Asad Waqar, Okasha Zulfiqar, Favour K Mbakwe, Talha Ali, Ghulam Mohayy Ud Din
Myasthenia gravis is an autoimmune disease of the neuromuscular junction, primarily caused by antibodies directed against the acetylcholine receptor. Follicular hyperplasia of the thymus can be seen in patients with acetylcholine receptor-positive myasthenia gravis and may remain asymptomatic for many years until unmasked by a specific medication. Myasthenia gravis induced by drugs has been reported with D-penicillamine and immune checkpoint inhibitors, but never with the sodium-glucose linked transporter-2 inhibitors. We report a case of a 62-year-old man with type 2 diabetes presenting with progressive, fluctuating bilateral ptosis, binocular diplopia, dysarthria, and dysphagia occurring eight weeks after starting treatment with 10 mg daily of empagliflozin. He had no history of any other medications or infections. Physical examination revealed fluctuating bilateral ptosis (more prominent on the right) with an ice pack test demonstrating a 2 mm improvement after two minutes. The anti-acetylcholine receptor antibody level was positive at 4.2 nmol/L. Repetitive nerve stimulation studies revealed an 18% decremental response at 3 Hz. A chest computed tomography scan showed diffuse bilateral symmetric thymic hyperplasia measuring 12 mm in size without any mass. Empagliflozin was discontinued. Pyridostigmine and prednisone 40 mg daily were started, with full resolution of his symptoms. The patient shows no symptoms at one year on pyridostigmine alone. This case represents the first description of the unmasking of acetylcholine receptor-positive myasthenia gravis by sodium-glucose linked transporter-2 inhibitors in a patient with thymic follicular hyperplasia. Myasthenia gravis should be considered in patients with newly acquired fatigable ptosis, diplopia, or bulbar symptoms who are being treated with sodium-glucose linked transporter-2 inhibitors.