective tissues within the joint. The purpose of our study was to identify and characterize osteogenic protein 1 (OP-1) in SF from patients with rheumatoid arthritis (RA) or with osteoarthritis (OA) and to correlate levels of OP-1 with those of hyaluronan (HA) and antigenic keratan sulfate (AgKS). SF was aspirated from the knees of patients with either RA or OA and from the knees of asymptomatic organ donors with no documented history of joint disease. The presence of detectable OP-1 in SF was demonstrated by western blots with specific anti-pro-OP-1 and anti-mature OP-1 antibodies. Measurement of levels of OP-1, HA and AgKS was performed using ELISAs. OP-1 was identified in human SF in two forms, pro-OP-1 and active (mature) OP-1--mature OP-1 being detected only in SF from OA patients and RA patients. Levels of OP-1 and HA were higher in RA patients than in OA patients and asymptomatic donors, while the level of AgKS was highest in SF from asymptomatic donors. Statistically significant differences were found between SF levels of OP-1 in RA and OA patients and between SF levels of AgKS among the three groups tested. The SF content of OP-1 tended to correlate positively with HA levels, but negatively with AgKS concentrations. In conclusion, the results of this study suggest that measurement of OP-1 in joint fluid may have value in the clinical evaluation of joint disease processes. | |
16083527 | Methotrexate dosage reduction in patients with rheumatoid arthritis beginning therapy with | 2005 Aug | OBJECTIVE: Infliximab plus methotrexate (MTX) is approved for the treatment of rheumatoid arthritis (RA). Based on the benefit/risk profile of this combination therapy, lower doses of MTX would be preferable when infliximab efficacy can be maintained. We evaluated the ability of patients receiving infliximab plus MTX to achieve and maintain a clinical response while the dose of MTX was tapered. METHODS: Infliximab infusions were administered at a minimum dosage of 3 mg/kg at 8-week intervals (following three loading doses at weeks 0, 2, and 6) to patients who had an inadequate response to MTX. MTX tapering was initiated at week 22 or later when at least a 40% improvement in the combined tender and swollen joint count was achieved; dosages were reduced by 5 mg every 8 weeks to a protocol-specified minimum dosage of 5 mg per week. If the required dosage of MTX after a flare was greater than the baseline dosage, the patient was considered a treatment failure. RESULTS: Of the 210 patients enrolled, 159 (76%) achieved a 40% or better improvement in the combined tender and swollen joint count and had their MTX doses tapered. In these 159 responders, the median (mean) dose of MTX was reduced from 15 (16.5) mg per week at baseline to 5 (7.1) mg per week at week 54. From the time of initial response, 79% of these patients had a zero- or a one-vial increase in infliximab, corresponding to an approximate dose increase of 1 mg/kg, through week 54. CONCLUSION: Approximately 75% of the patients participating in this trial achieved at least a 40% reduction in the combined swollen and tender joint count (correlating with an American College of Rheumatology 20% [ACR20] response in 83% of patients) while reducing the mean MTX dose by 57%. | |
15644119 | A novel model of fibroblast-mediated cartilage destruction. | 2005 Jan | In rheumatoid arthritis (RA), fibroblasts have been shown to be crucial for disease progression as well as joint destruction. In the model of human/murine SCID arthritis, synovial explants as well as fibroblasts from human rheumatoid synovial membrane induce destructive arthritis in immunodeficient mice. Hereby, the underlying cartilage destruction is accomplished by murine fibroblasts. Therefore, murine destructive fibroblasts represent a promising tool to investigate destruction of articular cartilage and bone. In this context, a novel destructive murine fibroblast line (LS48) was examined for morphological, ultrastructural, immunological and functional cellular parameters. These cells were injected into knees of SCID mice. Subsequently, the animals were monitored for joint swelling and serological parameters of arthritis by radiological methods. Finally, cartilage destruction was assessed morphologically. Cultured LS48 cells exhibit characteristic features that resemble those of activated synovial fibroblasts in human RA. Expression levels of inducible nitric oxide synthase, interleukin-6, tumour necrosis factor-alpha and matrix metalloproteinases were comparable to those detected in invasive human fibroblasts. The instillation of 5 x 10(5) LS48 cells into the knee joints of SCID mice initiated a rapid progressive process, that caused cartilage destruction within 10 days, and morphological examinations revealed that articular cartilage was infiltrated by the fibroblasts injected previously. In summary, the intra-articular application of LS48 cells represents a rapid and highly reproducible model to investigate the initiation and progression of cartilage destruction in connection with RA therapy and represents an easy-to-handle animal model. | |
16798046 | Recommendations of the French Society for Rheumatology. TNFalpha antagonist therapy in rhe | 2006 Jul | OBJECTIVES: To develop recommendations for TNFalpha-antagonist therapy in patients with rheumatoid arthritis (RA) seen in everyday practice, under the aegis of the French Society for Rheumatology. METHOD: We used the methods recommended by the French Agency for Healthcare Accreditation and Evaluation, the AGREE collaboration, and the European League against Rheumatism (EULAR). The recommendations focus on patient selection, monitoring, and treatment adjustments. RESULTS: Criteria for selecting patients eligible for TNFalpha-antagonist treatment of RA include: 1) a definitive diagnosis of RA; 2) disease activity for longer than 1 month, including presence of objective signs of inflammation; or radiographic progression; 3) previous failure of methotrexate in the highest tolerated dosage or of another disease-modifying antirheumatic drug in patients with contraindications to methotrexate; 4) absence of contraindications to TNFalpha-antagonist therapy. When starting TNFalpha-antagonist therapy 1) a thorough baseline evaluation should be conducted; 2) any of the three available agents can be used, as no differences in efficacy have been identified in patient populations; 3) concomitant methotrexate therapy is recommended regardless of the TNFalpha antagonist used; and 4) patients should receive standardized follow-up at regular intervals. Treatment adjustments should be based on the following: 1) the treatment objective is achievement of a EULAR response; 2) when such a response is not achieved, the dosage or dosing interval can be changed, or the patient can be switched to another TNFalpha antagonist; 3) in patients who experience intolerance to a TNFalpha antagonist, another TNFalpha antagonist may be tried, depending on the nature of the adverse event; 4) occurrence of a remission should lead to a reduction in symptomatic medications, most notably glucocorticoids where used; in the event of a prolonged remission, either the TNFalpha antagonist or the concomitant disease-modifying antirheumatic drug may be reduced. CONCLUSION: These recommendations are intended to help physicians use TNFalpha antagonists in their everyday practice with RA patients. They do not constitute regulations. | |
16129906 | Clinical studies in patients with Castleman's disease, Crohn's disease, and rheumatoid art | 2005 Jun | Interleukin (IL)-6 is a pleiotropic cytokine with a wide range of biological activities and regulates immunological reactions, inflammatory responses, and hematopoiesis. Overproduction of IL-6 has been shown to be pathologically involved in some inflammatory diseases, such as Castleman's disease, Crohn's disease, and rheumatoid arthritis. Clinical studies have been conducted to investigate a role of IL-6 and the therapeutic potential of anti-IL-6 therapy for these diseases using humanized anti-IL-6 receptor antibody (tocilizumab; currently known as MRA). Overall, tocilizumab was well-tolerated, and improvements of signs and symptoms were observed, confirming the pathological role of IL-6 and suggesting that the blockade of IL-6 could become a new and important treatment option in these refractory diseases. | |
15790350 | Rheumatoid arthritis. | 2005 Apr | Therapeutic efficacy of depleting B cells or blocking T-cell costimulation in rheumatoid arthritis (RA) has confirmed the critical pathogenic role of adaptive immune responses. Yet, RA preferentially affects elderly individuals, in whom adaptive immunity to exogenous antigens begins to fail. Here, we propose that senescence of the immune system is a risk factor for RA, with chronic inflammation resulting from the accumulation of degenerate T cells that have a low threshold for activation and utilize a spectrum of novel receptors to respond to microenvironmental cues. The process of immunosenescence is accelerated in RA and precedes the onset of disease, the acceleration, in part, being conferred by the HLA-DR4 haplotype. Naive CD4(+) T cells in RA are contracted in diversity and restricted in clonal burst. Senescence of effector CD4(+) T cells is associated with the loss of CD28 and the de novo expression of KIR2DS2, NKG2D, and CX(3)CR1, all of which function as costimulatory molecules and reduce the threshold for T-cell activation. The synovial microenvironment promotes chronic persistent immune responses by facilitating ectopic lymphoid neogenesis, such as the formation of aberrant germinal centers. With the propensity to develop complex lymphoid architectures and to provide optimal activation conditions for senescent CD4(+) T cells, the synovium becomes a natural target for pathogenic immune responses in prematurely aged individuals. | |
16897197 | Relation between atlantoaxial (C1/2) and cervical alignment (C2-C7) angles with Magerl and | 2006 Jul | BACKGROUND: A few studies have reported the relation between the atlantoaxial (C1/2) angle and cervical alignment (C2-C7) angle after a Magerl and Brooks (M&B) surgical procedure to treat atlantoaxial subluxation (AAS) in patients with rheumatoid arthritis (RA). However, no study has examined an optimum preoperative C1/2 angle reduction. We aimed to assess the relation between the C1/2 angle reduction and the C2-C7 angle change in patients with progressive RA who underwent the M&B procedure. METHODS: We retrospectively analyzed the relation between the preoperative C1/2 angle and C2-C7 angle in 28 consecutive RA patients using their clinical and radiological data. Differences in the preoperative and postoperative C1/2 and C2-C7 angles were detected. Correlations of these angles and the reduced degree of angles were examined. The Ranawat grading scale and Japanese Orthopaedic Association (JOA) scores were used to determine myelopathy. Pain was categorized into five categories according to severity. Clinical and X-ray evaluations were collected before surgery, at 3 and/or 6 months after surgery, and at final follow-up. RESULTS: Clinical symptoms, Ranawat grade, and JOA scores improved postoperatively, and patients achieved bony union within 3 months. We observed a strong and significant correlation between the reduced C1/2 angle and the change in the C2-C7 angle. Patients with a preoperative C1/2 angle of <20 degrees had markedly reduced cervical lordotic angle but this condition was not seen in patients with a preoperative C1/2 angle of >or=20 degrees . The optimum C1/2 angle was estimated as [20 degrees - (preoperative C1/2 angle)] in patients with a C1/2 angle <20 degrees or as an in situ angle in patients with a C1/2 angle of >or=20 degrees . CONCLUSIONS: Surgeons performing the M&B procedure need to select patients carefully and avoid complete or overreduction of the C1/2 angle to prevent serious postoperative SAS and myelopathy. | |
15378265 | Bronchiolitis obliterans with organizing pneumonia in rheumatoid arthritis--a fatal case a | 2005 Jun | Bronchiolitis obliterans with organizing pneumonia (BOOP) is characterized by excessive proliferation of granulation tissue within small airways (proliferative bronchiolitis) and alveolar ducts associated with chronic inflammation in the surrounding alveoli. It is generally idiopathic but may occur during the resolution of viral or mycoplasmic pneumonia. It is also associated with a variety of systemic illnesses and clinical settings. Complete resolution occurs in 65-85% of patients treated with corticosteroid therapy, and recurrence is not uncommon. Although rapidly fatal BOOP is rare, respiratory failure leading to death may occur in up to 5% of patients. We describe a fatal case of BOOP suspicious for pneumonia in a patient with rheumatoid arthritis. | |
16932627 | Mechanisms of Disease: the link between RANKL and arthritic bone disease. | 2005 Nov | Chronic inflammation and bone loss are closely linked pathophysiologic events. The most typical example of inflammatory bone loss is seen in patients with rheumatoid arthritis who develop systemic osteopenia as well as local breakdown of bone in the direct vicinity of inflamed joints. Understanding the mechanisms of arthritic bone degradation is crucial for designing therapies that can specifically protect joints from structural damage. Since osteoclast differentiation and activity are key events in arthritic bone damage, the signals that trigger osteoclastogenesis are potential therapeutic targets. Receptor activator of nuclear factor-kappaB (RANK) is activated by its ligand, RANKL, an essential molecule for osteoclast development: in the absence of RANKL or RANK, osteoclast differentiation from monocyte precursors does not occur. RANKL is expressed on T cells and fibroblasts within the synovial inflammatory tissue of patients with RA and its expression is regulated by proinflammatory cytokines. In animal models of arthritis, blockade of RANKL-RANK interactions, or a genetic absence of RANKL or RANK, protects against joint damage despite the presence of joint inflammation. Therefore, inhibition of RANKL is regarded as a promising future strategy for inhibiting inflammatory bone loss in patients with chronic inflammatory arthritis. | |
16461794 | Human B cell tolerance and its failure in rheumatoid arthritis. | 2005 Dec | Random V(D)J gene assembly generates many autoreactive B cell receptors (BCRs). In healthy donors, most autoreactive developing B cells are removed either in the bone marrow or in the periphery, revealing two B cell tolerance checkpoints. The regulation and the mechanisms that ensure this human B cell tolerance are poorly characterized, but they require proper BCR signaling. Indeed, patients with X-linked agammaglobulinemia who carry mutations in the BTK gene, which encodes an essential BCR signaling component, fail to establish proper central B cell tolerance, as demonstrated by the release of self-reactive B cells in the periphery. In autoimmune diseases such as rheumatoid arthritis (RA), B cell tolerance is broken and autoantibodies are secreted. Our recent results show that RA patients suffer from defective central and peripheral B cell tolerance checkpoints, which may favor the development of autoimmunity. Also, about half of our RA patients display unusual immunoglobulin light chain repertoires showing impaired secondary recombination regulation, which indicates that receptor editing, one of the mechanisms that normally ensures B cell tolerance, may often be defective in RA. | |
17075825 | Increased serum levels of soluble fractalkine (CX3CL1) correlate with disease activity in | 2006 Nov | OBJECTIVE: To determine levels of soluble fractalkine (sFkn) in rheumatoid arthritis (RA) patients with and without rheumatoid vasculitis (RV), and to assess the relationship of sFkn levels to disease activity. METHODS: Serum was obtained from 98 RA patients (54 without vasculitis, 36 with extraarticular manifestations but without histologically proven vasculitis, and 8 with histologically proven vasculitis) and from 38 healthy individuals. Levels of sFkn were measured by enzyme-linked immunosorbent assay. Expression of Fkn and CX(3)CR1 was quantified by real-time polymerase chain reaction. Vasculitis disease activity was assessed using the Birmingham Vasculitis Activity Score and the Vasculitis Activity Index. RESULTS: Serum sFkn levels were significantly higher in patients with RA than in controls and were significantly higher in RA patients with RV than in those without vasculitic complications. Statistically significant correlations were observed between serum sFkn levels in RA patients and levels of C-reactive protein, rheumatoid factor, immune complex, and complement. In the RV group, sFkn levels also correlated with disease activity. Immunohistochemical analysis indicated that Fkn levels were associated mainly with endothelial cells in vasculitic arteries. In addition, expression of CX(3)CR1 messenger RNA was significantly greater in peripheral blood mononuclear cells from patients with active RV than in those from other RA patients or controls. Notably, serum sFkn levels were significantly diminished following successful treatment and clinical improvement. CONCLUSION: These findings suggest that Fkn and CX(3)CR1 play crucial roles in the pathogenesis of RV and that sFkn may serve as a serologic inflammatory marker of disease activity in RA patients with vasculitis. | |
16437446 | Intra-articular steroids and splints/rest for children with juvenile idiopathic arthritis | 2006 Jan 25 | BACKGROUND: Resting or immobilizing a joint to enhance outcomes following intra-articular (IA) steroid injection is generally advocated. This systematic review aimed to determine the efficacy of IA steroid injections and the influence of post-injection rest. OBJECTIVES: 1. Compare IA steroid injections versus no treatment or placebo. 2. Determine the effects of rest following IA steroid injection in rheumatoid or juvenile idiopathic arthritis. SEARCH STRATEGY: The Cochrane Central Register of Controlled Trials (CENTRAL- Issue 4, 2003), Cochrane Database of Systematic Reviews (CDSR - Issue 4, 2003), Database of Abstracts of Reviews of Effectiveness (DARE - searched 8.1.04), MEDLINE (1966 to August Week 2 2004), EMBASE (1980 to August Week 2 2004) , CINAHL (1982 to December Week 2 2003), Clinical Trials site of the National Institute of Health, (USA - searched 8.1.04), OTseeker (Occupational Therapy Systematic Evaluation of Evidence - searched 8.1.04) and PEDro (Physiotherapy Evidence Database - searched 8.1.04) were searched. Journals and reference lists were hand searched. SELECTION CRITERIA: Eligible were randomised controlled trials of IA steroid injections or of rest following IA steroid injections in rheumatoid or juvenile idiopathic arthritis. DATA COLLECTION AND ANALYSIS: Potentially relevant references were evaluated and all data extracted by two independent reviewers. MAIN RESULTS: Five trials (n=346) examining IA steroid injection in the knee joint were included. It was not possible to pool data as outcome measures, timing of follow up and the methods of data reporting differed between trials. There was inconclusive conflicting evidence from two trials that walking time was reduced. There was evidence from one moderate quality trial that pain was reduced at 1-day post-injection (0-100 VAS from 28.33 to 13.46; McGill Pain Scale from 8.89 to 3.96) but not at 1 week or 7-12 weeks post-injection. There is some evidence that IA injections improved knee flexion (by 14 degrees) and reduced knee extension lag (by 20 degrees), knee circumference (median reduction = 0.3 cm) and morning stiffness (reduced from 60 mins to 7.6 mins). One trial (n=91) examined the effects of rest following injection in the knee. The rested group achieved significant improvement in pain, stiffness, knee circumference, and walking time when compared with the non-rested group (no point estimates provided). One trial evaluated rest following injection of the wrist (n=117). Relapse rate was higher in the rested group (rest relapse rate = 24/58, no-rest group = 14/59); but there were no differences between the rested and non-rested groups on pain, joint circumference, wrist function, grip strength or ROM. AUTHORS' CONCLUSIONS: There is some evidence to support the use of IA steroid injections and resting a knee following injections but that wrists should not be rested following injections. The included studies involved adult participants so any conclusions can only cautiously applied to children. Further research is required to examine the use and type of rest and the differential responses of different joints following injections. | |
15818652 | Impact of ultrasound imaging on local corticosteroid injections of symptomatic ankle, hind | 2005 Apr 15 | OBJECTIVE: To assess the impact of ultrasonography (US) on local corticosteroid (CS) injections of painful ankle, hindfoot, and midfoot in chronic inflammatory diseases. METHODS: Consecutive patients with chronic rheumatic diseases admitted to the hospital for local CS injections of painful ankle, hindfoot, or midfoot were enrolled in this study. Clinical and radiographic evaluation was performed by the physician in charge of CS injections, and US examination was performed by an independent examiner blinded to the clinical and radiologic findings. According to a randomized weekly-periods design, the physician planned CS injections either aware (G1 group) or unaware (G2 group) of US results. In the latter case, he was nonetheless informed of US results after he had performed the injections. Impact of this information on the treatment planning was assessed in all cases. Prognostic impact of US was also evaluated by comparing the change in global assessment of efficacy of CS injections, in activity of the disease, and in the Western Ontario and McMaster Universities (WOMAC) subscales after 1 and 3 months, between G1 and G2 groups. RESULTS: The knowledge of US findings led the physician to change his decision of local CS injections in 56 (82%) of 68 patients studied. Among 1,131 assessed sites, by clinical, radiographic, and US evaluation, injection was cancelled in 37 (15%) of 242 proposed sites, whereas it was decided in 74 (8%) additional sites. After 1 month, there was an improvement in G1 as compared with G2 groups. The mean +/- SD change in WOMAC physical function subscale was 15.6 +/- 17.5 in G1 versus 8 +/- 13 in G2 (P = 0.0305). After 3 months, only the global assessment of efficacy of CS injections was statistically greater in G1 than in G2 group (P = 0.0170). CONCLUSION: US frequently led the physician to change his diagnosis of inflammatory lesions in painful foot, and consequently his planning of CS injections. Moreover, US could improve the response to local treatment. | |
16541481 | Etanercept treatment in adults with established rheumatoid arthritis: 7 years of clinical | 2006 May | OBJECTIVE: To evaluate safety and efficacy of longterm etanercept treatment in patients with disease modifying antirheumatic drug (DMARD) refractory rheumatoid arthritis (RA). METHODS: Safety results are reported for 714 patients who received etanercept in one of 7 initial trials or a longterm extension. Efficacy results are reported for 581 patients who enrolled in the extension. RESULTS: Of the 714 patients enrolled in the initial trials, 581 (81%) enrolled in the extension, and 388 (54%) patients are continuing to receive etanercept therapy. The longest individual treatment was 8.2 years, with 3139 total patient-years of etanercept exposure. Rates of serious adverse events (overall rate=14.8 events/100 patient-yrs), serious infections (overall rate=4.2 events/100 patient-yrs), cancer (overall rate=1.0 events/100 patient-yrs), and deaths (overall rate=0.7 events/100 patient-yrs) were stable each year, through 8 years of etanercept exposure. For 356 patients who completed 6 years of etanercept treatment, response rates were ACR20=73%, ACR50=52%, ACR70=27%, DAS28 CRP good response=52%, and DAS28 CRP remission=37% of patients. Similar responses occurred in 167 patients who completed Year 7. Doses of concomitant methotrexate or corticosteroids were reduced in many patients who maintained clinical responses. CONCLUSION: The safety profile of etanercept was consistent over time, with rates of adverse events similar to those reported for patients with RA in general. Durable clinical responses were observed in some patients for 7 years or more. The benefit-to-risk ratio for longterm etanercept treatment remains highly favorable. | |
15466894 | Relationship between growth hormone-IGF-I-IGFBP-3 axis and serum leptin levels with bone m | 2005 Jan | OBJECTIVES: Hormonal factors playing a role in bone mass and body composition have been rarely assessed in rheumatoid arthritis (RA). In this study, we aimed to evaluate the growth hormone (GH)-insulin-like growth factor-I (IGF-I)-insulin-like growth factor binding protein-3 (IGFPB-3) axis and serum leptin levels in patients with RA and to determine whether these hormonal/growth factors may influence bone mass and body composition in RA. METHODS: Serum GH, IGF-I, IGFPB-3 and leptin were evaluated in 38 corticosteroid-treated RA patients, 14 non-RA patients under corticosteroids (corticosteroid controls, CC) and 32 healthy controls (HC). Bone density was evaluated using dual X-ray absorptiometry (DEXA), and expressed as bone mineral density (BMD), and quantitative ultrasound (QUS). Body composition was assessed by DEXA. RESULTS: The three groups differed regarding femoral neck, total body BMD, lean mass and QUS parameters with lower values in the RA group (all P < or = 0.05). Growth hormone was higher in RA patients (P=0.0001) while IGF-I and IGFBP-3 did not differ between the three groups. In RA patients there was a tendency to high serum leptin levels and leptin strongly correlated with fat mass (r=0.83, P<0.0001), but not with bone mass measurements or inflammatory parameters. There were no differences for lean mass, GH and leptin between CC and HC. CONCLUSION: Our results suggest that these GH and leptin modifications could have an influence on both bone mass and body composition in RA. |