Statins and Myasthenia Gravis: Clinical Implications and Pathogenesis

Statins are widely prescribed lipid-lowering agents and remain central to the prevention of atherosclerotic cardiovascular disease. Although generally well tolerated, they have been associated with neuromuscular adverse events, including new-onset or worsening myasthenia gravis (MG). Current evidence supports a primarily temporal association between statin exposure and MG onset or exacerbation; this signal has emerged largely from case reports, pharmacovigilance analyses, and retrospective observational studies, while more recent population-based observational data strengthen the association. Statin-associated MG should be distinguished from other statin-related neuromuscular syndromes, particularly toxic myopathy and immune-mediated necrotizing myopathy. Beyond cholesterol-lowering, statins may influence neuromuscular junction function through multiple converging mechanisms, including perturbation of the mevalonate-dolichol-glycosylation pathway, isoprenoid-dependent immune dysregulation, altered lipid raft integrity and acetylcholine receptor clustering, and coenzyme Q10-linked mitochondrial vulnerability. In this review, we summarize the clinical evidence linking statins to MG, outline key differential diagnostic considerations, and propose an integrated glycosylation-immune-structural-metabolic framework to guide future mechanistic studies and potential risk-stratified clinical management.