#3-43E. Beyond Glucocorticoids: Targeting the IL-6 Loop in Polymyalgia Rheumatica (Ann Rheum Dis, 2026)

Managing polymyalgia rheumatica (PMR) often leads to a clinical crossroads when glucocorticoids fail or cause toxicity, raising the question: what drives this inflammation? This comprehensive review by Choy et al. redefines PMR as a disease bridging autoinflammation and autoimmunity, detailing how the interplay between macrophages and fibroblast-like synoviocytes (FLS) in the bursa drives pathology. A critical insight is the identification of a self-sustaining IL-6 amplification loop within the bursal synovium, which fuels both local inflammation and systemic symptoms like fatigue and pain. This pathophysiological mechanism provides a robust rationale for using IL-6 receptor inhibitors, such as sarilumab, in steroid-refractory cases. However, clinicians should critically note that while the evidence for IL-6 blockade is strong, data supporting other targeted therapies—such as JAK inhibitors or anti-TNF agents—remains limited by small sample sizes or mixed results. For the practicing physician, understanding this distinct cytokine network is essential for navigating the shifting treatment landscape and confidently justifying the switch to biologic agents in difficult-to-treat patients.

Citation: Choy EH, et al. Understanding the immunopathophysiology of polymyalgia rheumatica: implications for treatment. Annals of the Rheumatic Diseases. 85(1), 6-21, 2026. DOI: 10.1016/j.ard.2025.09.005

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