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Myasthenia gravis, an autoimmune neurologic disorder, was associated with COVID-19 in three patients in Italy.

Symptoms of myasthenia gravis (MG) appeared 5 to 7 days after fever onset in three patients who had no previous neurologic or autoimmune disorders, reported Domenico Restivo, MD, PhS, of Garibaldi Hospital in Catania, and colleagues, in a case report in the .

"This finding is important because the association between COVID-19 infection and myasthenia gravis has not been reported before," Restivo said.

"The knowledge of such a possible association may help doctors to an earlier diagnosis of myasthenia gravis in patients with COVID-19 infection," he told 番茄社区app. "Moreover, these findings further underline the role of autoimmunity in neurological disorders associated with COVID-19 infection."

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, blocking signals transmitted from nerves to muscles. It causes fluctuating muscle weakness that can affect the respiratory system and can be debilitating.

"I am not surprised that new cases of myasthenia gravis are now being reported in the context of COVID-19," said Gil Wolfe, MD, of the University at Buffalo in New York, who was not involved with the case report.

"Although not as well established or reported as the link between infections -- that now includes SARS CoV-2 worldwide -- and Guillain-Barré syndrome, such a connection has also been observed with MG," he told 番茄社区app.

"Notable is that all three patients were positive for AChR-antibodies and that they responded to the conventional therapies we use for MG," Wolfe 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 (normal value is less than 0.4 pmol/L). Fevers were as high as 38.6 °C to 39 °C (101.5 °F to 102.2 °F) and ranged from 4 to 7 days. CT scans excluded thymoma in all three 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 hydroxychloroquine the day after the onset of her first neurologic symptoms (withdrawn a day later), so we do not believe that it caused her symptoms of myasthenia gravis," Restivo and colleagues 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," Restivo and colleagues wrote. "Alternatively, COVID-19 infection may break immunologic self-tolerance."

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