Key result
IL-1 receptor antagonism improves NSAID- and colchicine-resistant recurrent pericarditis linked to the MEFV E148Q variant.
Low-penetrance variants in autoinflammatory genes such as MEFV may amplify inflammasome activation and underlie treatment resistance in recurrent idiopathic pericarditis, which may selectively respond to IL-1 receptor antagonism.
Supports IL-1 antagonism in MEFV E148Q refractory recurrent pericarditis; extends autoinflammatory pathways to colchicine-resistant idiopathic disease.
Interleukin (IL)-1–mediated autoinflammation is increasingly recognised as a driver of recurrent idiopathic pericarditis, particularly in patients with systemic inflammation, glucocorticoid dependence, and suboptimal response to standard therapy, including nonsteroidal anti-inflammatory drugs (NSAIDs) and colchicine. Recent studies have shown that low-penetrance variants in autoinflammatory genes such as the Mediterranean fever gene (MEFV) may amplify inflammasome activation, which may underlie treatment resistance in some patients.
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Syed Waqas Haider (2026) studied this question. IL-1 receptor antagonism selectively improved refractory recurrent pericarditis associated with the MEFV E148Q variant resistant to NSAIDs and colchicine.
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