scholarly journals Multisystem Inflammatory-like Syndrome in a Child Following COVID-19 mRNA Vaccination

Vaccines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 43
Author(s):  
Tina Y. Poussaint ◽  
Kerri L. LaRovere ◽  
Jane W. Newburger ◽  
Janet Chou ◽  
Lise E. Nigrovic ◽  
...  

A 12-year-old male was presented to the hospital with acute encephalopathy, headache, vomiting, diarrhea, and elevated troponin after recent COVID-19 vaccination. Two days prior to admission and before symptom onset, he received the second dose of the Pfizer-BioNTech COVID-19 vaccine. Symptoms developed within 24 h with worsening neurologic symptoms, necessitating admission to the pediatric intensive care unit. Brain magnetic resonance imaging within 16 h of admission revealed a cytotoxic splenial lesion of the corpus callosum (CLOCC). Nineteen days prior to admission, he developed erythema migrans, and completed an amoxicillin treatment course for clinical Lyme disease. However, Lyme antibody titers were negative on admission and nine days later, making active Lyme disease an unlikely explanation for his presentation to hospital. An extensive workup for other etiologies on cerebrospinal fluid and blood samples was negative, including infectious and autoimmune causes and known immune deficiencies. Three weeks after hospital discharge, all of his symptoms had dissipated, and he had a normal neurologic exam. Our report highlights a potential role of mRNA vaccine-induced immunity leading to MIS-C-like symptoms with cardiac involvement and a CLOCC in a recently vaccinated child and the complexity of establishing a causal association with vaccination. The child recovered without receipt of immune modulatory treatment.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Caforio ◽  
S Gianstefani ◽  
A Baritussio ◽  
R Marcolongo ◽  
M Seguso ◽  
...  

Abstract Background Sarcoidosis is an immune-mediated disease; cardiac involvement, a granulomatous form of myocarditis, is under-recognised and prognostically relevant, as it can present with significant morbidity and mortality. Anti-heart autoantibodies (AHA) and anti-intercalated disk autoantibodies (AIDA) are reliable autoimmune markers in non-sarcoidosis myocarditis forms. Purpose The aim of this study was to assess the potential role of serum AHA and AIDA in cardiac sarcoidosis. Methods This is a cross-sectional study on a series of 29 patients with biopsy proven extra-cardiac sarcoidosis and with biopsy-proven or clinically suspected cardiac involvement, who were tested for AHA and AIDA. Patients were recruited in two recruiting tertiary centres, in USA and Italy. AHA and AIDA were detected by indirect immunofluorescence on human myocardium and skeletal muscle. Controls included sera from patients with non-inflammatory cardiac disease (NICD) (n=160), with ischemic heart failure (IHF) (n=141) and normal blood donors (NBD) (n=270). Results The frequencies of AHA and of AIDA were higher in sarcoidosis (86%; 62%) than in NICD (8%; 4%), IHF (7%; 2%), NBD (9%; 0%) (p=0.0001; p=0.0001 respectively). Sensitivity and specificity were: 86% and 92% for positive AHA and 62% and 98% for positive AIDA, respectively (see figure). Figure 1 Conclusions The detection of serum AHA and AIDA in biopsy-proven or clinically suspected cardiac sarcoidosis supports the involvement of heart-specific autoimmunity in the majority of our cases and may provide a novel non invasive diagnostic marker.


1995 ◽  
Vol 88 ◽  
pp. S142
Author(s):  
L. M. Shecterle ◽  
P. Gasper ◽  
J. A. St. Cyr. Jacqmar

2021 ◽  
Author(s):  
Andreia D. Magalhães ◽  
Marc Emmenegger ◽  
Elena De Cecco ◽  
Manfredi Carta ◽  
Karl Frontzek ◽  
...  

The microtubule-associated protein tau is involved in several neurodegenerative diseases and is currently being investigated as a plasma biomarker for the detection and monitoring of Alzheimer's disease and as an immunotherapeutical target in clinical trials. We assessed plasma anti-tau IgG reactivity in 40'098 unselected patients visiting a university hospital and healthy blood donors. We found that 4.97% patients and 1.58% healthy donors had natural anti-tau antibody titers >1.8 log10(EC50). In a multivariate model, female sex (P<0.001), age (P<0.001), cystitis (RR 1.59, 95%CI 1.14-2.16, P=0.004), other urinary disorders (RR 1.23, 95%CI 1.03-1.45, P=0.018), chronic kidney disease (RR 1.20, 95%CI 1.01-1.41, P=0.033), arterial embolism and thrombosis (RR 1.56, 95%CI 1.02-2.25, P=0.026) and atherosclerosis (RR 1.35, 95%CI 1.09-1.1.66, P=0.004) were independent predictors of anti-tau autoantibodies. We therefore conclude that anti-tau autoimmunity is associated with a systemic syndrome that includes vascular, kidney and urinary disorders. The expression of tau in these extraneural tissues suggests a potential role of autoimmunity in this syndrome.


1993 ◽  
Vol 2 (3) ◽  
pp. 225-228 ◽  
Author(s):  
E. Mayatepek ◽  
D. Hassler ◽  
M. Maiwald

The purpose of this study was to evaluate the potential role of LTB4and cysteinyl leukotrienes in Lyme disease (LD). Therefore, a total number of 34 patients divided into four groups was studied. The patients were classified as having Lyme arthritis (n = 7) or Lyme meningitis (n = 10), and as control groups patients with a noninflammatory arthropathy (NIA) (n = 7) and healthy subjects (n = 10). LTB4as well as LTC4secretion from stimulated polymorphonuclear leukocytes (PMNL) from all groups of patients showed no statistical differences. LTB4levels in synovial fluid were significantly increased in patients with Lyme arthritis (median 142 ng/ml, range 88–296) when compared to the control subjects with NIA (median 46 ng/ml, range 28–72) (p < 0.05). No statistical difference of urinary LTE4levels between all the different groups of patients was observed. These results show that cysteinyl leukotrienes do not play an important role in the pathogenesis of LD. In contrast to previous findings in rheumatoid arthritis, LTB4production from stimulated PMNL was not found to be increased in LD. However, the significantly elevated levels of LTB4in synovial fluid of patients with Lyme arthritis underline the involvement of LTB4in the pathogenesis of this disease.


2013 ◽  
Vol 19 (12) ◽  
Author(s):  
Marc Y. El Khoury ◽  
Jose F. Camargo ◽  
Jennifer L. White ◽  
Bryon P. Backenson ◽  
Alan P. Dupuis ◽  
...  

Discoveries ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. e120
Author(s):  
Abdul Rehman Arshad ◽  
◽  
Imtiaz Bashir ◽  
Farhat Ijaz ◽  
Nicholas Loh ◽  
...  

COVID-19 (coronavirus disease 2019) is a disease caused by the coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). COVID-19 has yielded many reported complications and unusual observations. In this article, we have reviewed one such observation: an association between malaria endemicity and reduced reported COVID-19 fatality. Malaria-endemic regions have a significantly lower reported COVID-19 fatality rate as compared to regions where malaria is non-endemic. Statistical analyses show that there is a strong negative correlation between the reported SARS-CoV-2 fatality and endemicity of malaria. In this review, we have discussed the potential role of CD-147, and potential malaria-induced immunity and polymorphisms in COVID-19 patients. Noteworthy, the results may also be due to underreported cases or due to the economic, political, and environmental differences between the malaria endemic and non-endemic countries. The study of this potential relationship might be of great help in COVID-19 therapy and prevention.


2019 ◽  
Vol 47 (5) ◽  
pp. 1393-1404 ◽  
Author(s):  
Thomas Brand

Abstract The Popeye domain-containing gene family encodes a novel class of cAMP effector proteins in striated muscle tissue. In this short review, we first introduce the protein family and discuss their structure and function with an emphasis on their role in cyclic AMP signalling. Another focus of this review is the recently discovered role of POPDC genes as striated muscle disease genes, which have been associated with cardiac arrhythmia and muscular dystrophy. The pathological phenotypes observed in patients will be compared with phenotypes present in null and knockin mutations in zebrafish and mouse. A number of protein–protein interaction partners have been discovered and the potential role of POPDC proteins to control the subcellular localization and function of these interacting proteins will be discussed. Finally, we outline several areas, where research is urgently needed.


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