Predictors of clinical improvement in rituximab-treated refractory adult and juvenile Dermatomyositis and adult polymyositis

Rohit Aggarwal, Andriy Bandos, Ann M. Reed, Dana Ascherman, Richard J. Barohn, Brian M. Feldman, Frederick W. Miller, Lisa G. Rider, Michael O. Harris-Love, Marc C. Levesque, Chester V. Oddis

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Abstract

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.

Original languageEnglish
Pages (from-to)740-749
Number of pages10
JournalArthritis and Rheumatology
Volume66
Issue number3
DOIs
StatePublished - Jan 1 2014

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Polymyositis
Myositis
Autoantibodies
Physicians
Signal Recognition Particle
Muscles
Dermatomyositis
Rituximab
Juvenile dermatomyositis
Proportional Hazards Models
Transcription Factors
Parents
Demography
Enzymes
Therapeutics

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Rheumatology

Cite this

Predictors of clinical improvement in rituximab-treated refractory adult and juvenile Dermatomyositis and adult polymyositis. / Aggarwal, Rohit; Bandos, Andriy; Reed, Ann M.; Ascherman, Dana; Barohn, Richard J.; Feldman, Brian M.; Miller, Frederick W.; Rider, Lisa G.; Harris-Love, Michael O.; Levesque, Marc C.; Oddis, Chester V.

In: Arthritis and Rheumatology, Vol. 66, No. 3, 01.01.2014, p. 740-749.

Research output: Contribution to journalArticle

Aggarwal, R, Bandos, A, Reed, AM, Ascherman, D, Barohn, RJ, Feldman, BM, Miller, FW, Rider, LG, Harris-Love, MO, Levesque, MC & Oddis, CV 2014, 'Predictors of clinical improvement in rituximab-treated refractory adult and juvenile Dermatomyositis and adult polymyositis', Arthritis and Rheumatology, vol. 66, no. 3, pp. 740-749. https://doi.org/10.1002/art.38270
Aggarwal, Rohit ; Bandos, Andriy ; Reed, Ann M. ; Ascherman, Dana ; Barohn, Richard J. ; Feldman, Brian M. ; Miller, Frederick W. ; Rider, Lisa G. ; Harris-Love, Michael O. ; Levesque, Marc C. ; Oddis, Chester V. / Predictors of clinical improvement in rituximab-treated refractory adult and juvenile Dermatomyositis and adult polymyositis. In: Arthritis and Rheumatology. 2014 ; Vol. 66, No. 3. pp. 740-749.
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abstract = "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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AU - Ascherman, Dana

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.

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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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