PMC:7597510 / 8898-10643 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7597510","sourcedb":"PMC","sourceid":"7597510","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7597510","text":"Among the 37 patients described by Caress et al, 17 were tested for anti-ganglioside antibodies, 15 of whom were negative. In addition, two patients were positive for Miller-Fisher syndrome, and all were negative for GBS. However, specific description of types of the anti-ganglioside antibodies tested were not provided in many cases. Although some reports specifically described the types of antiganglioside antibodies tested, patients appear to have been tested only for anti-GM1, anti-GQ1b and anti-GD1b antibodies.9 10 14 Although we tested for various additional antiganglioside antibodies, all tests were negative in the present case as well. GBS was also reported in a case–control study of the 2016 Zika virus, where most patients were negative for antiganglioside antibodies, suggesting the existence of unknown antibodies.18 Therefore, it is important to test for as many kinds of antibodies as possible when suspecting GBS associated with SARS-CoV-2. However, some authors have reported nearly simultaneous development of neurological and respiratory symptoms in patients with COVID-19 and GBS.19 20 Thus, the cause of GBS may not be immune related in all cases. Previous research has suggested that SARS-CoV-2 damages the vascular endothelium.21 Therefore, axonopathy may have been caused by a microvascular disorder. In addition, McGonagle et al proposed that hyperinflammation following macrophage activation syndrome (ie, ‘cytokine storm’) may be a cause of GBS in patients with SARS-CoV-2 infection.22 Together, these findings suggest that, if neurological symptoms develop early following the appearance of respiratory symptoms in patients with COVID-19, both autoimmune and other factors should be considered in the 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