CovidSeniorV1, Main, Exploration, bibRecord, 000107

Treatment of COVID-19 With Conestat Alfa, a Regulator of the Complement, Contact Activation and Kallikrein-Kinin System.

Identifieur interne : 000107 ( Main/Exploration ); précédent : 000106; suivant : 000108

Treatment of COVID-19 With Conestat Alfa, a Regulator of the Complement, Contact Activation and Kallikrein-Kinin System.

Auteurs : Pascal Urwyler [Suisse] ; Stephan Moser [Suisse] ; Panteleimon Charitos [Suisse] ; Ingmar A F M. Heijnen [Suisse] ; Melanie Rudin [Suisse] ; Gregor Sommer [Suisse] ; Bruno M. Giannetti [Pays-Bas] ; Stefano Bassetti [Suisse] ; Parham Sendi [Suisse] ; Marten Trendelenburg [Suisse] ; Michael Osthoff [Suisse]

Source :

Frontiers in immunology [ 1664-3224 ] ; 2020.

RBID : pubmed:32922409

Descripteurs français

KwdFr :
- Adulte d'âge moyen (MeSH), Betacoronavirus (effets des médicaments et des substances chimiques), C1 Inhibiteur (analyse), C1 Inhibiteur (usage thérapeutique), Charge virale (effets des médicaments et des substances chimiques), Complément C1 (antagonistes et inhibiteurs), Facteur XIa (antagonistes et inhibiteurs), Femelle (MeSH), Humains (MeSH), Infections à coronavirus (traitement médicamenteux), Kallicréines (antagonistes et inhibiteurs), Mâle (MeSH), Pandémies (MeSH), Pneumopathie virale (traitement médicamenteux), Protéines recombinantes (usage thérapeutique), Sujet âgé (MeSH), Sujet âgé de 80 ans ou plus (MeSH), Système kallicréine-kinine (effets des médicaments et des substances chimiques).
MESH :
- analyse : C1 Inhibiteur.
- antagonistes et inhibiteurs : Complément C1, Facteur XIa, Kallicréines.
- effets des médicaments et des substances chimiques : Betacoronavirus, Charge virale, Système kallicréine-kinine.
- traitement médicamenteux : Infections à coronavirus, Pneumopathie virale.
- usage thérapeutique : C1 Inhibiteur, Protéines recombinantes.
- Adulte d'âge moyen, Femelle, Humains, Mâle, Pandémies, Sujet âgé, Sujet âgé de 80 ans ou plus.

English descriptors

KwdEn :
- Aged (MeSH), Aged, 80 and over (MeSH), Betacoronavirus (drug effects), Complement C1 (antagonists & inhibitors), Complement C1 Inhibitor Protein (analysis), Complement C1 Inhibitor Protein (therapeutic use), Coronavirus Infections (drug therapy), Cytokine Release Syndrome (drug therapy), Factor XIa (antagonists & inhibitors), Female (MeSH), Humans (MeSH), Kallikrein-Kinin System (drug effects), Kallikreins (antagonists & inhibitors), Male (MeSH), Middle Aged (MeSH), Pandemics (MeSH), Pneumonia, Viral (drug therapy), Recombinant Proteins (therapeutic use), Viral Load (drug effects).
MESH :
- chemical , analysis : Complement C1 Inhibitor Protein.
- chemical , antagonists & inhibitors : Complement C1, Factor XIa, Kallikreins.
- drug effects : Betacoronavirus, Kallikrein-Kinin System, Viral Load.
- drug therapy : Coronavirus Infections, Cytokine Release Syndrome, Pneumonia, Viral.
- chemical , therapeutic use : Complement C1 Inhibitor Protein, Recombinant Proteins.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Pandemics.

Abstract

A dysregulated immune response with hyperinflammation is observed in patients with severe coronavirus disease 2019 (COVID-19). The aim of the present study was to assess the safety and potential benefits of human recombinant C1 esterase inhibitor (conestat alfa), a complement, contact activation and kallikrein-kinin system regulator, in severe COVID-19. Patients with evidence of progressive disease after 24 h including an oxygen saturation <93% at rest in ambient air were included at the University Hospital Basel, Switzerland in April 2020. Conestat alfa was administered by intravenous injections of 8400 IU followed by 3 additional doses of 4200 IU in 12-h intervals. Five patients (age range, 53-85 years; one woman) with severe COVID-19 pneumonia (11-39% lung involvement on computed tomography scan of the chest) were treated a median of 1 day (range 1-7 days) after admission. Treatment was well-tolerated. Immediate defervescence occurred, and inflammatory markers and oxygen supplementation decreased or stabilized in 4 patients (e.g., median C-reactive protein 203 (range 31-235) mg/L before vs. 32 (12-72) mg/L on day 5). Only one patient required mechanical ventilation. All patients recovered. C1INH concentrations were elevated before conestat alfa treatment. Levels of complement activation products declined after treatment. Viral loads in nasopharyngeal swabs declined in 4 patients. In this uncontrolled case series, targeting multiple inflammatory cascades by conestat alfa was safe and associated with clinical improvements in the majority of severe COVID-19 patients. Controlled clinical trials are needed to assess its safety and efficacy in preventing disease progression.

DOI: 10.3389/fimmu.2020.02072
PubMed: 32922409
PubMed Central: PMC7456998

Affiliations:

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

to stream Main, to step Corpus: 000231
to stream Main, to step Curation: 000231

Le document en format XML

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<front><div type="abstract" xml:lang="en">A dysregulated immune response with hyperinflammation is observed in patients with severe coronavirus disease 2019 (COVID-19). The aim of the present study was to assess the safety and potential benefits of human recombinant C1 esterase inhibitor (conestat alfa), a complement, contact activation and kallikrein-kinin system regulator, in severe COVID-19. Patients with evidence of progressive disease after 24 h including an oxygen saturation <93% at rest in ambient air were included at the University Hospital Basel, Switzerland in April 2020. Conestat alfa was administered by intravenous injections of 8400 IU followed by 3 additional doses of 4200 IU in 12-h intervals. Five patients (age range, 53-85 years; one woman) with severe COVID-19 pneumonia (11-39% lung involvement on computed tomography scan of the chest) were treated a median of 1 day (range 1-7 days) after admission. Treatment was well-tolerated. Immediate defervescence occurred, and inflammatory markers and oxygen supplementation decreased or stabilized in 4 patients (e.g., median C-reactive protein 203 (range 31-235) mg/L before vs. 32 (12-72) mg/L on day 5). Only one patient required mechanical ventilation. All patients recovered. C1INH concentrations were elevated before conestat alfa treatment. Levels of complement activation products declined after treatment. Viral loads in nasopharyngeal swabs declined in 4 patients. In this uncontrolled case series, targeting multiple inflammatory cascades by conestat alfa was safe and associated with clinical improvements in the majority of severe COVID-19 patients. Controlled clinical trials are needed to assess its safety and efficacy in preventing disease progression.</div>
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<DateCompleted><Year>2020</Year>
<Month>09</Month>
<Day>28</Day>
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<DateRevised><Year>2020</Year>
<Month>09</Month>
<Day>28</Day>
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<JournalIssue CitedMedium="Internet"><Volume>11</Volume>
<PubDate><Year>2020</Year>
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<Title>Frontiers in immunology</Title>
<ISOAbbreviation>Front Immunol</ISOAbbreviation>
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<ArticleTitle>Treatment of COVID-19 With Conestat Alfa, a Regulator of the Complement, Contact Activation and Kallikrein-Kinin System.</ArticleTitle>
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<Abstract><AbstractText>A dysregulated immune response with hyperinflammation is observed in patients with severe coronavirus disease 2019 (COVID-19). The aim of the present study was to assess the safety and potential benefits of human recombinant C1 esterase inhibitor (conestat alfa), a complement, contact activation and kallikrein-kinin system regulator, in severe COVID-19. Patients with evidence of progressive disease after 24 h including an oxygen saturation <93% at rest in ambient air were included at the University Hospital Basel, Switzerland in April 2020. Conestat alfa was administered by intravenous injections of 8400 IU followed by 3 additional doses of 4200 IU in 12-h intervals. Five patients (age range, 53-85 years; one woman) with severe COVID-19 pneumonia (11-39% lung involvement on computed tomography scan of the chest) were treated a median of 1 day (range 1-7 days) after admission. Treatment was well-tolerated. Immediate defervescence occurred, and inflammatory markers and oxygen supplementation decreased or stabilized in 4 patients (e.g., median C-reactive protein 203 (range 31-235) mg/L before vs. 32 (12-72) mg/L on day 5). Only one patient required mechanical ventilation. All patients recovered. C1INH concentrations were elevated before conestat alfa treatment. Levels of complement activation products declined after treatment. Viral loads in nasopharyngeal swabs declined in 4 patients. In this uncontrolled case series, targeting multiple inflammatory cascades by conestat alfa was safe and associated with clinical improvements in the majority of severe COVID-19 patients. Controlled clinical trials are needed to assess its safety and efficacy in preventing disease progression.</AbstractText>
<CopyrightInformation>Copyright © 2020 Urwyler, Moser, Charitos, Heijnen, Rudin, Sommer, Giannetti, Bassetti, Sendi, Trendelenburg and Osthoff.</CopyrightInformation>
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<ForeName>Pascal</ForeName>
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<AffiliationInfo><Affiliation>Division of Internal Medicine, University Hospital Basel, Basel, Switzerland.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Clinical Research and Department of Biomedicine, University Hospital Basel, Basel, Switzerland.</Affiliation>
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<AffiliationInfo><Affiliation>Division of Internal Medicine, University Hospital Basel, Basel, Switzerland.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Clinical Research and Department of Biomedicine, University Hospital Basel, Basel, Switzerland.</Affiliation>
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<Language>eng</Language>
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<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>08</Month>
<Day>14</Day>
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Treatment of COVID-19 With Conestat Alfa, a Regulator of the Complement, Contact Activation and Kallikrein-Kinin System.

Treatment of COVID-19 With Conestat Alfa, a Regulator of the Complement, Contact Activation and Kallikrein-Kinin System.

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