Interleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin?
OBJECTIVES:. To examine whether interleukin-6 in critical coronavirus disease 2019 is higher in arterial than in central venous blood, as a sign of predominantly local pulmonal rather than systemic interleukin-6 production. DESIGN:. Prospective cohort pilot study with repeated weekly measurements of...
Main Authors: | , , , , |
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Format: | Article |
Language: | English |
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Wolters Kluwer
2021-10-01
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Series: | Critical Care Explorations |
Online Access: | http://journals.lww.com/10.1097/CCE.0000000000000542 |
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author | Nikolai Ravn Aarskog, MD Hans Christian Aass, PhD Jan Cato Holter, MD, PhD Morten Rostrup, MD, PhD Aleksander Rygh Holten, MD, PhD |
author_facet | Nikolai Ravn Aarskog, MD Hans Christian Aass, PhD Jan Cato Holter, MD, PhD Morten Rostrup, MD, PhD Aleksander Rygh Holten, MD, PhD |
author_sort | Nikolai Ravn Aarskog, MD |
collection | DOAJ |
description | OBJECTIVES:. To examine whether interleukin-6 in critical coronavirus disease 2019 is higher in arterial than in central venous blood, as a sign of predominantly local pulmonal rather than systemic interleukin-6 production.
DESIGN:. Prospective cohort pilot study with repeated weekly measurements of interleukin-6 in arterial and central venous blood. Respiratory function, assessed with Pao2/Fio2 ratio, was measured at the time of blood sampling.
SETTING:. ICU at a university hospital.
SUBJECTS:. Nine adult patients with critical coronavirus disease 2019, actively treated and receiving mechanical ventilation.
MEASUREMENTS AND MAIN RESULTS:. No difference between arterial and central venous interleukin-6 was found. There was a significant negative relationship between interleukin-6 concentration and P/F ratio in both arterial (p = 0.04) and central venous (p = 0.03) blood.
CONCLUSIONS:. The absence of an arteriovenous interleukin-6 difference implies that interleukin-6 in critical coronavirus disease 2019 is mainly produced outside the lungs as part of a systemic inflammatory response syndrome and act as a driver of local inflammation and damage in the lungs. |
first_indexed | 2024-12-14T06:05:47Z |
format | Article |
id | doaj.art-77ff7ef076ce42c0bd7b814e4a482e9c |
institution | Directory Open Access Journal |
issn | 2639-8028 |
language | English |
last_indexed | 2024-12-14T06:05:47Z |
publishDate | 2021-10-01 |
publisher | Wolters Kluwer |
record_format | Article |
series | Critical Care Explorations |
spelling | doaj.art-77ff7ef076ce42c0bd7b814e4a482e9c2022-12-21T23:14:18ZengWolters KluwerCritical Care Explorations2639-80282021-10-01310e054210.1097/CCE.0000000000000542202110000-00003Interleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin?Nikolai Ravn Aarskog, MD0Hans Christian Aass, PhD1Jan Cato Holter, MD, PhD2Morten Rostrup, MD, PhD3Aleksander Rygh Holten, MD, PhD41 Department of Acute Medicine, Oslo University Hospital, Oslo, Norway.2 Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway.3 Department of Microbiology, Oslo University Hospital, Oslo, Norway.1 Department of Acute Medicine, Oslo University Hospital, Oslo, Norway.1 Department of Acute Medicine, Oslo University Hospital, Oslo, Norway.OBJECTIVES:. To examine whether interleukin-6 in critical coronavirus disease 2019 is higher in arterial than in central venous blood, as a sign of predominantly local pulmonal rather than systemic interleukin-6 production. DESIGN:. Prospective cohort pilot study with repeated weekly measurements of interleukin-6 in arterial and central venous blood. Respiratory function, assessed with Pao2/Fio2 ratio, was measured at the time of blood sampling. SETTING:. ICU at a university hospital. SUBJECTS:. Nine adult patients with critical coronavirus disease 2019, actively treated and receiving mechanical ventilation. MEASUREMENTS AND MAIN RESULTS:. No difference between arterial and central venous interleukin-6 was found. There was a significant negative relationship between interleukin-6 concentration and P/F ratio in both arterial (p = 0.04) and central venous (p = 0.03) blood. CONCLUSIONS:. The absence of an arteriovenous interleukin-6 difference implies that interleukin-6 in critical coronavirus disease 2019 is mainly produced outside the lungs as part of a systemic inflammatory response syndrome and act as a driver of local inflammation and damage in the lungs.http://journals.lww.com/10.1097/CCE.0000000000000542 |
spellingShingle | Nikolai Ravn Aarskog, MD Hans Christian Aass, PhD Jan Cato Holter, MD, PhD Morten Rostrup, MD, PhD Aleksander Rygh Holten, MD, PhD Interleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin? Critical Care Explorations |
title | Interleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin? |
title_full | Interleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin? |
title_fullStr | Interleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin? |
title_full_unstemmed | Interleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin? |
title_short | Interleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin? |
title_sort | interleukin 6 in critical coronavirus disease 2019 a driver of lung inflammation of systemic origin |
url | http://journals.lww.com/10.1097/CCE.0000000000000542 |
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