Anti-LGI1 encephalitis following COVID-19 vaccination: a case series.
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ABSTRACT:
SUBMITTER: Asioli GM
PROVIDER: S-EPMC9243946 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundData regarding thrombosis after COVID-19 vaccination are scarce.MethodsClinical and laboratory data were collected from all patients who developed thrombosis within 4 weeks of receiving the Pfizer or Oxford/AstraZeneca vaccine. None had a COVID-19-positive swab.ResultsSeventeen patients were included, with average age of 48.8 years and equal proportion of females to males. Our data suggest that thrombosis occurred in 1 in 163,000 of all individuals who had received any dose of any type of COVID-19 vaccine: six (1 in 123,000) patients after the first dose of Oxford/AstraZeneca, none after the second dose of Oxford/AstraZeneca, four (1 in 257,000) patients after the first dose of the Pfizer vaccine, and seven (1 in 102,000) patients after the second dose of Pfizer vaccine. Three of 17 patients with thrombosis (17.6%) died.ConclusionsWe believe this report to be one of the earliest in the literature to address the question of whether isolated thrombosis is a possible complication of COVID-19 vaccination.
| S-EPMC8734543 | biostudies-literature
Project description:Voltage-gated potassium channels are thought to be the target of antibodies associated with limbic encephalitis. However, antibody testing using cells expressing voltage-gated potassium channels is negative; hence, we aimed to identify the real autoantigen associated with limbic encephalitis.We analysed sera and CSF of 57 patients with limbic encephalitis and antibodies attributed to voltage-gated potassium channels and 148 control individuals who had other disorders with or without antibodies against voltage-gated potassium channels. Immunohistochemistry, immunoprecipitation, and mass spectrometry were used to characterise the antigen. An assay with HEK293 cells transfected with leucine-rich, glioma-inactivated 1 (LGI1) and disintegrin and metalloproteinase domain-containing protein 22 (ADAM22) or ADAM23 was used as a serological test. The identity of the autoantigen was confirmed by immunoabsorption studies and immunostaining of Lgi1-null mice.Immunoprecipitation and mass spectrometry analyses showed that antibodies from patients with limbic encephalitis previously attributed to voltage-gated potassium channels recognise LGI1, a neuronal secreted protein that interacts with presynaptic ADAM23 and postsynaptic ADAM22. Immunostaining of HEK293 cells transfected with LGI1 showed that sera or CSF from patients, but not those from control individuals, recognised LGI1. Co-transfection of LGI1 with its receptors, ADAM22 or ADAM23, changed the pattern of reactivity and improved detection. LGI1 was confirmed as the autoantigen by specific abrogation of reactivity of sera and CSF from patients after immunoabsorption with LGI1-expressing cells and by comparative immunostaining of wild-type and Lgi1-null mice, which showed selective lack of reactivity in brains of Lgi1-null mice. One patient with limbic encephalitis and antibodies against LGI1 also had antibodies against CASPR2, an autoantigen we identified in some patients with encephalitis and seizures, Morvan's syndrome, and neuromyotonia.LGI1 is the autoantigen associated with limbic encephalitis previously attributed to voltage-gated potassium channels. The term limbic encephalitis associated with antibodies against voltage-gated potassium channels should be changed to limbic encephalitis associated with LGI1 antibodies, and this disorder should be classed as an autoimmune synaptic encephalopathy.National Institutes of Health, National Cancer Institute, and Euroimmun.
| S-EPMC3086669 | biostudies-literature
Project description:ObjectiveThis single-center study was conducted in a cohort of patients with anti-LGI1 encephalitis to investigate the factors related to their functional recovery.MethodsWe retrospectively collected the clinical information of patients admitted to Xuanwu Hospital from January 2014 until December 2019, and followed up for at least 12 months.ResultsA total of 67 patients were included, and 57 completed the 12-month follow-up. Most of the patients (55/57, 96.5%) achieved functional improvement after immunotherapy, and 26 (45.6%) became symptom-free. Compared to patients with complete recovery, patients with partial or no recovery had significantly higher incidences of consciousness disorders (25.8% vs. 0%, P<0.05) and positive LGI1 antibodies in cerebrospinal fluid (CSF) (71.0% vs. 46.2%, P<0.05). These patients also had a lower Barthel Index both upon admission and at discharge, as well as a higher incidence of relapse (25.8% vs. 3.8%; P<0.05 each). Univariate logistic regression showed that positive LGI1 antibodies in CSF and relapse were associated with incomplete recovery at 1-year follow-up (both P<0.05), but only relapse remained statistically significant after multivariate logistic regression (P=0.034).ConclusionPatients with LGI1 antibodies in CSF and those who relapsed were more likely to experience worse outcome. Early recognition of these patients, combined with more aggressive immunotherapy may result in better recovery.
| S-EPMC8718904 | biostudies-literature
Project description:The coronavirus disease 2019 (COVID-19) vaccination frequently leads to minor side-effects, that may be more intense after the second dose, but more serious side effects have been reported. We report a case of a 24-year-old man who presented to the hospital with acute substernal chest pain, 4 days after his second COVID-19 Moderna vaccination. Laboratory studies revealed elevated troponins and negative viral serologies. Cardiac magnetic resonance imaging (cMRI) demonstrated edema and delayed gadolinium enhancement of the left ventricle in a midmyocardial and epicardial distribution. The patient was diagnosed with myocarditis following Moderna vaccination. Our case report raises concern that myocarditis is a rare side effect of COVID-19 vaccine. Despite our report, it appears that there is a significantly higher risk of cardiac involvement from COVID-19 infection compared to COVID-19 vaccination.
| S-EPMC8130498 | biostudies-literature
Project description:BackgroundMyocarditis following COVID-19 mRNA vaccines (Pfizer-BioNTech and Moderna) have been increasingly reported. Incidence rates in the general population are lacking, with pericarditis rather than myocarditis diagnostic codes being used to estimate background rates. This comparison is critical to balance the risk of vaccination with the risk of no vaccination.MethodsA retrospective case-series was performed utilizing the Mayo Clinic COVID-19 Vaccine Registry. We measured the incidence rate ratio for myocarditis temporally related to COVID-19 mRNA vaccination compared to myocarditis in a comparable population from 2016 through 2020. Clinical characteristics and outcomes of the affected patients was collected. A total of 21 individuals were identified, but ultimately 7 patients met the inclusion criteria for vaccine-associated myocarditis.ResultsThe overall incidence rate ratio (IRR) of COVID-19 related myocarditis was 4.18 (CI95% 1.63, 8.98) which was entirely attributable to an increased IRR among adult males (IRR 6.69, CI95% 2.35, 15.52) compared to females (IRR 1.41, CI95% 0.03, 8.45).All cases occurred within 2 weeks of a dose of the COVID-19 mRNA vaccine with the majority occurring within 3 days (range 1-13 days) following the second dose (6/7 patients, 86%). Overall, cases were mild, and all patients survived.ConclusionsMyocarditis is a rare adverse event associated with COVID-19 mRNA vaccines, and in adult males it occurs with significantly higher incidence than the background population rate. Recurrence of myocarditis after a subsequent mRNA vaccine dose is not known at this time.
| S-EPMC8767838 | biostudies-literature
Project description:Abstract Messenger RNA vaccines are the main COVID-19 vaccines authorized for use in the United States. Side effects are typically minor and transient. We report a case series of four subjects with an acute myocarditis-like illness following mRNA COVID-19 vaccination who were hospitalized at our hospital in Lubbock, Texas. Three patients were young men who presented with acute chest pain after the second dose of the mRNA-1273 vaccine. Another patient was a 53-year-old white woman who presented with acute left arm pain 3 days after the first dose of the mRNA-1273 vaccine. She was later found to have acute decompensated heart failure, and endomyocardial biopsy revealed eosinophilic injury–mediated myocarditis.
| S-EPMC8607537 | biostudies-literature
Project description: Not available
| S-EPMC8483649 | biostudies-literature
Project description:BackgroundClinical trials of the BNT162b2 vaccine, revealed efficacy and safety. We report six cases of myocarditis, which occurred shortly after BNT162b2 vaccination.MethodsPatients were identified upon presentation to the emergency department with symptoms of chest pain/discomfort. In all study patients, we excluded past and current COVID-19. Routine clinical and laboratory investigations for common etiologies of myocarditis were performed. Laboratory tests also included troponin and C-reactive protein levels. The diagnosis of myocarditis was established after cardiac MRI.FindingsFive patients presented after the second and one after the first dose of the vaccine. All patients were males with a median age of 23 years. Myocarditis was diagnosed in all patients, there was no evidence of COVID-19 infection. Laboratory assays excluded concomitant infection; autoimmune disorder was considered unlikely. All patients responded to the BNT162b2 vaccine. The clinical course was mild in all six patients.InterpretationOur report of myocarditis after BNT162b2 vaccination may be possibly considered as an adverse reaction following immunization. We believe our information should be interpreted with caution and further surveillance is warranted.
| S-EPMC8162819 | biostudies-literature
Project description:BackgroundCOVID-19 vaccines were efficacious and safe in clinical trials. We report nine events of acute pericarditis (AP) in eight patients following COVID-19 vaccination with BNT162b2 (6/9), AZD1222 (2/9) and mRNA-1273 (1/9).MethodsAll patients were referred for AP temporally linked with COVID-19 vaccination. Chest pain was the most common clinical manifestation. Alternative etiologies were excluded upon thorough diagnostic work up. AP diagnosis was established according to ESC guidelines.FindingsFive events occurred after the first vaccine dose and four after the second. The mean age in this cohort was 65.8 ± 10.2 years and the men/women ratio 3/5. All events resolved without sequelae; two events were complicated by cardiac tamponade requiring emergent pericardial decompression. Hospitalization was required in four cases.InterpretationAlthough causality cannot be firmly established, AP has emerged as a possible complication following COVID-19 vaccination. Further investigation is indispensable to fully characterize this new entity.
| S-EPMC8491922 | biostudies-literature
Project description:Magnetic resonance imaging has linked chronic voltage-gated potassium channel (VGKC) complex antibody-mediated limbic encephalitis with generalized hippocampal atrophy. However, autoantibodies bind to specific rodent hippocampal subfields. Here, human hippocampal subfield (subiculum, cornu ammonis 1-3, and dentate gyrus) targets of immunomodulation-treated LGI1 VGKC-complex antibody-mediated limbic encephalitis were investigated using in vivo ultra-high resolution (0.39 × 0.39 × 1.0 mm3) 7.0 T magnetic resonance imaging [n = 18 patients, 17 patients (94%) positive for LGI1 antibody and one patient negative for LGI1/CASPR2 but positive for VGKC-complex antibodies, mean age: 64.0 ± 2.55 years, median 4 years post-limbic encephalitis onset; n = 18 controls]. First, hippocampal subfield quantitative morphometry indicated significant volume loss confined to bilateral CA3 [F(1,34) = 16.87, P < 0.0001], despite hyperintense signal evident in 5 of 18 patients on presentation. Second, early and later intervention (<3 versus >3 months from symptom onset) were associated with CA3 atrophy. Third, whole-brain voxel-by-voxel morphometry revealed no significant grey matter loss. Fourth, CA3 subfield atrophy was associated with severe episodic but not semantic amnesia for postmorbid autobiographical events that was predicted by variability in CA3 volume. The results raise important questions about the links with histopathology, the impact of the observed focal atrophy on other CA3-mediated reconstructive and episodic mechanisms, and the role of potential antibody-mediated pathogenicity as part of the pathophysiology cascade in humans.
| S-EPMC5405234 | biostudies-literature