Inflammatory Biomarkers, HLA Associations and Comorbidities in Myasthenia Gravis: From Immunogenetic Signatures to Clinical Outcomes and Personalized Management

Résumé fourni par la source

Myasthenia gravis (MG) is a prototypical autoimmune neuromuscular disorder marked by considerable clinical and immunological heterogeneity. Growing evidence highlights the role of proinflammatory biomarkers, including cytokines, chemokines, and acute-phase proteins, not only as correlates of disease activity but also as contributors to systemic immune dysregulation. These inflammatory signatures may predispose patients to both autoimmune and nonautoimmune comorbidities, thereby influencing prognosis and therapeutic decisions. In parallel, human leukocyte antigen (HLA) alleles remain the most consistent genetic factors associated with MG susceptibility and phenotype stratification. Distinct HLA profiles across antibody-defined subtypes (AChR, MuSK, and double-seronegative) suggest shared yet divergent immunopathogenic pathways, while overlaps with HLA signatures of other autoimmune conditions provide a genetic rationale for the frequent cooccurrence of multiple autoimmune diseases. Comorbidity patterns in MG extend beyond classical autoimmune associations, encompassing cardiovascular and metabolic disorders likely mediated by chronic systemic inflammation. Integrating insights from inflammatory biomarkers, HLA predisposition, and comorbidity clustering can refine risk assessment, guide monitoring, and open opportunities for personalized management strategies. This chapter provides a comprehensive literature review of these interconnected dimensions, emphasizing their impact on clinical outcomes and their potential to inform precision medicine approaches in MG.

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