Myasthenia gravis as initial presentation of a pancreatic neuroendocrine tumor: A case report Journal Article


Authors: Stingu, E.; Dobrowolski, J. M.; Bombach, P.; Nann, D.; Singer, S.; Horger, M.; Lauer, U. M.; Zender, L.; Hinterleitner, C.; Hinterleitner, M.
Article Title: Myasthenia gravis as initial presentation of a pancreatic neuroendocrine tumor: A case report
Abstract: Myasthenia gravis (MG) is a heterogeneous autoimmune disease, which is characterized by a postsynaptic neuromuscular transmission defect, with antibodies directly targeting the acetylcholine receptor (AChR) or other structural proteins of the neuromuscular junction. The majority of MG cases are associated with thymic pathologies, including thymoma, thyroiditis, autoimmune diseases or malignant hematologic neoplasia. The present study reported a rare case of AChR-positive and late-onset ocular MG, which rapidly progressed to a generalized myasthenic syndrome as an initial presentation of a pancreatic neuroendocrine neoplasia (pNEN). Following complete surgical resection of the pNEN, the myasthenic syndrome was improved and the anti-AChR antibody titers were reduced. It has been reported that MG is a paraneoplastic syndrome in thymic neoplasms and less common in hematologic malignancies. However, currently, only few cases of MG as initial presentation of a solid tumor, and more particular of a neuroendocrine neoplasm, have been reported in the literature. In conclusion, surveillance for extrathymic solid malignancies in newly diagnosed patients with MG could promote the early diagnosis of associated tumor diseases.
Keywords: solid tumor; myasthenia gravis; paraneoplastic syndrome; pancreatic; chromogranin a; acetylcholine receptor; neuroendocrine neoplasia
Journal Title: Experimental and Therapeutic Medicine
Volume: 26
Issue: 5
ISSN: 1792-0981
Publisher: Spandidos Publications  
Date Published: 2023-11-01
Start Page: 523
Language: English
ACCESSION: WOS:001086119200001
DOI: 10.3892/etm.2023.12222
PROVIDER: wos
PMCID: PMC10580239
PUBMED: 37854502
Notes: Source: Wos
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