scholarly journals A fatal case of COVID‐19‐associated acute necrotizing encephalopathy

2021 ◽  
Vol 28 (11) ◽  
pp. 3870-3872
Author(s):  
Dace Ziemele ◽  
Gundega Ķauķe ◽  
Krista Skrējāne ◽  
Līga Jaunozoliņa ◽  
Guntis Karelis
2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Yu-Jin Lee ◽  
D. Scott Smith ◽  
Vivek A. Rao ◽  
Robert D. Siegel ◽  
Jon Kosek ◽  
...  

Acute necrotizing encephalopathy (ANE) is a severe neurological complication of influenza infection, including H1N1 influenza. Many cases of ANE have been reported in the pediatric literature, but very few cases have been described in adults. The cause of ANE remains unknown—the influenza virus is not known to be neurotropic, and evidence of direct viral involvement of the central nervous system (CNS) has not been demonstrated in the limited cases of ANE in which pathological specimens have been obtained. Here we report a fatal case of ANE from H1N1 influenza infection in an adult. Neuroimaging and postmortem analysis both showed widespread brain edema, necrosis, and hemorrhage, but molecular studies and postmortem pathology revealed no evidence of direct viral involvement of the CNS. This case of fatal ANE in an adult is consistent with the hypothesis generated from pediatric cases that the host immune response, and not direct viral invasion of the CNS, is responsible for pathogenesis of ANE.


2021 ◽  
pp. 194187442199137
Author(s):  
Yan Wang ◽  
John R. Younce ◽  
Joel S. Perlmutter ◽  
Soe S. Mar

Acute necrotizing encephalopathy (ANE) is a rare para-infectious encephalopathy that classically occurs in children. However, ANE should be considered in the differential diagnosis of adults with symmetric brain lesions after a prodromal illness given recent reports of coronavirus disease of 2019 (COVID-19) to presumably cause ANE in adults. We report a case of a 29-year-old male presenting with fever, malaise, and rapid deterioration into coma. Brain magnetic resonance imaging revealed multifocal symmetric areas of diffusion restriction and surrounding vasogenic edema involving bilateral thalami, pons and cerebellar hemispheres with a core of susceptibility artifact, and minimal thalamic contrast enhancement, most consistent with ANE. Extensive infectious workup revealed isolated Escherichia coli and Neisseria gonorrhoeae in his urine. Despite the severe encephalopathy on initial presentation, the patient improved with intravenous antibiotics and supportive management with minimal residual deficits at 9 months follow-up. We aim to provide an overview of the radiological features, differential diagnosis, treatment and prognosis of ANE. Becoming familiarized with this rare but devastating disease will improve detection, treatment, and ultimately prognosis, especially in the era of a new pandemic.


2018 ◽  
Vol 40 (3) ◽  
pp. 639-641 ◽  
Author(s):  
Vedran Stevanović ◽  
Zoran Barušić ◽  
Klaudija Višković ◽  
Oktavija Đaković Rode ◽  
Goran Tešović

2011 ◽  
Vol 45 (5) ◽  
pp. 344-346 ◽  
Author(s):  
Akira Kumakura ◽  
Chihiro Iida ◽  
Makiko Saito ◽  
Masashi Mizuguchi ◽  
Daisuke Hata

2019 ◽  
Vol 29 (07) ◽  
pp. 649-653 ◽  
Author(s):  
Farida Jan ◽  
Sidra Jafri ◽  
Shahnaz Ibrahim

2019 ◽  
Author(s):  
Qingtang Shen ◽  
Yifan E. Wang ◽  
Mathew Truong ◽  
Kohila Mahadevan ◽  
Jing Ze Wu ◽  
...  

SUMMARYRanBP2/Nup358 is one of the main components of the cytoplasmic filaments of the nuclear pore complex. It has been speculated that RanBP2, which has an E3 SUMO-ligase domain, may alter the composition of messenger ribonucleoprotein (mRNP) complexes as they emerge from the nuclear pore and thus regulate the ultimate fate of the mRNA in the cytoplasm. Four separate missense mutations in RanBP2 cause Acute Necrotizing Encephalopathy 1 (ANE1), which manifests as a sharp rise in cytokine production after common viral infections such as influenza and parainfluenza. However, how RanBP2 and its ANE1-associated mutations affect cytokine production is not well understood. Here we report that RanBP2 represses the translation of the interleukin-6 (IL6) mRNA, which encodes a cytokine that is aberrantly up-regulated in ANE1. Our data indicates that soon after its production, the IL6 mRNP recruits the RNA-induced silencing complex (RISC) bound to Let7 miRNA. After this mRNP is exported, RanBP2 sumoylates the RISC-component AGO1, thereby stabilizing it and enforcing mRNA silencing. Collectively, these results support a model whereby RanBP2 promotes an mRNP remodelling event that is critical for the miRNA-mediated suppression of clinically relevant mRNAs, such as IL6.


2015 ◽  
Vol 52 (1) ◽  
pp. 110-114 ◽  
Author(s):  
Kevin Y. Wang ◽  
Harvey S. Singer ◽  
Barbara Crain ◽  
Sachin Gujar ◽  
Doris D.M. Lin

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