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.