Goserelin-triggered immune-mediated rhabdomyolysis in a patient receiving long-term rosuvastatin therapy: A case report

Statins inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase to reduce cholesterol but can cause muscle-related side effects. A rare severe form, immune-mediated necrotizing myopathy (IMNM), is an autoimmune condition characterized by proximal weakness, very high creatine kinase (CK) levels, and muscle necrosis with minimal inflammation. We report a 73-year-old man on long-term rosuvastatin who developed acute proximal muscle weakness, dark urine, and acute kidney injury (AKI) shortly after receiving goserelin. Laboratory tests showed severe rhabdomyolysis with markedly elevated CK and renal failure requiring hemodialysis. Muscle biopsy and serology confirmed anti-HMG-CoA reductase (anti-HMGCR) IMNM with complement-mediated muscle injury. Treatment with high-dose corticosteroids led to gradual improvement in strength, although residual renal impairment persisted at discharge. We describe a rare presentation of anti-HMGCR IMNM with fulminant rhabdomyolysis temporally associated with initiation of goserelin in a patient on chronic rosuvastatin therapy. The findings raise the possibility that gonadotropin-releasing hormone (GnRH) agonists may act as additional immunomodulatory triggers in genetically or immunologically predisposed individuals. Early recognition and prompt immunosuppressive treatment are essential to prevent irreversible organ damage and improve outcomes.