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ID PMID Title PublicationDate abstract
16776848 The MHC2TA -168A>G gene polymorphism is not associated with rheumatoid arthritis in Austri 2006 An association between susceptibility to rheumatoid arthritis (RA) and a common -168A>G polymorphism in the MHC2TA gene with differential major histocompatibility complex (MHC) II molecule expression was recently reported in a Swedish population. The objective of the present study was to replicate this finding by examining the -168A>G polymorphism in an Austrian case-control study. Three hundred and sixty-two unrelated RA cases and 351 sex-matched and age-matched controls as well as 1,709 Austrian healthy individuals were genotyped. All participants were from the same ethnic background. Genotyping was performed using 5' allelic discrimination assays. The association between susceptibility to RA and the -168A>G single nucleotide polymorphism was examined by chi-square test. Comparison was made assuming a dominant effect (AG + GG genotypes versus AA genotype). In contrast to the primary report, the frequency of MHC2TA -168G allele carriers was not significantly different between patients and controls in the Austrian cohort. The homozygous MHC2TA -168 GG genotype was more frequent in matched controls than in Austrian RA patients. There was no association between the presence of RA-specific autoantibodies and the MHC2TA -168 GG genotype. In this cohort of Austrian patients, no association between the MHC2TA polymorphism and RA was found.
17907166 Fractalkine mediates T cell-dependent proliferation of synovial fibroblasts in rheumatoid 2007 Oct OBJECTIVE: In rheumatoid arthritis (RA), synovial fibroblasts proliferate excessively, eventually eroding bone and cartilage. The aim of this study was to examine the mechanisms through which CD4 T cells, the dominant lymphocyte population in patients with rheumatoid synovitis, regulate synoviocyte proliferation. METHODS: Fibroblast-like synoviocyte (FLS) lines were established from rheumatoid synovium. CD4 T cells from patients with RA and age-matched control subjects were cultured on FLS monolayers. FLS proliferation was quantified by cytometry, using carboxyfluorescein succinimidyl ester staining or microscopic enumeration of PKH26-stained FLS. Surface expression of the fractalkine (FKN) receptor CX(3)CR1 was monitored by fluorescence-activated cell sorting. The induction of CX(3)CR1 and its ligand FKN in FLS was quantified by real-time polymerase chain reaction. RESULTS: The proliferation of FLS was significantly increased in the presence of CD4 T cells from patients with RA compared with control T cells. CD4+,CD28- T cells were particularly effective in supporting FLS growth, inducing a 25-fold expansion compared with a 5-fold expansion induced by CD4+,CD28+ T cells. The growth-promoting activity of CD4+,CD28- T cells was mediated through CX(3)CR1, a chemokine receptor expressed on both T cells and FLS. Anti-CX(3)CR1 antibodies inhibited T cell production of tumor necrosis factor alpha (TNFalpha) and suppressed FLS proliferation. TNFalpha amplified the expansion of FLS by enhancing their expression of CX(3)CR1 and FKN. CONCLUSION: FKN-CX(3)CR1 receptor-ligand interactions regulate FLS growth and FLS-dependent T cell function. FLS stimulate autocrine growth by releasing FKN and triggering the activity of their own CX(3)CR1. This growth-promotion loop is amplified by TNFalpha produced by CX(3)CR1-expressing T cells upon stimulation by FKN-expressing FLS. These data assign a critical role to FKN and its receptor in fibroblast proliferation and pannus formation in RA.
16778341 Pulmonary infectious complications associated with anti-TNFalpha therapy (infliximab) for 2006 Two patients with rheumatoid arthritis (RA) that developed serious infectious complications following anti-TNFalpha therapy (infliximab) are reported. Patient 1 developed tuberculosis with high fever, refractory diarrhea and mediastinal lymphadenopathy. Trans-bronchial needle biopsy was useful to confirm the diagnosis. Patient 2 showed sudden onset of dyspnea with diffuse bilateral lung infiltration caused by pneumocystis jiroveci pneumonia and the diagnosis was confirmed by broncho-alveolar lavage. Physicians should be alerted to infectious complications with atypical presentation and rapid progression in infliximab-treated patients. Invasive diagnostic procedures including fiber-optic bronchoscopy may be necessary early in the course for such cases.
17109564 Anti-tumour necrosis factor-alpha therapy for rheumatoid and other inflammatory arthropath 2006 Anti-tumour necrosis factor (TNF)-alpha represents a major advance in the treatment of rheumatoid arthritis (RA), ankylosing spondylitis and psoriatic arthritis. It is usually well tolerated, but a potential increase in the incidence of some infections in patients taking anti-TNFalpha agents has been reported. Compared with younger people, elderly patients have more co-morbidities and are likely to be taking more medications. Moreover, the aging process induces an increase in the rate of infections. Nevertheless, in recent studies analysing the databases of etanercept trials, the normalised incidence of adverse events, serious adverse events, medically important infections and deaths was not increased in patients aged >or=65 years. However, these trials included patients who might have been healthier than elderly RA patients in the general population and therefore not truly representative. Conflicting results have been reported in several 'real-life' observational studies. Taken together, the available data are reassuring for carefully selected populations, at least for etanercept, but it is not possible to claim that anti-TNFalpha agents do, or do not, pose a particular risk for the general population of older patients. Additional studies aiming at determining the safety and benefit-risk ratio of anti-TNFalpha agents in elderly patients are needed. In addition, since the benefit-risk ratio of anti-TNFalpha agents might be different in patients aged 65, 75 or >80 years, when possible, subgroup analysis might also be useful.
17486519 Osseointegrated wrist-joint prostheses: a 15-year follow-up with focus on bony fixation. 2007 Five patients with rheumatoid arthritis or osteoarthrosis of the wrist joint were followed up for 15 (14-17) years after wrist-joint arthroplasty with semiconstrained artificial joint mechanisms that had been anchored to bone using the osseointegration principle. They were fixed by one titanium screw introduced into the radius, and two or more titanium screws introduced distally into the metacarpal bones. In four cases a screw was also introduced into the ulna thereby constituting one component in a distal radio-ulnar (DRU) joint mechanism. The titanium screw introduced into the radius and the distal metacarpal screws osseointegrated in all cases. In three cases the mechanism of the wrist joint or parts of it were replaced with new components that could be attached to the screws that were already osseointegrated. We conclude that wrist joint prostheses can be anchored to the surrounding bone using osseointegration and that they remain fixed for at least 15 years. The principle allows replacement of the joint mechanism, if needed, with maintenance of the osseointegrated anchoring elements.
18269922 Costimulation blockade in autoimmunity and transplantation. 2008 Feb Signaling through the costimulation receptors is a critical pathway in the regulation of T-cell activation. The selective costimulation inhibitor abatacept (cytotoxic T lymphocyte-associated antigen 4-Ig) binds to CD80 and CD86 on antigen-presenting cells, blocking interaction with CD28 on T cells, and is approved for the treatment of moderate to severe rheumatoid arthritis. Belatacept (LEA29Y), currently enrolling phase III trials in renal transplantation, was rationally designed from abatacept to bind with more avidity to CD86, providing the more potent immunosuppressive properties required for immunosuppression in transplantation. This review describes the relevant preclinical studies and summarizes recent clinical findings on these 2 molecules in autoimmune diseases and organ transplantation. Although both inhibit the CD28 costimulatory pathway, they are tailored for specific disease states--abatacept for autoimmune diseases and belatacept for transplantation.
17052893 Clinical, radiographic and MRI findings of the temporomandibular joint in patients with di 2006 Nov The aim of this study was to investigate the condition of the temporomandibular joint (TMJ) in patients with different rheumatic diseases, and report correlations between the clinical, radiographic and magnetic resonance imaging (MRI) findings. The 67 patients were divided into four groups: 16 with rheumatoid arthritis (RA), 15 with mixed connective tissue disease (MCTD), 18 with ankylosing spondylitis (AS) and 18 with spondyloarthropathy (SPA). They were clinically examined, and panoramic tomography, lateral panoramic radiography and MRI of the TMJ were performed. MRI showed reduced articular cartilage in 25% (4/16) of RA, 0% (0/15) of MCTD, 17% (3/18) of AS and 17% (3/18) of SPA patients. Condylar changes included erosion, osteophytes and abnormal shape. Disc alterations included perforation, abnormal anterior position and decreased movement. These abnormalities were most frequent in RA patients, and least frequent in MCTD and SPA patients. Crepitation and reduced maximum opening of the mouth correlated with abnormalities of the disc and articular cartilage as shown by MRI. Severe condylar erosion in panoramic tomograms significantly correlated with MRI findings of condylar erosion (P<0.01), diminished thickness of condylar cartilage, abnormal condylar shape, and abnormal shape of the temporal surface of the TMJ (P< or =0.001). The presence of crepitation, limited mandibular movement and/or pain on movement of the jaw often indicated structural damage to the TMJ. Panoramic radiographs provide an alternative method to MRI but, to obtain a more detailed anatomic picture, MRI is recommended for patients with acute unexplained pain or as part of preoperative work up. A panoramic recording is not indicated when MRI is planned.
17943259 Spontaneous regression of EBV-associated diffuse lymphoproliferative disease in a patient 2008 Mar We describe the case of a 64-year-old female patient with rheumatoid arthritis (RA), who presented with lymphoproliferative disease (LPD) soon after the administration of etanercept, and regressed very shortly after the withdrawal of it. The occurrence was also associated with the Epstein-Barr virus (EBV) infection. The case of our patient may provide the evidence that etanercept plays an etiologic role in LPD in patients with RA.
17596287 Radiosynoviorthesis of medium-sized joints with rhenium-186-sulphide colloid: a review of 2007 Oct Hypertrophy and inflammation of the synovium with various underlying pathologies - such as rheumatoid arthritis, osteoarthritis, haemophilia and spondyloarthropathy - can be treated successfully by radiosynoviorthesis (RSO). For medium-sized joints (shoulder, elbow, wrist, hip and ankle), the radionuclide of choice is rhenium-186. We review the evidence for the efficacy of this local, relatively non-invasive therapy and evaluate its benefits and risks. We conclude good evidence of rhenium-186 RSO in rheumatoid arthritis and haemophilic arthropathy. In the remaining pathologies, up to now, the therapeutic efficacy has not been confirmed by today's most stringent criteria for clinical studies. The available data support rhenium-186 RSO as a suitable second-line treatment for patients in whom other therapies (including locally injected corticoids) have failed, as long as proper attention is paid to correct administration - including post-treatment immobilization and the co-administration of corticoids.
18837597 Vulnerability and resilience in women with arthritis: test of a two-factor model. 2008 Oct The purpose of this study was to test a 2-factor model of affective health in women with rheumatoid arthritis (RA; n = 82) or osteoarthritis (OA; n = 88). Positive and negative social interactions and affect were assessed for 11 consecutive weeks. For each participant, Vulnerability and Resilience factors were created from factor analyses of positive and negative personal characteristics, respectively. Multilevel analyses tested the hypothesis that weekly changes in social interactions or affect would only be predicted by the factor of the same valence. The Vulnerability (and not the Resilience) factor predicted changes in negative interactions. The Resilience (and not the Vulnerability) factor predicted changes in positive interactions. The Vulnerability (and not the Resilience) factor predicted changes in current and next-week negative affect. The Resilience and Vulnerability factors each predicted changes in current and next-week positive affect, although the effects for Vulnerability were smaller than for Resilience. Finally, the Vulnerability factor interacted with pain to predict more future negative affect. The main implication is that both Vulnerability and Resilience should be considered in theory, research, and interventions.
17435845 [The hand: a reflection of arthritis]. 2007 Jan Hand joint involvement in rheumatic diseases is often precocious and predominant as compared to other skeleton-muscular regions. Clinical examination not always allows for easy detection of fluid outpouring and synovial involvement, and undoubtedly does not allow to diagnose pathognomonic bone alterations of several rheumatic conditions. Articular ultrasonography is an innocuous methodology, easily reproducible and directly applied by a rheumatologist. The aim of this vignette is to present ultrasonography elementary lesions of the hand for a prompt diagnosis.
16953659 Regulation of peripheral inflammation by spinal p38 MAP kinase in rats. 2006 Sep BACKGROUND: Somatic afferent input to the spinal cord from a peripheral inflammatory site can modulate the peripheral response. However, the intracellular signaling mechanisms in the spinal cord that regulate this linkage have not been defined. Previous studies suggest spinal cord p38 mitogen-activated protein (MAP) kinase and cytokines participate in nociceptive behavior. We therefore determined whether these pathways also regulate peripheral inflammation in rat adjuvant arthritis, which is a model of rheumatoid arthritis. METHODS AND FINDINGS: Selective blockade of spinal cord p38 MAP kinase by administering the p38 inhibitor SB203580 via intrathecal (IT) catheters in rats with adjuvant arthritis markedly suppressed paw swelling, inhibited synovial inflammation, and decreased radiographic evidence of joint destruction. The same dose of SB203580 delivered systemically had no effect, indicating that the effect was mediated by local concentrations in the neural compartment. Evaluation of articular gene expression by quantitative real-time PCR showed that spinal p38 inhibition markedly decreased synovial interleukin-1 and -6 and matrix metalloproteinase (MMP3) gene expression. Activation of p38 required tumor necrosis factor alpha (TNFalpha) in the nervous system because IT etanercept (a TNF inhibitor) given during adjuvant arthritis blocked spinal p38 phosphorylation and reduced clinical signs of adjuvant arthritis. CONCLUSIONS: These data suggest that peripheral inflammation is sensed by the central nervous system (CNS), which subsequently activates stress-induced kinases in the spinal cord via a TNFalpha-dependent mechanism. Intracellular p38 MAP kinase signaling processes this information and profoundly modulates somatic inflammatory responses. Characterization of this mechanism could have clinical and basic research implications by supporting development of new treatments for arthritis and clarifying how the CNS regulates peripheral immune responses.
17182109 Toll-like receptor 2 ligand mediates the upregulation of angiogenic factor, vascular endot 2007 Feb 15 Rheumatoid arthritis (RA) is characterized by infiltrations of inflammatory cells accompanied by neovascularization in the joint. We hypothesized that cell activation via the toll-like receptor (TLR) may be involved in the induction of angiogenic molecules, which are relevant to the pathogenesis of RA. RA fibroblast like synoviocytes (FLS) were stimulated with TLR-2 ligand bacterial peptidoglycan (PGN), TLR-4 ligand lipopolysaccharide (LPS) and various cytokines. Vascular endothelial growth factor (VEGF) and IL-8 were measured by ELISA in culture supernatants; mRNA levels were assessed by RT-PCR and real time PCR. The levels of TLR-2, VEGF and IL-8 were analyzed by dual immunohistochemistry in RA synovium and compared with osteoarthritis (OA). Regulation of MyD88, IRAK4, IRAK1, IRAK-M and TRAF-6 mRNA expression levels by PGN were analyzed by RT-PCR. Phosphorylation of I kappa B alpha was evaluated by western blotting. Levels of VEGF and IL-8 were upregulated in culture supernatants of RA FLS stimulated with PGN, similar to the levels of IL-1beta and IL-17 stimulation. Neutralization of TLR-2 with a blocking monoclonal antibody significantly reduced both VEGF and IL-8 levels (P<0.05), which reflected the functional relevance of TLR-2 activation to the induction of VEGF and IL-8 production. Downstream intracellular signaling following TLR-2 stimulation involved MyD88-IRAK-4-TRAF-6 pathways, resulting in NF-kappaB activation. Thus, TLR-2 activation in RA FLS by microbial constituents could be involved in the induction of VEGF and IL-8 and thereby promote inflammation either directly or via angiogenesis. This possibly contributes to the perpetuation of synovitis in patients with RA.
17343250 Tumour necrosis factor (TNF)alpha -308 G/G promoter polymorphism and TNFalpha levels corre 2006 Nov OBJECTIVE: To investigate the influence of -308 tumour necrosis factor-alpha (TNFalpha) promoter polymorphism and circulating TNFalpha levels in the clinical response to adalimumab treatment in patients with rheumatoid arthritis (RA). METHODS: Eighty-one patients with active RA were genotyped for the -308 TNFalpha polymorphism by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis and subdivided into two groups for each polymorphism (G/A and G/G genotype). All received 40 mg of adalimumab subcutaneously every other week. We compared the groups' clinical responses to adalimumab at 8, 16, and 24 weeks using the Disease Activity Score in 28 joints (DAS28). RESULTS: Both groups showed a significant improvement from baseline. A significant difference between groups was found at week 24. We found that 88.2% of G/G versus 68.4% of G/A for the -308 polymorphism were DAS28 responders (p = 0.05). The score improvement at week 24 was 2.5 +/- 1.3 in the G/G group and 1.8 +/- 1.3 in the G/A group for the -308 polymorphism (p = 0.04). The median of serum TNFalpha levels of the G/A group were lower than those of the G/G group, and statistically different at weeks 8 and 24 (p < 0.039 and p < 0.043). When comparing baseline levels to those achieved at 8, 16, and 24 weeks for the whole group, only responder patients showed a statistically significant overall increase in TNFalpha over time (p < 0.000001). CONCLUSION: A relationship between DAS28 improvement, the -308 G/G polymorphism, and increased circulating TNFalpha levels was found in Chilean RA patients treated with adalimumab.
16107514 Chemokine and chemokine receptor expression in paired peripheral blood mononuclear cells a 2006 Mar BACKGROUND: Chemokine receptors and chemokines have a crucial role in leucocyte recruitment into inflamed tissue. OBJECTIVE: To examine the expression of an extensive number of chemokines and receptors in a unique bank of paired samples of synovial tissue (ST) and peripheral blood (PB) from patients with different forms of arthritis to assist in identifying suitable targets for therapeutic intervention. METHODS: Synovial biopsy specimens were obtained from 23 patients with rheumatoid arthritis (RA), 16 with osteoarthritis, and 8 with reactive arthritis. ST chemokine (CCL2/MCP-1, CCL5/RANTES, CCL7/MCP-3, CCL8/MCP-2, CCL14/HCC-1, CCL15/HCC-2, CCL16/HCC-4), chemokine receptor (CCR1, CCR2b, CCR5, CXCR4), and CD13 expression was analysed by immunohistochemistry and two colour immunofluorescence. Chemokine receptor expression (CCR1, CCR3, CCR5, CCR6, CCR7) on PB cells was studied by flow cytometry. Non-parametric tests were used for statistical analysis. RESULTS: Abundant expression of CCR1, CXCR4, and CCR5 was found in all forms of arthritis, with a specific increase of CCL5 and CCL15 in RA. CCL7, CCL8, CCL14, CCL15, and CCL16 were detected for the first time in ST. The results for PB analysis were comparable among different arthritides. Interestingly, compared with healthy controls, significantly lower expression of CCR1 (p<0.005) and CCR5 (p<0.05) by PB monocytes in the patient groups was seen. DISCUSSION: A variety of chemokines and receptors might have an important role in several inflammatory joint disorders. Although other receptors are involved as well, migration of CCR1(+) and CCR5(+) cells towards the synovial compartment may play a part in the effector phase of various forms of arthritis.
17614755 Targeting pleiotropin to treat osteoarthritis. 2007 Jul Pleiotropin (PTN) is a secreted heparin-binding peptide expressed in mesodermal and neuroectodermal cells during development, but rarely in adult tissues. Although PTN is abundant in fetal or juvenile cartilage, it is undectable in mature cartilage. However, PTN is re-expressed in chondrocytes in early stages of osteoarthritis where it is detectable in situ and in synovial fluids from patients. PTN enhances chondrogenesis by stimulation of extra-cellular matrix synthesis, reduction of degrading matrix metalloproteases and induction of their inhibitors; PTN also slightly reduces pro-inflammatory factors, such as nitric oxide and vascular endothelial growth factor. Furthermore, PTN stimulates chondrocyte clustering and proliferation. Thus, PTN appears to mediate repair and protective processes in osteoarthritic cartilage and appears to be a promising factor to treat osteoarthritis.
18402776 Bmx regulates LPS-induced IL-6 and VEGF production via mRNA stability in rheumatoid synovi 2008 Jun 13 Discordant cytokine production is characteristic of chronic inflammatory conditions like rheumatoid arthritis (RA), and anti-cytokine therapeutics are becoming routinely used to treat RA in the clinic. Fibroblasts from rheumatoid synovium have been shown to contribute to cytokine production in inflamed joints; likewise these cells also produce cytokines in response to inflammatory mediators signalling through Toll like receptors (TLRs). Tyrosine kinase activity is essential to LPS-induced cytokine production, and we have previously implicated a role for the Tec kinase, Bmx, in inflammatory cytokine production. Here we show that Bmx kinase activity in RASF is increased following LPS stimulation and that Bmx is involved in the regulation of LPS-induced IL-6 and VEGF production via mRNA stabilisation. This is an important insight into the regulation of VEGF, which is involved in a wide range of different pathologies, and may lead to more effective design of novel anti-inflammatory/angiogenic therapeutics for conditions such as RA.
18071945 Humanized antihuman IL-6 receptor antibody, tocilizumab. 2008 Interleukin-6 (IL-6) is a pleiotropic cytokine that regulates immune responses and inflammatory reactions. Overproduction of IL-6 has been shown to play a role in inflammatory autoimmune diseases such as rheumatoid arthritis (RA), and juvenile idiopathic arthritis (JIA) and, therefore, an agent blocking IL-6 actions can be a therapy of these diseases. IL-6 belongs to a cytokine family, which shares the cytokine receptor subunit glycoprotein (gp) 130. This family also includes IL-11, oncostatin-M, and leukemia inhibitory factor (LIF). In the IL-6 receptor (IL-6R) system, both a membrane-bound IL-6R and a soluble form of IL-6R are able to mediate IL-6 signals into the cells through the interaction of gp130. Tocilizumab is a humanized antihuman IL-6 receptor antibody designed using genetic engineering technology. Tocilizumab recognizes both the membrane-bound and the soluble form IL-6R and specifically blocks IL-6 actions. Tocilizumab is expected to ameliorate the autoimmune inflammatory diseases with IL-6 overproduction and has been clinically developed as a therapeutic agent for RA, systemic-onset and articular types of JIA, Crohn's disease, etc. Tocilizumab has been shown to be effective not only for improving signs and symptoms but also for preventing joint destruction of RA. Immunopharmacology and clinical benefit of tocilizumab in RA is addressed.
18975334 Vertebral strength changes in rheumatoid arthritis patients treated with alendronate, as a 2008 Nov OBJECTIVE: Finite element analysis of clinical computed tomography (CT) scans provides a noninvasive means of assessing vertebral strength that is superior to dual x-ray absorptiometry (DXA)-measured areal bone mineral density. The present study was undertaken to compare strength changes, measured using this newer method, in rheumatoid arthritis (RA) patients who were treated with alendronate (ALN) versus those who were not. METHODS: Thirty female RA patients without radiologic signs of L3 compression fractures or a history of osteoporosis medication were enrolled in a prospective randomized clinical trial. Patients were randomly assigned to the ALN group (5 mg orally, once daily) or the control group not receiving antiresorptive treatment. All patients were evaluated by DXA and quantitative CT at baseline and reevaluated after a mean of 12.2 months. Nonlinear finite element analysis was performed on the CT scans (n = 29 available for analysis) to compute an estimate of vertebral compressive strength and to assess strength changes associated with changes in the trabecular compartment and the outer 2 mm of bone (peripheral compartment). RESULTS: On average, vertebral strength was significantly decreased from baseline in the control group (n = 15) (median change -10.6%; P = 0.008) but was maintained in the ALN group (n = 14) (median change +0.4%; P = 0.55), with a significant difference between the 2 groups (P < 0.01). Strength decreased more rapidly within the trabecular bone, and ALN treatment was much more effective in the peripheral than the trabecular compartment. CONCLUSION: Our results indicate that patients with RA can lose a substantial amount of vertebral strength over a relatively short period of time, and this loss can be prevented by ALN, primarily via its positive effect on the outer 2 mm of vertebral bone.
16696388 Validation of the Thai version of a screening questionnaire for detection of systemic lupu 2006 Apr OBJECTIVE: The present study was performed to assess the sensitivity and specificity of the translation questionnaire for Systemic Lupus Erythematosus (SLE) in Thai speaking populations. MATERIAL AND METHOD: The 10- item questionnaire was applied to out-patients at the rheumatology clinic of the Chiang Mai University Hospital. One hundred and thirty-nine SLE, 109 Rheumatoid Arthritis (RA), and 35 Scleroderma (Scl) patients, as well as 88 Healthy Controls (HC) were enrolled into the present study. RESULTS: All subjects completed the questionnaire within 2 minutes. A positive response to three or more questions of the questionnaire gave a sensitivity and specificity of 92.81% and 76. 39%, respectively, and was comparable to the original version. CONCLUSION: This Thai-version of the screening questionnaire should be applied in the general population to determine the prevalence of SLE.