SARS-CoV-2 Infection in Sjögren Syndrome can be Complicated by Myelitis and Guillain-Barré Syndrome

To the Editor The study by Funakoshi et al. is noteworthy, but several points should be discussed.

First, we do not believe that the patient had sensory neuropathy due to Sjögren syndrome (SS) (1). The patient developed weakness, sensory disturbances and ataxia three weeks after SARS-CoV-2 infection (SC2I), which makes it more likely that the viral infection, and not SS, was responsible for the acute abnormalities. Arguments in favor of SC2I as the cause of neuropathy are the fact that sensory neuropathy and Guillain-Barre syndrome, subtype acute motor and sensory axonal neuropathy (AMSAN) are common complications of SC2I, that there was dissociation cytoalbuminique, that compound muscle action potential was decreased in the ulnar nerve, that F-wave responses were prolonged, that interleukin-6 was elevated in the CSF, that there was swelling of the nerve roots on magnetic resonance imaging, and that the abnormalities responded favorably to intravenous methylprednisolone, intravenous immunoglobulins, and plasma exchange. In addition to AMSAN, the patient developed long-distance myelitis.

Second, we do not agree that the patient only had sensory neuropathy. In addition to sensory abnormalities, the patient developed muscle weakness and autonomic dysfunction (1). How can the discrepancy between the presence of muscle weakness before admission and normal muscle strength on admission be explained? Did muscle weakness improve before admission so that it returned to normal upon admission?

Third, the patient developed sinus tachycardia, but the underlying pathophysiology was not stated. Since SC2I can be complicated by endocarditis and myocarditis (2), we should know if these conditions have been thoroughly ruled out. What were the results of the long-term electrocardiogram recordings, echocardiography, thyroid function tests, tilt table examinations, and meta-Iodobenzylguanidine (123)I metaiodobenzylguanidine imaging? Was there evidence of hyperthyroidism or postural tachycardia syndrome, which are common complications of SC2I (3)?

Fourth, cerebral imaging was not reported, and antibodies to aquaporin-4, myelin oligodendrocyte glycoprotein (MOG), and neuromyelitis optica (NMO) were not determined. Since the patient had myelitis, it is important to rule out MOG-associated disease and NMO spectrum disorder, both of which are known complications of SC2I (4,5).

Finally, we should know which virus caused the infection that led to relapse of myelitis and AMSAN nine months after the first occurrence. Did she experience a second SC2I? We should also know what medications the patient was taking at the first and second admissions. Is it conceivable that immunosuppression in SS favors the development of myelitis and AMSAN?

The author states that he has no Conflict of Interest (COI).