Результаты исследований: Научные публикации в периодических изданиях › редакционная статья › Рецензирование
Hypothesis : AA amyloidosis is a factor causing systemic complications after coronavirus disease. / Galkin, Alexey P.
в: Prion, Том 15, № 1, 2021, стр. 53-55.Результаты исследований: Научные публикации в периодических изданиях › редакционная статья › Рецензирование
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TY - JOUR
T1 - Hypothesis
T2 - AA amyloidosis is a factor causing systemic complications after coronavirus disease
AU - Galkin, Alexey P.
N1 - Publisher Copyright: © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
PY - 2021
Y1 - 2021
N2 - The severe course of COVID-19 causes systemic chronic inflammation and thrombosis in a wide variety of organs and tissues. The nature of these inflammations remains a mystery, although they are known to occur against the background of a high level of cytokine production. The high level of cytokines provokes overproduction of the Serum amyloid A (SAA) protein. Moreover, the number of studies has shown that the severe COVID-19 causes SAA overproduction. The authors of these works regard a high level of SAA exclusively as a biomarker of COVID-19. However, it should be borne in mind that overproduction of SAA can cause systemic AA amyloidosis. SAA forms cytotoxic amyloid deposits in various organs and induces inflammation and thrombosis. The consequences of COVID-19 infection are surprisingly similar to the clinical picture that is observed in AA amyloidosis. Here I present the hypothesis that AA amyloidosis is a factor causing systemic complications after coronavirus disease.
AB - The severe course of COVID-19 causes systemic chronic inflammation and thrombosis in a wide variety of organs and tissues. The nature of these inflammations remains a mystery, although they are known to occur against the background of a high level of cytokine production. The high level of cytokines provokes overproduction of the Serum amyloid A (SAA) protein. Moreover, the number of studies has shown that the severe COVID-19 causes SAA overproduction. The authors of these works regard a high level of SAA exclusively as a biomarker of COVID-19. However, it should be borne in mind that overproduction of SAA can cause systemic AA amyloidosis. SAA forms cytotoxic amyloid deposits in various organs and induces inflammation and thrombosis. The consequences of COVID-19 infection are surprisingly similar to the clinical picture that is observed in AA amyloidosis. Here I present the hypothesis that AA amyloidosis is a factor causing systemic complications after coronavirus disease.
KW - AA amyloidosis
KW - chronic inflammation
KW - Coronavirus
KW - COVID-19
KW - serum amyloid A
KW - COVID-19/complications
KW - Humans
KW - Biomarkers
KW - Inflammation
KW - Amyloidosis/blood
KW - Serum Amyloid A Protein
UR - http://www.scopus.com/inward/record.url?scp=85104696292&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/a12f7b5b-cb92-30d1-b447-be5a0e532d1c/
U2 - 10.1080/19336896.2021.1910468
DO - 10.1080/19336896.2021.1910468
M3 - Editorial
C2 - 33876719
AN - SCOPUS:85104696292
VL - 15
SP - 53
EP - 55
JO - Prion
JF - Prion
SN - 1933-6896
IS - 1
ER -
ID: 88151247