Current data suggest that spondyloarthritis and Takayasu arteritis (TA) share common pathophysiological mechanisms, involving in particular the Th1 and Th17 pathways and a complex cytokine network. Paradoxically, although anti-TNF agents have an established role in the management of refractory forms of TA, their involvement in the development of systemic vasculitis-albeit rare-is now well documented.
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