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The preplanned analyses of clinical response and time to first symptom resolution also revealed statistically significant results.
Similarly, analyses of clinical response in arthritis and psoriasis after dose escalation from 50 to 100 mg q4wks suggesting improved efficacy, especially in PASI scores, were limited by lack of a control arm.
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Multiple subgroup analyses of clinical responses (eg, age, sex, race, geographic location) found consistently efficacious clinical responses between the treatment groups.
The clinical correlate of this observation was initially described in retrospective analyses of clinical responses to rituximab in which patients harbouring the Fc γRIIIA 158V/V genotype showed superior response to rituximab in the treatment of non-Hodgkin's lymphoma compared with homozygous F/F or heterozygous F/V patients (Cartron et al, 2002).
We applied multiple logistic regression analysis as well as univariate analyses to identify markers of clinical response to GMA (Tables 2, and 3).
Details of the GO-AFTER patients with RA [ 4] and the study methods have been reported previously; procedures and analyses specific to the LTE, including assessments of clinical response, quality of life, safety and immunogenicity [ 5- 14], are summarized in Additional file 1. Patient disposition through week 24 [ 1] and week 160 [ 2] of the GO-AFTER trial has been reported previously.
Associations between baseline serum biomarker levels and the achievement of clinical response were assessed via robust logistic regression analyses.
The efficacy measures, including the rates of clinical response, clinical remission and mucosal healing, were analysed using the ITT analysis population.
These patients were still included in the analysis of clinical response and biopsy vessel staining, but could not be analysed for pathological response.
Evidence from recent trials supports early measurement of clinical response.
There were no strong predictors of clinical response.
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