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...

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Autores principales: Nikolai Ravn Aarskog, MD, Hans Christian Aass, PhD, Jan Cato Holter, MD, PhD, Morten Rostrup, MD, PhD, Aleksander Rygh Holten, MD, PhD
Formato: article
Lenguaje:EN
Publicado: Wolters Kluwer 2021
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Acceso en línea:https://doaj.org/article/77ff7ef076ce42c0bd7b814e4a482e9c
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spelling oai:doaj.org-article:77ff7ef076ce42c0bd7b814e4a482e9c2021-11-25T07:56:43ZInterleukin-6 in Critical Coronavirus Disease 2019, a Driver of Lung Inflammation of Systemic Origin?2639-802810.1097/CCE.0000000000000542https://doaj.org/article/77ff7ef076ce42c0bd7b814e4a482e9c2021-10-01T00:00:00Zhttp://journals.lww.com/10.1097/CCE.0000000000000542https://doaj.org/toc/2639-8028OBJECTIVES:. 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.Nikolai Ravn Aarskog, MDHans Christian Aass, PhDJan Cato Holter, MD, PhDMorten Rostrup, MD, PhDAleksander Rygh Holten, MD, PhDWolters KluwerarticleMedical emergencies. Critical care. Intensive care. First aidRC86-88.9ENCritical Care Explorations, Vol 3, Iss 10, p e0542 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medical emergencies. Critical care. Intensive care. First aid
RC86-88.9
spellingShingle Medical emergencies. Critical care. Intensive care. First aid
RC86-88.9
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?
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.
format article
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
title 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_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_sort interleukin-6 in critical coronavirus disease 2019, a driver of lung inflammation of systemic origin?
publisher Wolters Kluwer
publishDate 2021
url https://doaj.org/article/77ff7ef076ce42c0bd7b814e4a482e9c
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