CovidFranceV1, Main, Exploration, bibRecord, 000768

Renin-angiotensin-aldosterone system and COVID-19 infection.

Identifieur interne : 000768 ( Main/Exploration ); précédent : 000767; suivant : 000769

Renin-angiotensin-aldosterone system and COVID-19 infection.

Auteurs : Joachim Alexandre [France] ; Jean-Luc Cracowski [France] ; Vincent Richard [France] ; Béatrice Bouhanick [France]

Source :

Annales d'endocrinologie [ 2213-3941 ] ; 2020.

RBID : pubmed:32370986

Descripteurs français

KwdFr :
- Abstention thérapeutique (MeSH), Aldostérone (métabolisme), Aldostérone (physiologie), Antagonistes du récepteur de type 1 de l'angiotensine-II (usage thérapeutique), Betacoronavirus (métabolisme), Comorbidité (MeSH), Guides de bonnes pratiques cliniques comme sujet (MeSH), Humains (MeSH), Hypertension artérielle (physiopathologie), Hypertension artérielle (traitement médicamenteux), Hypertension artérielle (épidémiologie), Indice de gravité de la maladie (MeSH), Infections à coronavirus (anatomopathologie), Infections à coronavirus (physiopathologie), Infections à coronavirus (épidémiologie), Inhibiteurs de l'enzyme de conversion de l'angiotensine (usage thérapeutique), Pandémies (MeSH), Peptidyl-Dipeptidase A (métabolisme), Pneumopathie virale (anatomopathologie), Pneumopathie virale (physiopathologie), Pneumopathie virale (épidémiologie), Pression sanguine (physiologie), Système rénine-angiotensine (physiologie).
MESH :
- anatomopathologie : Infections à coronavirus, Pneumopathie virale.
- métabolisme : Aldostérone, Betacoronavirus, Peptidyl-Dipeptidase A.
- physiologie : Aldostérone, Pression sanguine, Système rénine-angiotensine.
- physiopathologie : Hypertension artérielle, Infections à coronavirus, Pneumopathie virale.
- traitement médicamenteux : Hypertension artérielle.
- usage thérapeutique : Antagonistes du récepteur de type 1 de l'angiotensine-II, Inhibiteurs de l'enzyme de conversion de l'angiotensine.
- épidémiologie : Hypertension artérielle, Infections à coronavirus, Pneumopathie virale.
- Abstention thérapeutique, Comorbidité, Guides de bonnes pratiques cliniques comme sujet, Humains, Indice de gravité de la maladie, Pandémies.

English descriptors

KwdEn :
- Aldosterone (metabolism), Aldosterone (physiology), Angiotensin II Type 1 Receptor Blockers (therapeutic use), Angiotensin-Converting Enzyme Inhibitors (therapeutic use), Betacoronavirus (metabolism), Blood Pressure (physiology), Comorbidity (MeSH), Coronavirus Infections (epidemiology), Coronavirus Infections (pathology), Coronavirus Infections (physiopathology), Humans (MeSH), Hypertension (drug therapy), Hypertension (epidemiology), Hypertension (physiopathology), Pandemics (MeSH), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (epidemiology), Pneumonia, Viral (pathology), Pneumonia, Viral (physiopathology), Practice Guidelines as Topic (MeSH), Renin-Angiotensin System (physiology), Severity of Illness Index (MeSH), Withholding Treatment (MeSH).
MESH :
- chemical , metabolism : Aldosterone, Peptidyl-Dipeptidase A.
- chemical , physiology : Aldosterone.
- chemical , therapeutic use : Angiotensin II Type 1 Receptor Blockers, Angiotensin-Converting Enzyme Inhibitors.
- drug therapy : Hypertension.
- epidemiology : Coronavirus Infections, Hypertension, Pneumonia, Viral.
- metabolism : Betacoronavirus.
- pathology : Coronavirus Infections, Pneumonia, Viral.
- physiology : Blood Pressure, Renin-Angiotensin System.
- physiopathology : Coronavirus Infections, Hypertension, Pneumonia, Viral.
- Comorbidity, Humans, Pandemics, Practice Guidelines as Topic, Severity of Illness Index, Withholding Treatment.

Abstract

With the multiplication of COVID-19 severe acute respiratory syndrome cases due to SARS-COV2, some concerns about angiotensin-converting enzyme 1 (ACE1) inhibitors (ACEi) and angiotensin II type 1 receptor blockers (ARB) have emerged. Since the ACE2 (angiotensin-converting enzyme 2) enzyme is the receptor that allows SARS COV2 entry into cells, the fear was that pre-existing treatment with ACEi or ARB might increase the risk of developing severe or fatal severe acute respiratory syndrome in case of COVID-19 infection. The present article discusses these concerns. ACE2 is a membrane-bound enzyme (carboxypeptidase) that contributes to the inactivation of angiotensin II and therefore physiologically counters angiotensin II effects. ACEis do not inhibit ACE2. Although ARBs have been shown to up-regulate ACE2 tissue expression in experimental animals, evidence was not always consistent in human studies. Moreover, to date there is no evidence that ACEi or ARB administration facilitates SARS-COV2 cell entry by increasing ACE2 tissue expression in either animal or human studies. Finally, some studies support the hypothesis that elevated ACE2 membrane expression and tissue activity by administration of ARB and/or infusion of soluble ACE2 could confer protective properties against inflammatory tissue damage in COVID-19 infection. In summary, based on the currently available evidence and as advocated by many medical societies, ACEi or ARB should not be discontinued because of concerns with COVID-19 infection, except when the hemodynamic situation is precarious and case-by-case adjustment is required.

DOI: 10.1016/j.ando.2020.04.005
PubMed: 32370986
PubMed Central: PMC7172808

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 001444
to stream Main, to step Curation: 001444

Le document en format XML

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<term>Angiotensin II Type 1 Receptor Blockers (therapeutic use)</term>
<term>Angiotensin-Converting Enzyme Inhibitors (therapeutic use)</term>
<term>Betacoronavirus (metabolism)</term>
<term>Blood Pressure (physiology)</term>
<term>Comorbidity (MeSH)</term>
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<term>Hypertension (physiopathology)</term>
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<term>Pneumonia, Viral (epidemiology)</term>
<term>Pneumonia, Viral (pathology)</term>
<term>Pneumonia, Viral (physiopathology)</term>
<term>Practice Guidelines as Topic (MeSH)</term>
<term>Renin-Angiotensin System (physiology)</term>
<term>Severity of Illness Index (MeSH)</term>
<term>Withholding Treatment (MeSH)</term>
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<term>Aldostérone (métabolisme)</term>
<term>Aldostérone (physiologie)</term>
<term>Antagonistes du récepteur de type 1 de l'angiotensine-II (usage thérapeutique)</term>
<term>Betacoronavirus (métabolisme)</term>
<term>Comorbidité (MeSH)</term>
<term>Guides de bonnes pratiques cliniques comme sujet (MeSH)</term>
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<term>Hypertension artérielle (traitement médicamenteux)</term>
<term>Hypertension artérielle (épidémiologie)</term>
<term>Indice de gravité de la maladie (MeSH)</term>
<term>Infections à coronavirus (anatomopathologie)</term>
<term>Infections à coronavirus (physiopathologie)</term>
<term>Infections à coronavirus (épidémiologie)</term>
<term>Inhibiteurs de l'enzyme de conversion de l'angiotensine (usage thérapeutique)</term>
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<term>Pneumopathie virale (physiopathologie)</term>
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<term>Système rénine-angiotensine</term>
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<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Hypertension artérielle</term>
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<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antagonistes du récepteur de type 1 de l'angiotensine-II</term>
<term>Inhibiteurs de l'enzyme de conversion de l'angiotensine</term>
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<term>Guides de bonnes pratiques cliniques comme sujet</term>
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<term>Indice de gravité de la maladie</term>
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<front><div type="abstract" xml:lang="en">With the multiplication of COVID-19 severe acute respiratory syndrome cases due to SARS-COV2, some concerns about angiotensin-converting enzyme 1 (ACE1) inhibitors (ACEi) and angiotensin II type 1 receptor blockers (ARB) have emerged. Since the ACE2 (angiotensin-converting enzyme 2) enzyme is the receptor that allows SARS COV2 entry into cells, the fear was that pre-existing treatment with ACEi or ARB might increase the risk of developing severe or fatal severe acute respiratory syndrome in case of COVID-19 infection. The present article discusses these concerns. ACE2 is a membrane-bound enzyme (carboxypeptidase) that contributes to the inactivation of angiotensin II and therefore physiologically counters angiotensin II effects. ACEis do not inhibit ACE2. Although ARBs have been shown to up-regulate ACE2 tissue expression in experimental animals, evidence was not always consistent in human studies. Moreover, to date there is no evidence that ACEi or ARB administration facilitates SARS-COV2 cell entry by increasing ACE2 tissue expression in either animal or human studies. Finally, some studies support the hypothesis that elevated ACE2 membrane expression and tissue activity by administration of ARB and/or infusion of soluble ACE2 could confer protective properties against inflammatory tissue damage in COVID-19 infection. In summary, based on the currently available evidence and as advocated by many medical societies, ACEi or ARB should not be discontinued because of concerns with COVID-19 infection, except when the hemodynamic situation is precarious and case-by-case adjustment is required.</div>
</front>
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<Abstract><AbstractText>With the multiplication of COVID-19 severe acute respiratory syndrome cases due to SARS-COV2, some concerns about angiotensin-converting enzyme 1 (ACE1) inhibitors (ACEi) and angiotensin II type 1 receptor blockers (ARB) have emerged. Since the ACE2 (angiotensin-converting enzyme 2) enzyme is the receptor that allows SARS COV2 entry into cells, the fear was that pre-existing treatment with ACEi or ARB might increase the risk of developing severe or fatal severe acute respiratory syndrome in case of COVID-19 infection. The present article discusses these concerns. ACE2 is a membrane-bound enzyme (carboxypeptidase) that contributes to the inactivation of angiotensin II and therefore physiologically counters angiotensin II effects. ACEis do not inhibit ACE2. Although ARBs have been shown to up-regulate ACE2 tissue expression in experimental animals, evidence was not always consistent in human studies. Moreover, to date there is no evidence that ACEi or ARB administration facilitates SARS-COV2 cell entry by increasing ACE2 tissue expression in either animal or human studies. Finally, some studies support the hypothesis that elevated ACE2 membrane expression and tissue activity by administration of ARB and/or infusion of soluble ACE2 could confer protective properties against inflammatory tissue damage in COVID-19 infection. In summary, based on the currently available evidence and as advocated by many medical societies, ACEi or ARB should not be discontinued because of concerns with COVID-19 infection, except when the hemodynamic situation is precarious and case-by-case adjustment is required.</AbstractText>
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Renin-angiotensin-aldosterone system and COVID-19 infection.

Renin-angiotensin-aldosterone system and COVID-19 infection.

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