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SpA Patients (spa + patient)
Selected AbstractsThe Ankylosing Spondylitis Quality of Life Questionnaire: validation in a New Zealand cohortINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 4 2010Katherine JENKS Abstract Aim:, To examine the validity of the Ankylosing Spondylitis Quality of Life Questionnaire (ASQoL) in a New Zealand population with defined axial spondyloarthritis (SpA). Once validated, the ASQoL will be included as an outcome measure in a proposed multicentre New Zealand study. Methods:, Five healthy participants were interviewed to identify any issues related to local dialect or linguistic comprehension of the questionnaire. Cognitive debriefing interviews were conducted with four participants with SpA to assess the relevance and comprehensiveness of the questionnaire. Internal consistency was established by determining the Cronbach's alpha. Finally, convergent validity of the ASQoL was assessed by testing the correlation with the Bath Ankylosing Spondylitis Functional Index (BASFI), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and patient global visual analogue scale (VAS) scores in a cohort of 63 SpA patients. Results:, The language used in the ASQoL was considered clear, comprehensible and accessible to speakers of New Zealand English. The questionnaire displayed content validity for patients with SpA. The ASQoL had good internal consistency in the present sample (, = 0.854). A positive correlation was found between the ASQoL and the BASFI (rho = 0.635, P < 0.001), BASDAI (rho = 0.521, P < 0.001) and patient global assessment VAS (rho = 0.546, P < 0.001), providing evidence that the ASQoL has convergent validity among patients with SpA in New Zealand. Test,retest reliability was good over 16 weeks (rho = 0.730, P < 0.001). Conclusions:, The ASQoL has been demonstrated in this study to be feasible, internally consistent and to have content and convergent validity in a New Zealand population of patients with axial spondyloarthritis; it is a measure of quality of life which is both easy to employ and reliable. [source] Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis,ARTHRITIS & RHEUMATISM, Issue 4 2009Bernard Vandooren Objective Peripheral spondylarthritis (SpA) is characterized by macrophages that express CD163, a marker of alternative activation (M2). The purpose of this study was to assess whether this differential infiltration with macrophage subsets was associated with a different local inflammatory milieu in SpA as compared with rheumatoid arthritis (RA). Methods The effect of SpA and RA synovial fluid (SF) on macrophage polarization was tested in vitro on normal peripheral blood monocytes. SF levels of classically activated macrophage (M1),derived and alternatively activated macrophage (M2),derived mediators were analyzed by enzyme-linked immunosorbent assay and multiparameter Luminex bead assay in 47 patients with non-psoriatic SpA, 55 with RA, and 15 with psoriatic arthritis (PsA). Paired synovial biopsy samples were analyzed histologically. Results SF from SpA patients promoted preferential expression of the M2 markers CD163 and CD200R in vitro, even if SF levels of the prototypical M2-polarizing factors (interleukin-4 [IL-4], IL-13, and IL-10) were not increased as compared with those in RA SF. Despite a similar degree of overall joint inflammation in SpA and RA, SpA synovitis displayed strongly reduced SF levels of M1-derived, but not M2-derived, mediators, such as tumor necrosis factor , (TNF,), IL-1,, IL-12p70, and interferon-,,inducible protein 10. SF levels of M1-derived mediators correlated well with peripheral joint inflammation in RA, but neither these mediators nor IL-1, and IL-17 did so in SpA. Of interest, the SF cytokine profile in PsA, a more destructive subtype of SpA, was similar to that in non-psoriatic SpA. Conclusion The local inflammatory milieu is clearly different in SpA as compared with RA peripheral arthritis. Synovitis in SpA, including that in PsA, is characterized by a selective decrease in M1-derived proinflammatory mediators, such as TNF, and IL-1,. [source] Identification of interleukin-7 as a candidate disease mediator in spondylarthritis,ARTHRITIS & RHEUMATISM, Issue 11 2008Markus Rihl Objective Understanding of the molecular pathophysiology of spondylarthritis (SpA) remains largely elusive. This is related both to the complexity of the disease (axial versus peripheral disease, inflammation versus tissue remodeling) and to the difficulty in obtaining samples from primary disease sites. This study was undertaken to explore a gene expression approach for identifying novel candidate mediators of SpA. Methods Sacroiliac joint fluid aspirates from 3 SpA patients with active sacroiliitis were studied by microarray analysis. The expression of selected candidate molecules in peripheral synovitis was confirmed by reverse transcriptase,polymerase chain reaction and enzyme-linked immunosorbent assay. Results Microarray analysis identified 4 sacroiliitis gene clusters, containing a total of 47 messenger RNA (mRNA) transcripts. Two clusters contained genes expressed in all sacroiliitis samples, corresponding to both known and unsuspected candidate mediators of SpA pathology. These included proinflammatory molecules as well as molecules involved in tissue remodeling, such as transforming growth factor ,2. Of the novel candidate genes selected for confirmation, interleukin-7 (IL-7) mRNA expression was higher in SpA peripheral synovial fluid and synovial tissue samples than in osteoarthritis samples, and similar to expression in rheumatoid arthritis (RA) samples. At the protein level, synovial fluid IL-7 levels were even higher in SpA than in RA, despite lower levels of tumor necrosis factor , and IL-1,. Conclusion In the present study, both known and unsuspected candidate mediators of SpA pathogenesis were identified, including IL-7. The specific overexpression of IL-7 at sites of peripheral synovitis in SpA suggests that further functional investigations of the role of this cytokine in SpA pathogenesis are warranted. [source] Antinuclear antibodies following infliximab treatment in patients with rheumatoid arthritis or spondylarthropathyARTHRITIS & RHEUMATISM, Issue 4 2003Leen De Rycke Objective To investigate the effect of infliximab treatment on antinuclear antibodies (ANAs), anti,double-stranded DNA (anti-dsDNA), antinucleosome, antihistone, and anti,extractable nuclear antigen (anti-ENA) antibodies in rheumatoid arthritis (RA) and spondylarthropathy (SpA) patients. Methods Sera from 62 RA and 35 SpA patients treated with infliximab were tested at baseline and week 30 (RA group) or week 34 (SpA group). ANAs were tested by indirect immunofluorescence (IIF) on HEp-2 cells. Anti-dsDNA antibodies were detected by IIF on Crithidia luciliae and by enzyme-linked immunosorbent assay (ELISA) and were further isotyped with ,, ,, and , chain,specific conjugates at various time points. Antinucleosome antibodies were tested by ELISA. Antihistone and anti-ENA antibodies were detected by line immunoassay. Results Initially, 32 of 62 RA patients and 6 of 35 SpA patients tested positive for ANAs. After infliximab treatment, these numbers shifted to 51 of 62 (P < 0.001) and 31 of 35 (P < 0.001), respectively. At baseline, none of the RA or SpA patients had anti-dsDNA antibodies. After infliximab treatment, 7 RA patients (P = 0.016) and 6 SpA patients (P = 0.031) became positive for anti-dsDNA antibodies. All 7 anti-dsDNA,positive RA patients had IgM and IgA anti-dsDNA antibodies. Three of the 6 anti-dsDNA,positive SpA patients had IgM and IgA anti-dsDNA antibodies, and 2 had IgM anti-dsDNA antibodies alone. In both diseases, the IgM anti-dsDNA antibodies appeared before the IgA anti-dsDNA antibodies. During the observation period, no IgG anti-dsDNA antibodies or lupus symptoms were observed. The development of antinucleosome, antihistone, or anti-ENA antibodies following infliximab treatment was observed in some patients, but the numbers were not statistically significant. Conclusion Infliximab treatment may induce ANAs, and especially IgM and IgA anti-dsDNA antibodies, in RA and SpA patients. However, no anti-dsDNA IgG antibodies or lupus symptoms were observed during the period of observation in this study, and the development of antinucleosome, antihistone, or anti-ENA antibodies was not statistically significant. These observations do not exclude potential induction of clinically significant lupus in the long term, and further followup is therefore mandatory. [source] | ||||||||||