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Advances in understanding the biology of inflammation have spurred drug development and revolutionized the care of both adults and children with rheumatic diseases. Among the most dramatic examples of this progress are the clinical trials, reported by Ruperto et al.1 and De Benedetti et al.2 in this issue of the Journal, of two different biologic agents — the interleukin-1 inhibitor, canakinumab, and the interleukin-6 inhibitor, tocilizumab — for the treatment of systemic juvenile idiopathic arthritis (JIA). These studies represent the culmination of work begun in small, but encouraging studies involving patients with systemic JIA who received treatment with interleukin-1 or . . .
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Sandborg et al. (2012) studied this question.
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