Conclusion
Considering that 10 out of the 13 patients in our cohort had positive
auto-antibodies though only 4 of them had thymic hyperplasia, we
hypothesize that the bone marrow proliferation was responsible for the
production of autoantibodies in these patients. We assume that MG occurs
as a neurologic paraneoplastic syndrome due to AChR/ MuSK
auto-antibodies produced from abnormal bone marrow, which act at the
NMJ, in patients with MPNs. As the clonal cell population cannot be
eliminated entirely in the bone marrow even after treatment with
tyrosine kinase inhibitors (TKI) in Ph +ve MPNs and JAK2 inhibitors in
Ph -ve MPNS, MG can occur even in patients who are treated with these
agents. A high index of suspicion is needed to diagnose it early, and
treatment should be initiated immediately with steroids and
anticholinergic agents.