Myasthenia Gravis and Chronic Myeloid Leukemia: A Rare Intersection of Autoimmunity and Malignancy
Esha Butala1
1Nuvance Health
Objective:
NA
Background:

Myasthenia gravis (MG) is an autoimmune disorder caused by antibodies against acetylcholine receptors (AChR) or related proteins at the neuromuscular junction. It causes fatigable weakness involving ocular, bulbar, and respiratory muscles. It affects 150-200 people out of every million, 10-12% having another autoimmune disease. Coexistence with a hematologic malignancy such as chronic myeloid leukemia (CML) is exceedingly rare.

CML is a myeloproliferative neoplasm driven by the BCR-ABL1 fusion oncogene, accounting for 15% of adult leukemias. The incidence is 1-2 per 100,000 persons annually. Tyrosine kinase inhibitors (TKIs) such as dasatinib have transformed CML into a chronic disease. Although autoimmune complications of TKIs and paraneoplastic syndromes can occur, concurrent MG and CML have been described only in isolated reports.

Design/Methods:
NA
Results:

An 81-year-old man with recently diagnosed MG presented with dysphagia, ptosis, and respiratory distress. After one dose of IVIG, he rapidly declined, requiring intubation and plasmapheresis (PLEX). Marked leukocytosis to 24,700 prompted hematology evaluation, revealing BCR–ABL positivity consistent with CML. After completing five PLEX sessions, he improved and was discharged on prednisone and pyridostigmine. Outpatient therapy with dasatinib 100 mg daily stabilized his CML. Later, he transitioned to efgartigimod (Vyvgart) infusions every eight weeks, enabling steroid taper, cessation of pyridostigmine, and sustained neurologic remission. 12 months later, he remained asymptomatic and in hematologic remission.


Conclusions:
This rare coexistence of MG and CML suggests shared immune dysregulation. In MG, loss of tolerance drives autoantibody formation. In CML, BCR–ABL-mediated clonal expansion alters cytokine and immune signaling. Chronic immune activation may link these processes. Future studies should explore immune profiling to identify convergent pathways, such as Fc receptor signaling and cytokine cross-talk, to guide precision therapies addressing both autoimmunity and malignancy
10.1212/WNL.0000000000216630
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