<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Engelen MM</submitter><funding>Fonds Wetenschappelijk Onderzoek</funding><pagination>e12826</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9618401</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>6(7)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Thromboinflammation plays a central role in severe COVID-19. The kallikrein pathway activates both inflammatory pathways and contact-mediated coagulation. We investigated if modulation of the thromboinflammatory response improves outcomes in hospitalized COVID-19 patients.&lt;h4>Methods&lt;/h4>In this multicenter open-label randomized clinical trial (EudraCT 2020-001739-28), patients hospitalized with COVID-19 were 1:2 randomized to receive standard of care (SOC) or SOC plus study intervention. The intervention consisted of aprotinin (2,000,000 IE IV four times daily) combined with low molecular weight heparin (LMWH; SC 50 IU/kg twice daily on the ward, 75 IU/kg twice daily in intensive care). Additionally, patients with predefined hyperinflammation received the interleukin-1 </pubmed_abstract><journal>Research and practice in thrombosis and haemostasis</journal><pubmed_title>Modulation of thromboinflammation in hospitalized COVID-19 patients with aprotinin, low molecular weight heparin, and anakinra: The DAWn-Antico study.</pubmed_title><pmcid>PMC9618401</pmcid><funding_grant_id>G0G4720N</funding_grant_id><pubmed_authors>Heytens L</pubmed_authors><pubmed_authors>De Tavernier B</pubmed_authors><pubmed_authors>Ceunen H</pubmed_authors><pubmed_authors>Van Thillo Q</pubmed_authors><pubmed_authors>Wouters C</pubmed_authors><pubmed_authors>Robberecht W</pubmed_authors><pubmed_authors>Dupont L</pubmed_authors><pubmed_authors>Ruttens D</pubmed_authors><pubmed_authors>Liesenborghs L</pubmed_authors><pubmed_authors>Dolhain J</pubmed_authors><pubmed_authors>Engelen MM</pubmed_authors><pubmed_authors>Van Wijngaerden E</pubmed_authors><pubmed_authors>Vos R</pubmed_authors><pubmed_authors>Servaes V</pubmed_authors><pubmed_authors>Wauters J</pubmed_authors><pubmed_authors>Meyfroidt G</pubmed_authors><pubmed_authors>Hoppenbrouwers M</pubmed_authors><pubmed_authors>Wens K</pubmed_authors><pubmed_authors>Vandenbriele C</pubmed_authors><pubmed_authors>Cludts K</pubmed_authors><pubmed_authors>Gunst J</pubmed_authors><pubmed_authors>Neyts J</pubmed_authors><pubmed_authors>Spalart V</pubmed_authors><pubmed_authors>Mesotten D</pubmed_authors><pubmed_authors>Spriet I</pubmed_authors><pubmed_authors>Van den Berghe G</pubmed_authors><pubmed_authors>Devos T</pubmed_authors><pubmed_authors>Jacobs C</pubmed_authors><pubmed_authors>Dauwe D</pubmed_authors><pubmed_authors>Janssens W</pubmed_authors><pubmed_authors>Meersseman P</pubmed_authors><pubmed_authors>Roebroek D</pubmed_authors><pubmed_authors>Claes K</pubmed_authors><pubmed_authors>Belmans A</pubmed_authors><pubmed_authors>Van Geet C</pubmed_authors><pubmed_authors>Smet N</pubmed_authors><pubmed_authors>Devooght C</pubmed_authors><pubmed_authors>Daems K</pubmed_authors><pubmed_authors>Rex S</pubmed_authors><pubmed_authors>Verhamme P</pubmed_authors><pubmed_authors>De Munter P</pubmed_authors><pubmed_authors>Thomeer M</pubmed_authors><pubmed_authors>Betrains A</pubmed_authors><pubmed_authors>Verbeke G</pubmed_authors><pubmed_authors>Fivez T</pubmed_authors><pubmed_authors>Dreesen P</pubmed_authors><pubmed_authors>Vanassche T</pubmed_authors><pubmed_authors>Ockerman A</pubmed_authors><pubmed_authors>Martens CP</pubmed_authors><pubmed_authors>Debaveye B</pubmed_authors><pubmed_authors>D'hondt M</pubmed_authors><pubmed_authors>Wilmer A</pubmed_authors><pubmed_authors>DAWn Consortium Members</pubmed_authors><pubmed_authors>Dapper I</pubmed_authors><pubmed_authors>Vanheule K</pubmed_authors><pubmed_authors>Tuyls S</pubmed_authors><pubmed_authors>Gyselinck I</pubmed_authors></additional><is_claimable>false</is_claimable><name>Modulation of thromboinflammation in hospitalized COVID-19 patients with aprotinin, low molecular weight heparin, and anakinra: The DAWn-Antico study.</name><description>&lt;h4>Background&lt;/h4>Thromboinflammation plays a central role in severe COVID-19. The kallikrein pathway activates both inflammatory pathways and contact-mediated coagulation. We investigated if modulation of the thromboinflammatory response improves outcomes in hospitalized COVID-19 patients.&lt;h4>Methods&lt;/h4>In this multicenter open-label randomized clinical trial (EudraCT 2020-001739-28), patients hospitalized with COVID-19 were 1:2 randomized to receive standard of care (SOC) or SOC plus study intervention. The intervention consisted of aprotinin (2,000,000 IE IV four times daily) combined with low molecular weight heparin (LMWH; SC 50 IU/kg twice daily on the ward, 75 IU/kg twice daily in intensive care). Additionally, patients with predefined hyperinflammation received the interleukin-1 </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Oct</publication><modification>2026-05-27T20:42:27.033Z</modification><creation>2026-04-08T01:48:54.355Z</creation></dates><accession>S-EPMC9618401</accession><cross_references><pubmed>36324831</pubmed><doi>10.1002/rth2.12826</doi></cross_references></HashMap>