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#3-28E. Unraveling the Immunopathophysiology of Polymyalgia Rheumatica (Ann Rheum Dis, 2026)
2026年2月4日 05:00·4分54秒
How do we move beyond glucocorticoids in managing difficult-to-treat polymyalgia rheumatica (PMR)? This comprehensive review by Choy et al. redefines PMR as a condition with both autoinflammatory and autoimmune components, driven by specific cytokine networks rather than just aging. The authors detail the critical mechanism of bursal inflammation, where the interaction between macrophages and fibroblast-like synoviocytes (FLS) creates a self-sustaining IL-6 amplification loop responsible for systemic symptoms. The most significant clinical takeaway is that this distinct IL-6 signature provides a robust mechanistic rationale for using IL-6 receptor inhibitors in steroid-refractory cases. However, when critically appraising the therapeutic landscape, it is crucial to note that while evidence for IL-6 blockade is strong, data supporting other targeted therapies—such as JAK inhibitors and anti-TNF agents—remains limited or inconsistent. This paper is essential for clinicians as it validates the shift toward personalized medicine, offering a pathophysiological basis for selecting steroid-sparing agents in patients who cannot tolerate prolonged glucocorticoid toxicity.
Citation: Choy, E. H., et al. Understanding the immunopathophysiology of polymyalgia rheumatica: implications for treatment. Ann Rheum Dis. 2026. DOI: 10.1016/j.ard.2025.09.005
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