ABSTRACT
Introduction: In patients with Multiple Sclerosis (pwMS) disease- modifying therapies (DMTs) are known to affect immune response to antigens and possibly to SARS-CoV2 vaccine. Therefore, post-vaccination serological assessments are needed to evaluate the effect of the vaccine on SARS-CoV-2 antibody response. Objectives and aims: We designed a prospective multicenter cohort study enrolling pwMS who were scheduled for SARSCov- 2 vaccination with mRNA vaccines (BNT162b2, Pfizer/ BioNTech, Inc or mRNA-1273, Moderna Tx, Inc) to evaluate their effect on SARS-CoV-2 antibody response. Methods: A blood collection for the measure of SARS-CoV-2 antibody before the first vaccine dose and 4 weeks after the second dose was planned, with a centralized and blinded serological assessment (electrochemiluminescence immunoassay, ECLIA, Roche Diagnostics). Results: Preliminary data were collected on 780 pwMS (76% BNT162b2 and 24% mRNA-1273) who had pre- and 4-week post-vaccination blood assessments. 87 (11.2%) were untreated, 154 (19.7%) on ocrelizumab, 25 (3.2%) on rituximab, 85 (10.9%) on fingolimod, 25 (3.2%) on cladribine and 404 (51.7%) on other DMTs. 677 patients (86.8%) had detectable post-vaccination SARS-CoV-2 antibodies. At multivariate analysis, the antibody levels of patients on ocrelizumab (178-fold decrease, p<0.001), fingolimod (26-fold decrease, p<0.001) and rituximab (17-fold decrease, p<0.001) were significantly reduced as compared to untreated patients. Vaccination with mRNA-1273 resulted in a systematically 3.5-fold higher antibody level than with the BNT162b2 vaccine (p<0.001). Interpretation: In pwMS, anti-CD20 treatment and fingolimod led to a reduced humoral response to mRNA-based SARS-CoV-2 vaccines. As mRNA-1273 elicits 3.5-higher antibody levels than BNT162b2, this vaccine may be preferentially considered for patients under anti-CD20 treatment or fingolimod. Combining our data with those that will be produced by studying the cellular immune response to vaccines, and including clinical follow-up, will contribute to better define the most appropriate SARS-CoV-2 vaccine strategies in the context of DMTs and MS. At the time of the ECTRIMS presentation data on the full sample (about 2000 subjects) will be presented.
ABSTRACT
Background and aims: Several neurological complications related to SARS-CoV-2 infection have been reported. The involvement of peripheral nervous system (PNS) consists in the development of immune-mediated neuropathies such as Guillain-Barrè Syndrome. In this study we aim at assessing the presence of asymptomatic abnormalities in peripheral nerves conduction during the acute phase of COVID-19 and, their correlation with blood circulating inflammatory markers. Methods: Thirty-nine patients with COVID-19 were assessed by electroneurographic study of lower limbs and blood tests within one week of hospital admission (T0) and after 30 ± 10 days (T1). Results: Electroneurographic changes were found at least on one nerve at T0 in 12 patients, consisting of axonal or demyelinating changes. Two biological markers were found to be significantly correlated with the presence of neuropathic changes: Reactive Protein C and lymphocyte count. Patients with pathological electrophysiology at T0 showed significant improvement of electrophysiological parameters at T1. The improvements in electroneurographic data were significantly correlated with the trend of laboratory parameters, in particular with fibrinogen, D-Dimer, ferritin, C Reactive protein and lymphocytes. None of the patients with neuropathic changes developed clinical evidence of a full-blown peripheral neuropathy over time. Conclusions: Our study shows that asymptomatic alterations of the PNS can be found during the acute phase of COVID-19. These alterations significantly improve after 20–40 days from the acute phase of infection and that the improvement correlates significantly with the trend of laboratory parameters. Further studies are needed to evaluate possible long-term neurological complications and the predictive value of subclinical damage of PNS in the acute phase of infection.