Increased levels of plasma cytokines and correlations to organ failure and 30-day mortality in critically ill Covid-19 patients.

Bülow Anderberg S, Luther T, Berglund M, Larsson R, Rubertsson S, Lipcsey M, Larsson A, Frithiof R, Hultström M

Cytokine 138 (-) 155389 [2021-02-00; online 2020-12-14]

The infection caused by SARS CoV-2 has been postulated to induce a cytokine storm syndrome that results in organ failure and even death in a considerable number of patients. However, the inflammatory response in Corona virus disease-19 (Covid-19) and its potential to cause collateral organ damage has not been fully elucidated to date. This study aims to characterize the acute cytokine response in a cohort of critically ill Covid-19 patients. 24 adults with PCR-confirmed Covid-19 were included at time of admission to intensive care a median of eleven days after initial symptoms. Eleven adult patients admitted for elective abdominal surgery with preoperative plasma samples served as controls. All patients were included after informed consent was obtained. 27 cytokines were quantified in plasma. The expression of inflammatory mediators was then related to routine inflammatory markers, SAPS3, SOFA score, organ failure and 30-day mortality. A general increase in cytokine expression was observed in all Covid-19 patients. A strong correlation between respiratory failure and IL-1ra, IL-4, IL-6, IL-8 and IP-10 expression was observed. Acute kidney injury development correlated well with increased levels of IL-1ra, IL-6, IL-8, IL-17a, IP-10 and MCP-1. Generally, the cohort demonstrated weaker correlations between cytokine expression and 30-day mortality out of which IL-8 showed the strongest signal in terms of mortality. The present study found that respiratory failure, acute kidney injury and 30-day mortality in critically ill Covid-19 patients are associated with moderate increases of a broad range of inflammatory mediators at time of admission.

Category: Health

Funder: KAW/SciLifeLab

Funder: VR

Research Area: Biobanks for COVID-19 research

Type: Journal article

PubMed 33348065

DOI 10.1016/j.cyto.2020.155389

Crossref 10.1016/j.cyto.2020.155389

pii: S1043-4666(20)30405-1
pmc: PMC7833204

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