First COVID-19, then Myasthenia Gravis- A report of 3 cases
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Myasthenia gravis is an autoimmune disease in which antibodies bind to acetylcholine receptors (AChRs) or to functionally related molecules in the postsynaptic membrane at the neuromuscular junction.

This report describes 3 patients without previous neurologic or autoimmune disorders who were diagnosed with myasthenia gravis after the onset of COVID-19.

Notable is that all three patients were positive for AChR-antibodies and that they responded to the conventional therapies we use for MG," researchers pointed out.

The three patients ranged in age from 64 to 71; two were men, and all were without previous neurologic or autoimmune disorders. Their serum AChR antibody levels were elevated, ranging from 22.8 pmol/L to 35.6 pmol/L. Fevers were as high as 38.6 °C to 39 °C and ranged from 4 to 7 days. CT scans excluded thymoma in all 3 patients.

In the first patient, repetitive stimulation of his facial nerve showed a 57% decrement, confirming involvement of the postsynaptic neuromuscular junction. In the second, it showed postsynaptic deficit of neuromuscular transmission in facial (52%) and ulnar (21%) nerves.

The first patient was treated with pyridostigmine bromide and prednisone and "had a response typical for someone with myasthenia gravis," the authors noted. The second patient improved after one cycle of intravenous immunoglobulin treatment.

The third patient developed dysphagia and respiratory failure and was transferred to the ICU for mechanical ventilation. Repetitive nerve stimulation showed postsynaptic deficit of the ulnar nerve (56%). She was extubated after plasmapheresis treatment. "This patient received HCQ the day after the onset of her first neurologic symptoms, so we do not believe that it caused her symptoms of myasthenia gravis," authors wrote.

Time from presumed infection with SARS-CoV-2 to onset of myasthenia gravis symptoms -- 5 to 7 days -- was consistent with times seen in other neurologic disorders triggered by infections, the authors observed.

Several possible explanations exist, they noted. Antibodies directed against SARS-CoV-2 proteins may cross-react with AChR subunits because the virus has epitopes similar to components of the neuromuscular junction. "This is known to occur in other neurologic autoimmune disorders after infection," authors wrote. "Alternatively, COVID-19 infection may break immunologic self-tolerance."

Source: https://www.acpjournals.org/doi/10.7326/L20-0845
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