srjcmsSRJCMSSRJCMS2788-8851https://doi.org/10.47310/srjcms.2022.v02i02.007Treat SARS-CoV-2 Related Gullain-Barre Syndrome Early and AppropriatelyJosefFinstererAnaCFioriniFulvioAScorzaCarlaAScorzaWe read with interest the article by Pichardo-Rodriguez et al. on a 48 years-old male who developed spontaneous multifocal bleeding 25 days after a moderate infection with SARS-CoV-2, treated with glucocorticoids, anticoagulation, and oxygen for 6 days [1]. Thereafter, the patient developed paresthesias and “burning sensations” in the lower limbs followed by lower limb weakness and weakness of the left upper limb [1]. Guillain-Barre syndrome (GBS) was diagnosed in the absence of a dissociation cyto-albuminiqe and therapy with gluco-corticosteroids was started three months after the first symptoms [1]. Thrombocytopenia was treated with platelet transfusions and steroids. Under this regimen the patient achieved an incomplete recovery at the last follow-up [1]. The study is promising but raises concerns that should be discussed. The results of “electromyography” (most likely the authors meant nerve conduction studies (NCSs)) are unclear having been described as “subacute, axonal motor-sensory demyelinating polyneuropathy” [1]. The two main subtypes of GBS are acute, inflammatory demyelinating polyneuropathy (AIDP) and acute, motor axonal neuropathy (AMAN). We should know which subtype of GBS was diagnosed by NCSs in the index patient.  We also should know which type of anticoagulation the patient received for the treatment of COVID-19. In case the patient received low-molecular weight heparin it is conceivable that he produced heparin-induced thrombocytopenia (HIT) antibodies, which could be responsible for thrombocytopenia and spontaneous bleeding. We therefore should know if HIT antibodies were elevated or not.  Unfortunately, the patient did not receive any treatment immediately after diagnosing GBS [1]. Treatment started with a prolonged delay of >3 months after the initial diagnosis. We should know why the patient was exposed towards a high risk of further deterioration and involvement of the respiratory muscles. We disagree with the statement that GBS is rarely associated with other autoimmune disease [1]. Several reports have shown that GBS can be associated with transverse myelitis [2], encephalitis [3], thyroiditis [4], or myocarditis [5]. There is no general agreement on how to delineate an acute and chronic SARS-CoV-2 infection, and how to define post-COVID respectively long-COVID. Such definitions may be irrelevant as long as complications of a SARS-CoV-2 infection are recognised as such and managed appropriately. There is a discrepancy between the description “complete response” and “motor improvement” [1]. We should know if there was complete or incomplete recovery of GBS and of thrombocytopenia. Given the delayed onset of GBS treatment, it can be speculated that clinical manifestations of GBS had resolved only partially at the 2 months follow-up.  Overall, the interesting study has limitations that call the results and their interpretation into question. Clarifying these weaknesses would strengthen the conclusions and could improve the study. A delay of >3months between the onset of GBS and the start of GBS treatment with corticosteroids is unacceptable, as the outcome improves the earlier a treatment for GBS is initiated. AcknowledgementsFunding: No funding was received                Author contributionJF: design, literature search, discussion, first draft, critical comments, final approval.  DisclosuresThe author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Compliance with Ethics GuidelinesThis article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.