Myasthenia gravis (MG) is a complex autoimmune neuromuscular disorder marked by fluctuating weakness in voluntary muscles. The pathogenesis primarily involves antibodies targeting components of the neuromuscular junction, most commonly the nicotinic acetylcholine receptor (AChR). In less frequent cases, antibodies may target other proteins such as muscle-specific kinase (MuSK) or low-density lipoprotein receptor-related protein 4 (LRP4) (Alcantara et al., 2022).

The underlying mechanism of MG involves T-cell-mediated, antibody-driven blocking and destruction of AChRs and the postsynaptic membrane. This process justifies using immunosuppressive and immunomodulating therapies as cornerstone treatments (Alcantara et al., 2022). The thymus gland plays a crucial role in the pathophysiology of AChR antibody-mediated MG, making thymectomy an important management option, particularly for AChR-antibody-positive younger adults and those with thymoma (Alipour-Faz et al., 2017, Bonilla, 2008, Bril et al., 2023, Barth et al., 2011).

Managing MG requires both chronic symptom control and effective treatment of acute exacerbations, including life-threatening myasthenic crises. These crises often necessitate hospitalization and intensive care due to bulbar and respiratory muscle failure. Various triggers, such as infections, immunizations, surgery, or stress, can precipitate symptom fluctuations.

Rescue therapy is vital during acute exacerbations and myasthenic crises, providing rapid, short-term relief by stabilizing neuromuscular transmission and improving respiratory function. This approach is crucial for managing severe symptoms while long-term treatments with delayed onset of action take effect. IVIG and PLEX have long been the cornerstone of rescue therapy.