Arthritis and rheumatism
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Arthritis and rheumatism · May 2009
ReviewMeasuring shoulder function: a systematic review of four questionnaires.
To conduct a systematic review of the quality and content of the psychometric evidence relating to 4 shoulder disability scales: the Disabilities of the Arm, Shoulder, and Hand (DASH) questionnaire, the Shoulder Pain and Disability Index (SPADI), the American Shoulder and Elbow Surgeons (ASES) score, and the Simple Shoulder Test (SST). ⋯ The psychometric properties of the ASES, DASH, and SPADI have been shown to be acceptable for clinical use. Conversely, some properties of the SST still need be evaluated, particularly the absolute errors of measurement. Overall, validation studies have focused on less clinically relevant properties (construct validity or group reliability) than estimates of MDC and MCID.
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Arthritis and rheumatism · May 2009
Randomized Controlled TrialEfficacy, pharmacodynamics, and safety of VX-702, a novel p38 MAPK inhibitor, in rheumatoid arthritis: results of two randomized, double-blind, placebo-controlled clinical studies.
To assess the efficacy and safety of VX-702, a p38 MAPK inhibitor, in patients with active, moderate-to-severe rheumatoid arthritis (RA). ⋯ The modest clinical efficacy plus the transient suppression of biomarkers of inflammation observed in this study suggest that p38 MAPK inhibition may not provide meaningful, sustained suppression of the chronic inflammation seen in RA.
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Arthritis and rheumatism · May 2009
Indoleamine 2,3 dioxygenase-mediated tryptophan catabolism regulates accumulation of Th1/Th17 cells in the joint in collagen-induced arthritis.
Indoleamine 2,3 dioxygenase (IDO) is a catabolic enzyme that initiates the kynurenine pathway of tryptophan degradation and has immunomodulatory properties. The aim of this study was to investigate the regulation of collagen-induced arthritis by tryptophan catabolism mediated by IDO. ⋯ Our data indicate that the induction of IDO controls the accumulation of Th1 and Th17 pathogenic T cells at the site of inflammation during collagen-induced arthritis. Therefore, manipulation of the kynurenine pathway of tryptophan degradation provides the potential for therapeutic intervention in rheumatoid arthritis.