OBJECTIVE: There are few treatments for reactive arthritis (ReA). Since concentrations of tumor necrosis factor α (TNFα) are high in the serum and joints of patients with persistent ReA, this cytokine could be targeted in patients who do not respond to nonsteroidal antiinflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs). We under-took this study to investigate the safety and efficacy of TNF antagonists in patients with recent-onset and refractory ReA. METHODS: All French rheumatology and internal medicine practitioners registered on the Club Rhumatisme et Inflammation web site were asked to report on patients with ReA (defined by the criteria of the Third International Workshop on Reactive Arthritis) who had received anti-TNF therapy within the 12 months following the triggering infection. Tolerance and efficacy were retrospectively assessed using a standardized questionnaire. RESULTS: Ten patients with ReA previously refractory to NSAIDs and DMARDs, for which there was clinical and microbiologic evidence of a triggering bacterial infection, received anti-TNF therapy within a median of 6 months (range 2-12 months) between the beginning of ReA and the initiation of the treatment. The median followup was 20.6 months (range 6-50 months). We observed no severe adverse event and no infection related to the bacterium that triggered the ReA. Anti-TNF therapy was rapidly effective in 9 patients (90%), as shown by the rapid effect on a visual analog scale pain score, tender joint count, swollen joint count, and extraarticular manifestations, and by the corticosteroid-sparing effect. CONCLUSION: Anti-TNF therapy appears to be a safe and effective treatment of rheumatic and extraarticular manifestations in patients with recent-onset and refractory ReA, with a corticosteroid-sparing effect. Thus, TNFα could be a relevant target for ReA therapy.
OBJECTIVE: There are few treatments for reactive arthritis (ReA). Since concentrations of tumor necrosis factor α (TNFα) are high in the serum and joints of patients with persistent ReA, this cytokine could be targeted in patients who do not respond to nonsteroidal antiinflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs). We under-took this study to investigate the safety and efficacy of TNF antagonists in patients with recent-onset and refractory ReA. METHODS: All French rheumatology and internal medicine practitioners registered on the Club Rhumatisme et Inflammation web site were asked to report on patients with ReA (defined by the criteria of the Third International Workshop on Reactive Arthritis) who had received anti-TNF therapy within the 12 months following the triggering infection. Tolerance and efficacy were retrospectively assessed using a standardized questionnaire. RESULTS: Ten patients with ReA previously refractory to NSAIDs and DMARDs, for which there was clinical and microbiologic evidence of a triggering bacterial infection, received anti-TNF therapy within a median of 6 months (range 2-12 months) between the beginning of ReA and the initiation of the treatment. The median followup was 20.6 months (range 6-50 months). We observed no severe adverse event and no infection related to the bacterium that triggered the ReA. Anti-TNF therapy was rapidly effective in 9 patients (90%), as shown by the rapid effect on a visual analog scale pain score, tender joint count, swollen joint count, and extraarticular manifestations, and by the corticosteroid-sparing effect. CONCLUSION: Anti-TNF therapy appears to be a safe and effective treatment of rheumatic and extraarticular manifestations in patients with recent-onset and refractory ReA, with a corticosteroid-sparing effect. Thus, TNFα could be a relevant target for ReA therapy.
Authors: Terhi M Uotila; Jaakko A Antonen; Antti S Paakkala; Jukka T Mustonen; Markku M Korpela Journal: Clin Rheumatol Date: 2013-04-05 Impact factor: 2.980