TY - JOUR
T1 - Predictors of clinical improvement in rituximab-treated refractory adult and juvenile Dermatomyositis and adult polymyositis
AU - Aggarwal, Rohit
AU - Bandos, Andriy
AU - Reed, Ann M.
AU - Ascherman, Dana P.
AU - Barohn, Richard J.
AU - Feldman, Brian M.
AU - Miller, Frederick W.
AU - Rider, Lisa G.
AU - Harris-Love, Michael O.
AU - Levesque, Marc C.
AU - Oddis, Chester V.
PY - 2014/3
Y1 - 2014/3
N2 - 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 timedependent 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.
AB - 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 timedependent 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.
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U2 - 10.1002/art.38270
DO - 10.1002/art.38270
M3 - Article
C2 - 24574235
AN - SCOPUS:84896277090
SN - 2326-5191
VL - 66
SP - 740
EP - 749
JO - Arthritis and Rheumatology
JF - Arthritis and Rheumatology
IS - 3
ER -