Biomarkers and prognostic models for severe COVID-19 in comparison with other etiologies of sepsis
- 作者: Sсherbak S.1,2, Sarana A.2,3, Vologzhanin D.1,2, Golota A.1, Kamilova T.1, Makarenko S.1,2
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隶属关系:
- City Hospital No. 40 Kurortny District
- St Petersburg University
- Health Committee of the Administration of Saint Petersburg
- 期: 卷 29, 编号 4 (2023)
- 页面: 325-348
- 栏目: Reviews
- URL: https://journals.rcsi.science/0869-2106/article/view/133935
- DOI: https://doi.org/10.17816/medjrf545995
- ID: 133935
如何引用文章
详细
Severe COVID-19 shares pathophysiological, immunological, metabolic, and clinical features with classic bacterial sepsis. Patients with severe COVID-19 have sepsis-like manifestations, such as acute respiratory distress syndrome and multiple organ failure. However, research indicates that COVID-19 leads to acute respiratory distress syndrome and that septic syndrome is more fatal than septic syndrome of other etiologies. SARS-CoV-2 initially infects the lungs; however, in COVID-19-associated sepsis, the majority of deaths are caused by the subsequent involvement of multiple organs. Many patients who died because of COVID-19 died from sepsis, a life-threatening dysfunctional response to infection that is accompanied by respiratory and multiple organ failure.
Overlapping molecular characteristics are found in patients with severe COVID-19 and sepsis from all causes. Endotypes that reflect different etiologies of sepsis have been identified in patients with severe COVID-19. Whole-blood proteomics and transcriptomics are useful in identifying the pathogenetic mechanisms and multimolecular signatures of COVID-associated sepsis and other sepsis, which allow for the development of more specific criteria for early diagnosis, patient classification, and therapeutic choices.
The detection of sepsis endotypes in patients with COVID-19 implies that sepsis endotypes may be useful for clinical risk stratification in COVID-associated sepsis and the potential opportunity to treat these patients with targeted immunomodulatory therapies that can correct endotype-specific dysfunctional immune processes.
作者简介
Sergey Sсherbak
City Hospital No. 40 Kurortny District; St Petersburg University
Email: b40@zdrav.spb.ru
ORCID iD: 0000-0001-5036-1259
SPIN 代码: 1537-9822
MD, dr. sci. (med.), professor
俄罗斯联邦, 9B Borisova street, 197706 SestroretskAndrey Sarana
St Petersburg University; Health Committee of the Administration of Saint Petersburg
Email: asarana@mail.ru
ORCID iD: 0000-0003-3198-8990
SPIN 代码: 7922-2751
MD, cand. sci. (med.), associate professor
俄罗斯联邦, Saint-PetersburgDmitry Vologzhanin
City Hospital No. 40 Kurortny District; St Petersburg University
Email: volog@bk.ru
ORCID iD: 0000-0002-1176-794X
SPIN 代码: 7922-7302
MD, dr. sci. med.)
俄罗斯联邦, 9B Borisova street, Sestroretsk, 197706Aleksandr Golota
City Hospital No. 40 Kurortny District
Email: golotaa@yahoo.com
ORCID iD: 0000-0002-5632-3963
MD, cand. sci. (med.), associate professor
俄罗斯联邦, 9B Borisova street, 197706 SestroretskTatiana Kamilova
City Hospital No. 40 Kurortny District
Email: kamilovaspb@mail.ru
ORCID iD: 0000-0001-6360-132X
SPIN 代码: 2922-4404
cand. sci. (biol.)
俄罗斯联邦, 9B Borisova street, 197706 SestroretskStanislav Makarenko
City Hospital No. 40 Kurortny District; St Petersburg University
编辑信件的主要联系方式.
Email: st.makarenko@gmail.com
ORCID iD: 0000-0002-1595-6668
SPIN 代码: 8114-3984
俄罗斯联邦, 9B Borisova street, 197706 Sestroretsk
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