The Cross-Talk between Age, Hypertension and Inflammation in COVID-19 Patients: Therapeutic Targets.
Identifieur interne : 000B50 ( Main/Exploration ); précédent : 000B49; suivant : 000B51The Cross-Talk between Age, Hypertension and Inflammation in COVID-19 Patients: Therapeutic Targets.
Auteurs : Gerardo Casucci [Italie] ; Domenico Acanfora [Italie] ; Raffaele Antonelli Incalzi [Italie]Source :
- Drugs & aging [ 1179-1969 ] ; 2020.
Descripteurs français
- KwdFr :
- Antagonistes des récepteurs aux angiotensines (pharmacologie), Betacoronavirus (effets des médicaments et des substances chimiques), Betacoronavirus (physiologie), Facteurs immunologiques (pharmacologie), Humains (MeSH), Hypertension artérielle (traitement médicamenteux), Infections à coronavirus (immunologie), Infections à coronavirus (métabolisme), Infections à coronavirus (traitement médicamenteux), Infections à coronavirus (virologie), Inflammation (immunologie), Inflammation (traitement médicamenteux), Inhibiteurs de l'enzyme de conversion de l'angiotensine (pharmacologie), Néprilysine (antagonistes et inhibiteurs), Pandémies (MeSH), Peptidyl-Dipeptidase A (métabolisme), Pneumopathie virale (immunologie), Pneumopathie virale (métabolisme), Pneumopathie virale (traitement médicamenteux), Pneumopathie virale (virologie), Sujet âgé (MeSH), Système rénine-angiotensine (effets des médicaments et des substances chimiques).
- MESH :
- antagonistes et inhibiteurs : Néprilysine.
- effets des médicaments et des substances chimiques : Betacoronavirus, Système rénine-angiotensine.
- immunologie : Infections à coronavirus, Inflammation, Pneumopathie virale.
- métabolisme : Infections à coronavirus, Peptidyl-Dipeptidase A, Pneumopathie virale.
- pharmacologie : Antagonistes des récepteurs aux angiotensines, Facteurs immunologiques, Inhibiteurs de l'enzyme de conversion de l'angiotensine.
- physiologie : Betacoronavirus.
- traitement médicamenteux : Hypertension artérielle, Infections à coronavirus, Inflammation, Pneumopathie virale.
- virologie : Infections à coronavirus, Pneumopathie virale.
- Humains, Pandémies, Sujet âgé.
English descriptors
- KwdEn :
- Aged (MeSH), Angiotensin Receptor Antagonists (pharmacology), Angiotensin-Converting Enzyme 2 (MeSH), Angiotensin-Converting Enzyme Inhibitors (pharmacology), Betacoronavirus (drug effects), Betacoronavirus (physiology), COVID-19 (MeSH), Coronavirus Infections (drug therapy), Coronavirus Infections (immunology), Coronavirus Infections (metabolism), Coronavirus Infections (virology), Cytokine Release Syndrome (drug therapy), Cytokine Release Syndrome (immunology), Humans (MeSH), Hypertension (drug therapy), Immunologic Factors (pharmacology), Inflammation (drug therapy), Inflammation (immunology), Neprilysin (antagonists & inhibitors), Pandemics (MeSH), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (drug therapy), Pneumonia, Viral (immunology), Pneumonia, Viral (metabolism), Pneumonia, Viral (virology), Renin-Angiotensin System (drug effects), SARS-CoV-2 (MeSH).
- MESH :
- chemical , antagonists & inhibitors : Neprilysin.
- chemical , metabolism : Peptidyl-Dipeptidase A.
- chemical , pharmacology : Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Immunologic Factors.
- drug effects : Betacoronavirus, Renin-Angiotensin System.
- drug therapy : Coronavirus Infections, Cytokine Release Syndrome, Hypertension, Inflammation, Pneumonia, Viral.
- immunology : Coronavirus Infections, Cytokine Release Syndrome, Inflammation, Pneumonia, Viral.
- metabolism : Coronavirus Infections, Pneumonia, Viral.
- physiology : Betacoronavirus.
- virology : Coronavirus Infections, Pneumonia, Viral.
- Aged, Angiotensin-Converting Enzyme 2, COVID-19, Humans, Pandemics, SARS-CoV-2.
Abstract
This paper presents a brief overview of the complex interaction between age, hypertension, the renin-angiotensin-aldosterone system (RAAS), inflammation, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection. Coronavirus disease 2019 (COVID-19) is more frequent and more severe in comorbid elderly patients, especially those with hypertension, diabetes, obesity, or cardiovascular diseases. There are concerns regarding the use of RAAS inhibitors in patients with COVID-19. Some physicians have considered the need for interrupting RAAS inhibition in order to reduce the possibility of SARS-CoV2 entering lung cells after binding to angiotensin-converting enzyme 2 (ACE2) receptors. We offer a different point of view in relation to the need for continuing to use RAAS inhibitors in patients with COVID-19. We focused our article on elderly patients because of the distinctive imbalance between the immune response, which is depressed, and the exacerbated inflammatory response, 'inflammaging', which makes the geriatric patient an appropriate candidate for therapeutic strategies aimed at modulating the inflammatory response. Indeed, COVID-19 is an inflammatory storm that starts and worsens during the course of the disease. During the COVID-19 pandemic, various therapeutic approaches have been tested, including antiviral drugs, interferon, anti-interleukins, hydroxychloroquine, anti-inflammatories, immunoglobulins from recovered patients, and heparins. Some of these therapeutic approaches did not prove to be beneficial, or even induced serious complications. Based on current evidence, in the early stages of the disease modulation of the inflammatory response through the inhibition of neprilysin and modulation of the RAAS could affect the course and outcome of COVID-19.
DOI: 10.1007/s40266-020-00808-4
PubMed: 33084001
PubMed Central: PMC7575413
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged (MeSH)</term>
<term>Angiotensin Receptor Antagonists (pharmacology)</term>
<term>Angiotensin-Converting Enzyme 2 (MeSH)</term>
<term>Angiotensin-Converting Enzyme Inhibitors (pharmacology)</term>
<term>Betacoronavirus (drug effects)</term>
<term>Betacoronavirus (physiology)</term>
<term>COVID-19 (MeSH)</term>
<term>Coronavirus Infections (drug therapy)</term>
<term>Coronavirus Infections (immunology)</term>
<term>Coronavirus Infections (metabolism)</term>
<term>Coronavirus Infections (virology)</term>
<term>Cytokine Release Syndrome (drug therapy)</term>
<term>Cytokine Release Syndrome (immunology)</term>
<term>Humans (MeSH)</term>
<term>Hypertension (drug therapy)</term>
<term>Immunologic Factors (pharmacology)</term>
<term>Inflammation (drug therapy)</term>
<term>Inflammation (immunology)</term>
<term>Neprilysin (antagonists & inhibitors)</term>
<term>Pandemics (MeSH)</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
<term>Pneumonia, Viral (drug therapy)</term>
<term>Pneumonia, Viral (immunology)</term>
<term>Pneumonia, Viral (metabolism)</term>
<term>Pneumonia, Viral (virology)</term>
<term>Renin-Angiotensin System (drug effects)</term>
<term>SARS-CoV-2 (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Antagonistes des récepteurs aux angiotensines (pharmacologie)</term>
<term>Betacoronavirus (effets des médicaments et des substances chimiques)</term>
<term>Betacoronavirus (physiologie)</term>
<term>Facteurs immunologiques (pharmacologie)</term>
<term>Humains (MeSH)</term>
<term>Hypertension artérielle (traitement médicamenteux)</term>
<term>Infections à coronavirus (immunologie)</term>
<term>Infections à coronavirus (métabolisme)</term>
<term>Infections à coronavirus (traitement médicamenteux)</term>
<term>Infections à coronavirus (virologie)</term>
<term>Inflammation (immunologie)</term>
<term>Inflammation (traitement médicamenteux)</term>
<term>Inhibiteurs de l'enzyme de conversion de l'angiotensine (pharmacologie)</term>
<term>Néprilysine (antagonistes et inhibiteurs)</term>
<term>Pandémies (MeSH)</term>
<term>Peptidyl-Dipeptidase A (métabolisme)</term>
<term>Pneumopathie virale (immunologie)</term>
<term>Pneumopathie virale (métabolisme)</term>
<term>Pneumopathie virale (traitement médicamenteux)</term>
<term>Pneumopathie virale (virologie)</term>
<term>Sujet âgé (MeSH)</term>
<term>Système rénine-angiotensine (effets des médicaments et des substances chimiques)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Neprilysin</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Peptidyl-Dipeptidase A</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Angiotensin Receptor Antagonists</term>
<term>Angiotensin-Converting Enzyme Inhibitors</term>
<term>Immunologic Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Néprilysine</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Betacoronavirus</term>
<term>Renin-Angiotensin System</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronavirus Infections</term>
<term>Cytokine Release Syndrome</term>
<term>Hypertension</term>
<term>Inflammation</term>
<term>Pneumonia, Viral</term>
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<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Betacoronavirus</term>
<term>Système rénine-angiotensine</term>
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<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Inflammation</term>
<term>Pneumopathie virale</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus Infections</term>
<term>Cytokine Release Syndrome</term>
<term>Inflammation</term>
<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Coronavirus Infections</term>
<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Pneumopathie virale</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antagonistes des récepteurs aux angiotensines</term>
<term>Facteurs immunologiques</term>
<term>Inhibiteurs de l'enzyme de conversion de l'angiotensine</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Betacoronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Betacoronavirus</term>
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<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Hypertension artérielle</term>
<term>Infections à coronavirus</term>
<term>Inflammation</term>
<term>Pneumopathie virale</term>
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<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Pneumopathie virale</term>
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<term>Pandémies</term>
<term>Sujet âgé</term>
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<front><div type="abstract" xml:lang="en">This paper presents a brief overview of the complex interaction between age, hypertension, the renin-angiotensin-aldosterone system (RAAS), inflammation, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection. Coronavirus disease 2019 (COVID-19) is more frequent and more severe in comorbid elderly patients, especially those with hypertension, diabetes, obesity, or cardiovascular diseases. There are concerns regarding the use of RAAS inhibitors in patients with COVID-19. Some physicians have considered the need for interrupting RAAS inhibition in order to reduce the possibility of SARS-CoV2 entering lung cells after binding to angiotensin-converting enzyme 2 (ACE2) receptors. We offer a different point of view in relation to the need for continuing to use RAAS inhibitors in patients with COVID-19. We focused our article on elderly patients because of the distinctive imbalance between the immune response, which is depressed, and the exacerbated inflammatory response, 'inflammaging', which makes the geriatric patient an appropriate candidate for therapeutic strategies aimed at modulating the inflammatory response. Indeed, COVID-19 is an inflammatory storm that starts and worsens during the course of the disease. During the COVID-19 pandemic, various therapeutic approaches have been tested, including antiviral drugs, interferon, anti-interleukins, hydroxychloroquine, anti-inflammatories, immunoglobulins from recovered patients, and heparins. Some of these therapeutic approaches did not prove to be beneficial, or even induced serious complications. Based on current evidence, in the early stages of the disease modulation of the inflammatory response through the inhibition of neprilysin and modulation of the RAAS could affect the course and outcome of COVID-19.</div>
</front>
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<DateCompleted><Year>2020</Year>
<Month>11</Month>
<Day>11</Day>
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<Month>01</Month>
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<Title>Drugs & aging</Title>
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<ArticleTitle>The Cross-Talk between Age, Hypertension and Inflammation in COVID-19 Patients: Therapeutic Targets.</ArticleTitle>
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<Abstract><AbstractText>This paper presents a brief overview of the complex interaction between age, hypertension, the renin-angiotensin-aldosterone system (RAAS), inflammation, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection. Coronavirus disease 2019 (COVID-19) is more frequent and more severe in comorbid elderly patients, especially those with hypertension, diabetes, obesity, or cardiovascular diseases. There are concerns regarding the use of RAAS inhibitors in patients with COVID-19. Some physicians have considered the need for interrupting RAAS inhibition in order to reduce the possibility of SARS-CoV2 entering lung cells after binding to angiotensin-converting enzyme 2 (ACE2) receptors. We offer a different point of view in relation to the need for continuing to use RAAS inhibitors in patients with COVID-19. We focused our article on elderly patients because of the distinctive imbalance between the immune response, which is depressed, and the exacerbated inflammatory response, 'inflammaging', which makes the geriatric patient an appropriate candidate for therapeutic strategies aimed at modulating the inflammatory response. Indeed, COVID-19 is an inflammatory storm that starts and worsens during the course of the disease. During the COVID-19 pandemic, various therapeutic approaches have been tested, including antiviral drugs, interferon, anti-interleukins, hydroxychloroquine, anti-inflammatories, immunoglobulins from recovered patients, and heparins. Some of these therapeutic approaches did not prove to be beneficial, or even induced serious complications. Based on current evidence, in the early stages of the disease modulation of the inflammatory response through the inhibition of neprilysin and modulation of the RAAS could affect the course and outcome of COVID-19.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Casucci</LastName>
<ForeName>Gerardo</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Unit of Internal Medicine, San Francesco Hospital, Viale Europa 21, 82037, Telese Terme, BN, Italy.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Acanfora</LastName>
<ForeName>Domenico</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Unit of Internal Medicine, San Francesco Hospital, Viale Europa 21, 82037, Telese Terme, BN, Italy. domenico.acanfora29@gmail.com.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Incalzi</LastName>
<ForeName>Raffaele Antonelli</ForeName>
<Initials>RA</Initials>
<AffiliationInfo><Affiliation>Unit of Geriatrics, Policlinico Universitario Campus Bio-Medico di Roma, Via Álvaro del Portillo 21, 00128, Rome, Italy.</Affiliation>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
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<MeshHeading><DescriptorName UI="D007155" MajorTopicYN="N">Immunologic Factors</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D007249" MajorTopicYN="Y">Inflammation</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
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<MeshHeading><DescriptorName UI="D015260" MajorTopicYN="N">Neprilysin</DescriptorName>
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