OBJECTIVE: To identify the clinical and laboratory predictors of clinical improvement in a cohort of myositis patients treated with rituximab. METHODS: We analyzed data for 195 patients with myositis (75 with adult polymyositis [PM], 72 with adult dermatomyositis [DM], and 48 with juvenile DM) in the Rituximab in Myositis trial. Clinical improvement was defined as 20% improvement in at least 3 of the following 6 core set measures of disease activity: physician's and patient's/parent's global assessment of disease activity, manual muscle testing, physical function, muscle enzymes, and extramuscular disease activity. We analyzed the association of the following baseline variables with improvement: myositis clinical subgroup, demographics, myositis damage, clinical and laboratory parameters, core set measures, rituximab treatment, and myositis autoantibodies (antisynthetase, anti-Mi-2, anti-signal recognition particle, anti-transcription intermediary factor 1γ [TIF-1γ], anti-MJ, other autoantibodies, and no autoantibodies). All measures were univariately assessed for association with improvement using time-to-event analyses. A multivariable time-dependent proportional hazards model was used to evaluate the association of individual predictive factors with improvement. RESULTS: In the final multivariable model, the presence of an antisynthetase, primarily anti-Jo-1 (hazard ratio [HR] 3.08, P < 0.01), anti-Mi-2 (HR 2.5, P < 0.01), or other autoantibody (HR 1.4, P = 0.14) predicted a shorter time to improvement compared to the absence of autoantibodies. A lower physician's global assessment of damage (HR 2.32, P = 0.02) and juvenile DM (versus adult myositis) (HR 2.45, P = 0.01) also predicted improvement. Unlike autoantibody status, the predictive effect of physician's global assessment of damage and juvenile DM diminished by week 20. Rituximab treatment did not affect these associations. CONCLUSION: Our findings indicate that the presence of antisynthetase and anti-Mi-2 autoantibodies, juvenile DM subset, and lower disease damage strongly predict clinical improvement in patients with refractory myositis.
RCT Entities:
OBJECTIVE: To identify the clinical and laboratory predictors of clinical improvement in a cohort of myositispatients treated with rituximab. METHODS: We analyzed data for 195 patients with myositis (75 with adult polymyositis [PM], 72 with adult dermatomyositis [DM], and 48 with juvenile DM) in the Rituximab in Myositis trial. Clinical improvement was defined as 20% improvement in at least 3 of the following 6 core set measures of disease activity: physician's and patient's/parent's global assessment of disease activity, manual muscle testing, physical function, muscle enzymes, and extramuscular disease activity. We analyzed the association of the following baseline variables with improvement: myositis clinical subgroup, demographics, myositis damage, clinical and laboratory parameters, core set measures, rituximab treatment, and myositis autoantibodies (antisynthetase, anti-Mi-2, anti-signal recognition particle, anti-transcription intermediary factor 1γ [TIF-1γ], anti-MJ, other autoantibodies, and no autoantibodies). All measures were univariately assessed for association with improvement using time-to-event analyses. A multivariable time-dependent proportional hazards model was used to evaluate the association of individual predictive factors with improvement. RESULTS: In the final multivariable model, the presence of an antisynthetase, primarily anti-Jo-1 (hazard ratio [HR] 3.08, P < 0.01), anti-Mi-2 (HR 2.5, P < 0.01), or other autoantibody (HR 1.4, P = 0.14) predicted a shorter time to improvement compared to the absence of autoantibodies. A lower physician's global assessment of damage (HR 2.32, P = 0.02) and juvenile DM (versus adult myositis) (HR 2.45, P = 0.01) also predicted improvement. Unlike autoantibody status, the predictive effect of physician's global assessment of damage and juvenile DM diminished by week 20. Rituximab treatment did not affect these associations. CONCLUSION: Our findings indicate that the presence of antisynthetase and anti-Mi-2 autoantibodies, juvenile DM subset, and lower disease damage strongly predict clinical improvement in patients with refractory myositis.
Authors: M F G van der Meulen; I M Bronner; J E Hoogendijk; H Burger; W J van Venrooij; A E Voskuyl; H J Dinant; W H J P Linssen; J H J Wokke; M de Visser Journal: Neurology Date: 2003-08-12 Impact factor: 9.910
Authors: L A Love; R L Leff; D D Fraser; I N Targoff; M Dalakas; P H Plotz; F W Miller Journal: Medicine (Baltimore) Date: 1991-11 Impact factor: 1.889
Authors: M C Dalakas; I Illa; J M Dambrosia; S A Soueidan; D P Stein; C Otero; S T Dinsmore; S McCrosky Journal: N Engl J Med Date: 1993-12-30 Impact factor: 91.245
Authors: Lisa G Rider; Adrienne L Yip; Iren Horkayne-Szakaly; Rita Volochayev; Joseph A Shrader; Maria L Turner; Heidi H Kong; Minal S Jain; Anna V Jansen; Chester V Oddis; Thomas A Fleisher; Frederick W Miller Journal: Clin Exp Rheumatol Date: 2014-07-28 Impact factor: 4.473
Authors: Allison A Throm; Joshua B Alinger; Jeanette T Pingel; Allyssa L Daugherty; Lauren M Pachman; Anthony R French Journal: JCI Insight Date: 2018-11-15