[Pubmed] Physiological and pathological roles of the thymus and value of thymectomy in myasthenia gravis: a narrative re

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[Pubmed] Physiological and pathological roles of the thymus and value of thymectomy in myasthenia gravis: a narrative re

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Mediastinum. 2024 May 21;8:31. doi: 10.21037/med-23-43. eCollection 2024.

ABSTRACT

BACKGROUND AND OBJECTIVE: Myasthenia gravis (MG) is a well-elucidated autoimmune disorder affecting the neuromuscular junction. Given the relationship between MG and thymic pathologies, with T cell and antibody-mediated pathogenesis, surgical (i.e., thymectomy) and non-surgical approaches remain a mainstay of management of the disease. This review seeks to outline the involvement of the thymus in the development of lymphocytes leading to MG.

METHODS: Different databases were searched exploring the role of thymectomy in treatment and outcomes in various MG patient subpopulations, including in ocular versus generalized disease, different age groups, and antibody status.

KEY CONTENT AND FINDINGS: Overall, the findings of multiple studies and reviews provide evidence to support the efficacy and long-term success of thymectomy in the management of MG; outcomes have included remission status, symptom severity, and need for adjunctive therapy. However, the heterogeneity in the MG population suggests that there are multiple factors that may confound the results of thymectomy and still need further examination. Separately, other autoimmune diseases develop following thymectomy, and further research is required to elucidate this susceptibility. Finally, our review will discuss the different surgical approaches for thymectomy, including their advantages, limitations, and perioperative complications.

CONCLUSIONS: Overall, in light of the known pathogenesis and association of the thymus with MG, thymectomy remains an extremely effective approach for long-term management and improved clinical outcomes.

PMID:38881805 | PMC:PMC11177005 | DOI:10.21037/med-23-43


Source: https://pubmed.ncbi.nlm.nih.gov/3888180 ... t9+e462414
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