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ID PMID Title PublicationDate abstract
17513569 Tumour necrosis factor blockers and structural remodelling in ankylosing spondylitis: what 2007 Jun A delineation of the differences in pathology between AS and RA
17605053 Differential diagnoses of suspected Lyme borreliosis or post-Lyme-disease syndrome. 2007 Sep The symptoms of Lyme borreliosis are similar to those of a variety of autoimmune musculoskeletal diseases. Persistence of complaints is frequently interpreted as unsuccessful antibiotic treatment of Borrelia-associated infections. However, such refractory cases are rare, and re-evaluation of differential diagnoses helps to avoid the substantial risk of long-term antibiotic therapy. In this study, we analyzed patients who presented to our rheumatology unit with previous suspected or diagnosed Lyme borreliosis. Eighty-six patients from a 3.5-year period were evaluated. The mean age of patients was 49.2 +/- 17.2 years; 60% (n = 52) reported a tick bite and 33% (n = 28) an erythema. Forty-seven percent (n = 39) had positive enzyme-linked immunoassay results and Western blots (Mikrogen, Martinsried, Germany). All but 12 patients had already received antibiotic treatment previously. Nine percent (n = 8) had ongoing or recent Lyme borreliosis. Twenty-nine percent (n = 25) showed clinical symptoms and radiographic changes compatible with degenerative disorders of the cervical and/or lumbar spine. These patients were significantly older when compared to the other patients (59.3 +/- 13.7 years vs 46.1 +/- 17.2 years, p = 0.001). Seventeen percent (n = 16) had arthropathies related to psoriasis or rheumatoid arthritis. Twelve percent (n = 10) were positive for the HLA B27 antigen. Other diseases were less frequent. Six patients (7%) could not be diagnosed conclusively, and four of these patients had negative Borrelia immunoassay results. In conclusion, Borrelia-associated diseases were rare in this study. Differential diagnoses helped to initiate a successful disease-specific therapeutic strategy.
17114190 A randomised, double-blind, placebo-controlled trial of a recombinant version of human alp 2007 May BACKGROUND: Rheumatoid arthritis (RA) tends to remit during pregnancy, with more patients achieving remission in the third trimester, coinciding with an increase in levels of alpha-fetoprotein (AFP). In vitro and animal studies have shown that AFP has immunomodulatory properties. MM-093 is a non-glycosylated, recombinant version of human AFP. OBJECTIVE: To assess the safety, tolerability and clinical effects of MM-093 during a 12-week, randomised, double-blind, placebo-controlled study. METHODS: 12 patients with RA, who had active disease and were on stable doses of methotrexate, received weekly subcutaneous injections of placebo or 21 mg of MM-093. Assessments were carried out at baseline and weekly thereafter. RESULTS: Baseline characteristics were similar in both groups. There was one dropout in the placebo group, due to flare of disease. Treatment with MM-093 was well tolerated. No serious adverse event was observed. By day 85, MM-093 produced a significant mean improvement from baseline in Disease Activity Score 28 (DAS28; 0.913 vs 0.008, p = 0.033) and patient's global assessment (28.9% vs -36.3%, p = 0.02) compared with placebo. CONCLUSION: This is the first randomised, controlled trial of MM-093, a recombinant version of human AFP, in patients with RA. MM-093 was well tolerated. Evidence of efficacy was observed, suggesting that MM-093 may have therapeutic potential in RA.
17520870 PGE synthase inhibitors as an alternative to COX-2 inhibitors. 2007 May NSAIDs and selective COX-2 inhibitors reduce the formation of prostanoids, particularly PGE2, to diminish inflammation. However, these drugs exhibit toxicities, including gastrointestinal bleeding and myocardial infarction. In cells, arachidonic acid is converted to PGE2 by the action of COX enzymes and terminal PGE synthase. This review discusses the problems associated with selective COX-2 inhibitors and describes the microsomal PGE synthase-1 enzyme, its regulation and role in inflammatory diseases, its known inhibitors, and its potential as an alternative target for the development of novel anti-inflammatory agents.
16855170 Neuroendocrine modulation induced by selective blockade of TNF-alpha in rheumatoid arthrit 2006 Jun Tumor necrosis factor-alpha (TNFalpha) is a main actor in the pathogenesis of rheumatoid arthritis (RA), interacting with other molecules in complex mechanisms. The neuroendocrine system is known to be involved and Chromogranin A (CHGA) serum levels are elevated in patients with RA. We evaluated the effect of the selective blockade of TNF-alpha, induced by treatment with anti-TNF-alpha monoclonal antibodies (mAbs), on the serum levels of CHGA and on its correlation with TNF-alpha and TNF-alpha receptors (TNFRs) serum levels. Seven patients with RA have been treated with the anti-TNF-alpha mAb, infliximab. We measured the serum levels of TNF-alpha, its receptors (tumor necrosis factor receptor-I [TNFR-I] and tumor necrosis factor receptor-II [TNFR-II]), and CHGA before and during the treatment. We also measured, as a control, the serum levels of CHGA, TNF-alpha, and soluble TNFRs in 14 patients who were being treated with infliximab, adalimumab, or etanercept and in 20 matching negative controls. The serum levels of TNFR-I and TNFR-II, which are a sensitive marker for the TNF-alpha pathway, correlated with those of CHGA before treatment (Pearson's coefficient, respectively, 0.59 and 0.53). Treatment with anti-TNF-alpha mAb provided a significant clinical response in all patients and the correlation between CHGA and TNFR-I and TNFR-II was no more evident during treatment (respectively, -0.09 and -0.07). TNF-alpha blockade allows a clinical effect in patients with RA and modifies the correlation between CHGA and TNFRs, suggesting that TNF-alpha and CHGA reciprocally interfere in the pathogenesis of RA, through intermediate adaptors, whose identification warrants further studies.
17543158 Advanced magnetic resonance imaging of the brain in patients treated with TNF-alpha blocki 2007 Mar OBJECTIVE: Neurological symptoms have been reported in patients treated with anti-TNF-alpha. In a pilot study we evaluated the effect of anti-TNF-alpha on cerebral parenchyma using advanced Magnetic Resonance (MR) techniques. METHODS: Seven patients with a systemic inflammatory disease (5 rheumatoid arthritis, 2 psoriatic arthritis) had Magnetization Transfer Imaging, Diffusion Weighted Imaging (DWI) and Magnetic Resonance Spectroscopy (MRS) of the brain before and after administration of anti-TNF-alpha. Four patients were neuropsychologically evaluated. RESULTS: After treatment with TNF-alpha blocking agents the Magnetization Transfer Ratio histogram Peak-heights (MTR-Pht) of the white and gray matter decreased (p < 0.01 and p < 0.05 respectively). The Apparent Diffusion Coefficient for the white and gray matter and the metabolite ratios in the centrum semiovale did not significantly change after therapy. Neuropsychological assessment showed no difference before and after anti-TNF-alpha. CONCLUSION: The decrease of the MTR-Pht after anti-TNF-alpha therapy suggests loss of parenchyma integrity; however, these changes could not be attributed to inflammation or demyelination based on our complementary DWI and MRS data. The decrease of the MTR-Pht did not result in decreased cognitive function.
18178071 Clinical features of lung cancer in patients with connective tissue diseases: a 10-year ho 2008 Apr BACKGROUND: Connective tissue diseases (CTD) might be associated with various malignancies, and one of the most frequent is lung cancer (LC). Despite our understanding of pathogenesis, this association remains still unclear. The aim of the present study is to describe the clinical characteristics of patients with CTD who developed LC. METHODS: Of 375 successive patients with CTD followed up to University Hospital between 1995 and 2004, 24 patients were diagnosed with LC: 11 (46%) had systemic sclerosis (SSc), 6 (25%) rheumatoid arthritis (RA), 6 (25%) systemic lupus erythematosus (SLE), and 1 (4%) dermatomyositis. We analyzed LC stage, radiological presentation, histological type, patients' smoking status, method of diagnosis, treatment applied, and disease outcome. RESULTS: Average duration of CTD was 13.95 (range 0-30) years. Non-small cell lung cancer (NSCLC) was significantly more frequent than small-cell lung cancer (SCLC). Among patients with NSCLC, 21 patients (85%) presented with stage III or IV. With regard to treatment, 13% patients underwent surgery, 25% chemotherapy, 4% patients combined chemo- and radiotherapy and 58% patients had only supportive therapy. The median survival was 5 months (range 1-96 months). CONCLUSION: The majority of CTD patients who developed LC were diagnosed at advanced stage and had poor survival. Efforts for early detection of LC in CTD patients' group are warranted.
17543152 Antiprothrombin antibodies: a comparative analysis of homemade and commercial methods. A c 2007 Mar OBJECTIVE: Prothrombin (PT) is a target for antibodies with lupus anticoagulant (LA) activity, suggesting the possible application of anti-prothrombin antibody (aPT) assays in patients with antiphospholipid syndrome (APS). Different methods - both homemade and commercial - for the detection of aPT are available, but they seem to produce conflicting results. The purpose of this study was to compare the performance of different assays on a set of well-characterized serum samples. PATIENTS AND METHODS: Sera were gathered from 4 FIRMA institutions, and distributed to 15 participating centres. Forty-five samples were from patients positive for LA and/or anticardiolipin antibodies (aCL) with or without APS, and 15 were from rheumatoid arthritis (RA) patients negative for antiphospholipid antibodies. The samples were evaluated for IgG and IgM antibodies using a homemade direct aPT assay (method 1), a homemade phosphatidylserine-dependent aPT assay (aPS/PT, method 2), and two different commercial kits (methods 3 and 4). In addition, a commercial kit for the detection of IgG-A-M aPT (method 5) was used. RESULTS: Inter-laboratory results for the 5 methods were not always comparable when different methods were used. Good inter-assay concordance was found for IgG antibodies evaluated using methods 1, 3, and 4 (Cohen k > 0.4), while the IgM results were discordant between assays. In patients with thrombosis and pregnancy losses, method 5 performed better than the others. CONCLUSION: While aPT and aPS/PT assays could be of interest from a clinical perspective, their routine performance cannot yet be recommended because of problems connected with the reproducibility and interpretation of the results.
16267598 The incidence of Proteus mirabilis infection increases in patients on treatment but does n 2006 Jul The aim of this study is to determine whether treatment increases the levels of anti-Proteus antibodies (APA) in patients with rheumatoid arthritis (RA). The blood samples of 32 patients suffering from RA who were recruited in our previous study and continued to participate in our follow-up study were collected after 1 year. Their first and follow-up samples were analysed for the presence of IgG isotype and total immunoglobulins (IgG+IgA+IgM) against Proteus mirabalis (PM) using enzyme-linked immunosorbent assay with two kinds of antigen preparations: whole bacteria and sodium dodecyl sulphate (SDS) lysed bacterial extract. All patients were treated with methotrexate and hydroxychloroquine with adequate dose of non-steroidal anti-inflammatory drug. After 1 year, 11 patients were in clinical remission [erythrocyte sedimentation rate (ESR) less than 30 mm/h and C-reactive protein (CRP) less than or equal to 10 mg/l], while the rest of the 21 were in the state of active disease. Correlation and Student's t test were used for statistical analysis. APA titres were significantly elevated in patients after 1 year of therapy. However, the rise was not different between patients who were in clinical remission and those in the state of active disease. APA titre increases in the treatment of RA, and the probable mechanisms are discussed.
18330608 Delayed spinal infection after laminectomy in a patient with rheumatoid arthritis interrup 2008 Jul We report a case of spondylodiscitis caused by Staphylococcus aureus 8 months after laminectomy of the lumbar spine, occurring in a rheumatoid arthritis (RA) patient interruptedly treated with anti-tumor necrosis alpha (TNFalpha) agents. The patient had suffered from seropositive RA for 2 years. An intravenous infusion (200 mg) of infliximab, a chimeric antibody against human TNFalpha, was introduced; however, due to Pneumocystis jiroveci pneumonia, this therapy was withdrawn. Four months later, the patient underwent an L3-L4 and L4-L5 laminectomy for spinal stenosis. Two months after surgery, we started treatment with 25 mg of etanercept, a soluble humanized TNF receptor dimer, subcutaneously twice a week. At that time, wound healing was satisfactory and no evidence of infection was obtained. Eight months after surgery, septic spondylodiscitis of the lumbar spine occurred. To the best of our knowledge, this is the first case in the literature to show a delayed type of postoperative infection as a complication of non-instrumented orthopedic surgical procedures. Despite interruption of anti-TNFalpha therapy before surgery, patients may remain at risk of developing postoperative infections.
17720725 Infliximab inhibits bone resorption by circulating osteoclast precursor cells in patients 2008 May OBJECTIVE: To examine the effects of infliximab on bone resorption by osteoclast precursor cells (OCPs) in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS) and to compare the results with changes in disease activity. METHODS: Before and during 24 weeks of infliximab treatment, peripheral blood mononuclear cells of 9 RA and 10 AS patients were seeded onto ivory wafers and adherent cells, including OCPs, were grown in medium promoting osteoclast differentiation. Bone resorption was evaluated morphometrically and correlated to disease activity. A total of 19 healthy individuals were studied in parallel. In addition, biochemical bone markers were assessed in all patients at baseline and after 24 weeks. RESULTS: OCPs from RA patients showed a higher bone resorption at baseline when compared to AS patients. Blocking of tumour necrosis factor (TNF)alpha with infliximab resulted in a strong reduction of bone resorption by OCPs in both cohorts and occurred faster in RA compared to AS patients. This inhibition coincided with a reduction of clinical disease activity in both patient cohorts and with an increase of serum osteocalcin levels and a relative decrease of collagen crosslinks in RA compared to AS patients. CONCLUSION: These results provide an explanation on the cellular level for the anticatabolic effect of TNF neutralisation on bone. The variation in the kinetics of bone resorption by the OCPs in patients with RA and AS suggests disease-specific differences in the type or in the preactivation of OCPs.
17195211 Interleukin-17 as a molecular target in immune-mediated arthritis: immunoregulatory proper 2007 Jan OBJECTIVE: Our previous studies have shown that murine dendritic cells (DCs) genetically modified to express interleukin-4 (IL-4) reduce the incidence and severity of murine collagen-induced arthritis. The present studies were performed to assess the immunoregulatory mechanisms underlying this response, by assessing the effects of IL-4 DCs on cytokine production by subsets of T helper cells. METHODS: Male DBA mice ages 6-8 weeks old were immunized with type II collagen. Splenic T cells obtained during the initiation phase and the end stage of arthritis were cultured with IL-4 DCs or untransduced DCs in the presence of collagen rechallenge. Interferon-gamma (IFNgamma) and IL-17 responses were measured. Antibodies to IL-4, IL-12, and IL-23, and recombinant IL-4, IL-12, and IL-23 were used to further study the regulation of T cell cytokine production by IL-4 DCs. RESULTS: Splenic T cells obtained during the initiation phase of arthritis produced less IL-17 when cultured in the presence of IL-4 DCs, despite their production of increased quantities of other proinflammatory cytokines (IFNgamma and tumor necrosis factor). T cell IL-17 production after collagen rechallenge was not inhibited by a lack of IL-23, since IL-4-mediated suppression of IL-17 was not reconstituted by IL-23, an otherwise potent inducer of IL-17 production by T cells. Although IL-4 DCs can produce increased quantities of IL-12 and IFNgamma, suppression of IL-17 production by IL-4 DCs was independent of both. While IL-17 production by T cells obtained during the initiation phase of arthritis was regulated by IL-4 DCs, IL-17 production by T cells obtained during end-stage arthritis was not altered. CONCLUSION: Our data suggest that IL-4 DCs exert a therapeutic effect on collagen-induced arthritis by targeting IL-17. IL-17 suppression by IL-4 DCs is robust and is not reversed by IL-23. Timing might be important in IL-17-targeted therapy, since IL-17 production by T cells obtained during end-stage arthritis did not respond to suppression by IL-4 DCs.
18163955 Protective effects of overexpression TCR Vbeta5.2-HSP70 and TCR Vbeta8.2-HSP70 against col 2007 Dec Collagen-induced arthritis (CIA) is an animal model, which closely resembles human rheumatoid arthritis (RA) in pathogenesis and pathology. Evidence suggests that the inhibition of T lymphocytes or their functions can alleviate the progression of arthritis. So the administration of arthritogenic T cell receptor (TCR) variable region peptide or DNA vaccines encoding pathogenic TCR Vbeta variable region may provide useful information for designing specific immunotherapies against autoimmune diseases. Heat shock proteins (HSPs) have the function of raising antigenic immunogenicity and HSP70 has a protective effect against arthritis. We previously demonstrated the presence of pathogenic predominant T cell receptor Vbeta5.2 and Vbeta8.2 clonotypes in the joints of CIA rats. In this study, we constructed the recombinant eukaryotic expression vectors pTARGET-TCR Vbeta5.2/8.2-HSP70, and evaluated their protective effects on CIA rats. Protective effects were observed in CIA rats by injecting these recombinant DNA vaccines, which could alleviate arthritis index, decrease the levels of IFN-gamma and anti-CII antibody in serum, and increase the levels of IL-4. Pathological changes were not as serious as those observed in control CIA rats. The rat injected with two combined vaccines showed better protective effects than CIA rats administered with individual vaccine. These results showed that recombinant DNA vaccines pTARGET-TCR Vbeta5.2-HSP70 and pTARGET-TCR Vbeta8.2-HSP70 could significantly alleviate the arthritic symptoms of CIA rats, and better protective effects could be achieved if these two vaccines were used in combination.
17718385 [Characterization of the HtrA family of proteins]. 2007 The HtrA family of proteins consists of evolutionary conserved serine proteases, which are homologues of the HtrA protein from a model bacterium Escherichia coli. They are widely distributed among organisms, prokaryotic as well as eukaryotic including humans. HtrA proteins participate in defense against stresses causing aberrations in protein structure, for example heat or oxidative stress. At least four human homologues have been identified. They are involved in cell growth and differentiation, apoptosis, and disturbances in their function may induce carcinogenesis, arthritic and neurodegenerative disorders. This article summarizes recent studies regarding the HtrA family of proteins, their structure, regulation and function. It also presents practical applications of this knowledge and perspective of its use in the future.
16760833 [Cutaneous vasculitis with necrotic ulcers in rheumatoid arthritis: treatment with anti-TN 2006 May INTRODUCTION: Anti-TNFalpha has occasionally been used in the treatment of recalcitrant forms of systemic vasculitis such as Behçet's disease, Wegener's granulomatosis and Churg-Strauss syndrome. We report on the outcome of treatment in rheumatoid arthritis patients with cutaneous vasculitis lesions on anti-TNFalpha. OBSERVATIONS: Two patients with rheumatoid arthritis present for several years had necrotic ulcers of the lower limbs due to cutaneous vasculitis. After the failure of various immunosuppressive drugs (cyclophosphamide, azathioprine, methotrexate), the two patients were treated with anti-TNFalpha: infliximab in the first case and adalimumab in the second. Cutaneous ulcers healed within two to four months of the start of anti-TNFalpha treatment. Despite ongoing anti-TNFalpha treatment, these cutaneous ulcers relapsed four to six months after complete healing. CONCLUSION: Initially spectacular healing of cutaneous vasculitis ulcers under anti-TNF alpha treatment followed by relapse after several months of treatment is suggestive of an escape mechanism.
18830904 Modulatory effects of inflammation and therapy on GDF-5 expression in rheumatoid arthritis 2008 Nov OBJECTIVE: Growth differentiation factor-5 (GDF-5), a member of the transforming growth factor (TGF)-beta family, is involved in joint development during embryogenesis and has the potential to regenerate cartilage in adult animals. As progression of chronic joint diseases is influenced by cytokines of the synovial tissue, we examined the expression and effects of GDF-5 in this tissue. METHODS: Microarray experiments were investigated for differential expression of GDF-5 in synovial tissues, synovial fibroblasts, and peripheral blood cells. GDF-5 expression was validated by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR), immunohistochemistry, double immunofluorescence, and in situ hybridization in synovial tissue of normal donors (ND) and patients with osteoarthritis (OA) and rheumatoid arthritis (RA). Effects of inflammation and therapy were investigated in RA and OA fibroblasts after stimulation with interleukin (IL)-1beta, tumour necrosis factor (TNF)-alpha, methotrexate (MTX), and prednisolone. The influence of GDF-5 on macrophages was studied by chemotaxis assay. RESULTS: Microarray analysis and immunostaining revealed expression predominantly in synovial fibroblasts. Compared to patients without immunomodulating drugs, expression of GDF-5 was decreased significantly in patients receiving glucocorticoids and/or disease-modifying antirheumatic drugs (DMARDs) (p = 0.007), but did not differ between the total group of ND, OA, and RA. Stimulation with prednisolone and TNFalpha reduced GDF-5 expression in OA and RA fibroblasts, whereas MTX and IL-1beta revealed minor or no relevant change. GDF-5 also reduced cell migration of macrophages (p<0.001). CONCLUSION: GDF-5 is expressed in synovial fibroblasts and may counteract macrophage infiltration. Its modulation by inflammation and therapy suggests that glucocorticoids play a conflicting role by suppressing not only inflammation but also putative mechanisms of repair.
17642248 [Tuberculosis associated with anti-TNF therapy]. 2007 Jul Accumulated studies have shown that anti-TNF therapy increases risk of tuberculosis. Most of anti-TNF therapy associated tuberculosis develops within the first six months after initiation of the therapy, suggesting reactivation of latent infection. Atypical clinical features such as extrapulmonary tuberculosis and disseminated disease are frequently found, leading to delay in diagnosis. Official Japanese guidelines recommend tuberculosis risk evaluation before the use of anti-TNF therapy based on physical examination, chest X-ray, and tuberculin skin test(TST). However, a positive TST in BCG vaccinated individuals and false negative due to anti-rheumatic agents diminish the diagnostic value of TST. Alternative immunological assays which detect mycobacterial antigen specific interferon (IFN)-gamma secretion by ELISA or ELISPOT are more sensitive and specific than TST. These procedures are helpful for a screening and monitoring system for tuberculosis in patients receiving anti-TNF therapy.
17242466 Progressive and concordant expression of PKC-eta and iNOS phenotypes in monocytes from pat 2007 May Rheumatoid arthritis (RA) is a relatively common autoimmune disease with strong genetic and environmental determinants. The disease manifests itself as inflammation of the synovia and usually progresses to joint erosion and destruction. The disease can also be considered as a systemic disease because extra-articular manifestations are often observed throughout many organs and tissues of the body. Patients with severe RA have altered peripheral blood monocytes (PBM) that express activation markers. Two such markers, PKC-eta and iNOS, were studied using confocal laser scanning microscopy to determine how these markers are expressed during disease progression. Healthy individuals expressed neither of the two markers, but there was an elevated level of PKC-eta observed as the disease progressed (40% in mild RA and 100% in severe RA patients). Concordant expression of the two markers was observed in only 3% of PBM from mild RA patients, reaching 38% in severe RA patients. No cells expressing iNOS alone were observed in any of the patients studied. These data support the hypothesis linking PKC-eta expression with the regulation and predisposition to the development of the iNOS phenotype in severe RA patients. PKC-eta may therefore be a key regulator in the production of elevated plasma nitric oxide (NO) and corresponding circulating reactive nitrogen intermediates in severe RA and may be a possible target to regulate iNOS induction and NO production by monocytic cells in RA patients and possibly other inflammatory diseases.
17610322 Patients with rheumatoid arthritis have higher levels of mannan-binding lectin than their 2007 Aug OBJECTIVE: Mannan-binding lectin (MBL) is present in serum and synovial fluid; its levels vary widely, and the variations are strongly associated with polymorphisms in the MBL2 gene. Studies have compared MBL in patients with rheumatoid arthritis (RA) and in unrelated controls, but the findings have been contradictory. In the first family-based study, we compared MBL levels in patients with RA to population controls and also to their nonaffected first-degree relatives, who may be regarded as optimal controls because of less genetic variation. METHODS: Serum levels of MBL and rheumatoid factor were analyzed in 210 patients with RA and 406 of their first-degree relatives from 74 extended families. Population controls for MBL levels were 330 randomly selected adult Icelanders. RESULTS: Patients with RA had higher MBL levels in serum (median 1553 microg/l) than their first-degree relatives (1073 microg/l; p = 0.003) and the unrelated controls (938 microg/l; p < 0.0001). No association was found between MBL and rheumatoid factor. CONCLUSION: Patients with RA had markedly higher MBL levels than their close relatives and controls, indicating that high MBL may predispose to RA. As MBL has been shown to bind potential arthritogenic agents including modified immunoglobulins, cellular debris, and microorganisms, our findings suggest that high MBL could trigger complement mediated inflammation within joints.
16987681 Expression of CXCR-1 and CXCR-2 chemokine receptors on synovial neutrophils in inflammator 2006 Dec OBJECTIVE: To analyze the CXCR-1 and CXCR-2 chemokine receptor expression on peripheral blood neutrophils (PBN) and synovial fluid neutrophils (SFN) of patients with rheumatoid arthritis (RA) and Behçet's disease (BD) (characterized by erosive and non-erosive arthritis, respectively), and to compare them with those of patients with osteoarthritis (OA). METHODS: We used flow cytometry to investigate the expression of CXCR-1 and CXCR-2 chemokine receptors on PBN and SFN of fifty-five (22 RA, 22 BD and 11 OA) age and sex-matched patients. RESULTS: In respect to chemokine receptor expression on neutrophils isolated from patients with RA, mean fluorescein intensity (MFI) of CXCR-1 chemokine receptors on PBN from active and inactive RA patients, and SFN from patients with RA were 151 (90-395), 129 (81-539) and 136 (64-220), respectively, and there were not statistically significant difference each other. But MFI of CXCR-2 chemokine receptors on SFN of patients with RA was 18 (10-32), and significantly higher than PBN of active and inactive RA patients (MFI: 10 (6-15) and 12 (7-16), P=0.002 and 0.037, respectively). In respect to chemokine receptor expression on neutrophils isolated from patients with BD, MFI of CXCR-1 chemokine receptors on PBN of active BD patients was 245 (97-844), and higher than PBN of active RA patients and SFN of BD patients (MFI: 151 (90-395) and 134 (61-231), P=0.047 and 0.017, respectively). MFI of CXCR-2 chemokine receptors on PBN of active and inactive BD patients, and SFN of patients BD were 10 (6-14), 10 (2-16), and 12 (8-24), respectively, there were not statistically significant difference each other. MFI of CXCR-1 chemokine receptors on SFN from patients with RA, BD, and OA were 136 (64-220), 134 (61-231), and 114 (60-180), respectively, and there was no difference between the study groups. MFI of CXCR-2 chemokine receptors on SFN of patients with RA was 18 (10-32), and higher than patients with BD and OA (MFI: 12 (8-24) and 11 (9-18), P=0.037 and 0.005, respectively), though there was no difference between last two groups. CONCLUSION: Our study points that CXCR-1 and CXCR-2 chemokine receptors of SFN may have diverse functions in the course of inflammatory arthritides. These results indicate that CXCR-2 chemokine receptor might play more critical role in long lasting accumulation of neutrophils within the synovial fluid of patients with RA.