Is rosuvastatin protective against sepsis-associated encephalopathy? A secondary analysis of the SAILS trial.
Adverse reactions
Anti-inflammatory agents
Rosuvastatin calcium
Sepsis
Sepsis-associated encephalopathy
Journal
World journal of emergency medicine
ISSN: 1920-8642
Titre abrégé: World J Emerg Med
Pays: China
ID NLM: 101549691
Informations de publication
Date de publication:
2022
2022
Historique:
received:
19
12
2021
accepted:
20
04
2022
entrez:
19
9
2022
pubmed:
20
9
2022
medline:
20
9
2022
Statut:
ppublish
Résumé
Sepsis is a common cause of death in emergency departments and sepsis-associated encephalopathy (SAE) is a major complication. Rosuvastatin may play a neuroprotective role due to its protective effects on the vascular endothelium and its anti-inflammatory functions. Our study aimed to explore the potential protective function of rosuvastatin against SAE. Sepsis patients without any neurological dysfunction on admission were prospectively enrolled in the "Rosuvastatin for Sepsis-Associated Acute Respiratory Distress Syndrome" study (SAILS trial, ClinicalTrials.gov number: NCT00979121). Patients were divided into rosuvastatin and placebo groups. This is a secondary analysis of the SAILS dataset. Baseline characteristics, therapy outcomes, and adverse drug events were compared between groups. A total of 86 patients were eligible for our study. Of these patients, 51 were treated with rosuvastatin. There were significantly fewer cases of SAE in the rosuvastatin group than in the placebo group (32.1% vs. 57.1%, P=0.028). However, creatine kinase levels were significantly higher in the rosuvastatin group than in the placebo group (233 [22-689] U/L vs. 79 [12-206] U/L, P=0.034). Rosuvastatin appears to have a protective role against SAE but may result in a higher incidence of adverse events.
Sections du résumé
BACKGROUND
BACKGROUND
Sepsis is a common cause of death in emergency departments and sepsis-associated encephalopathy (SAE) is a major complication. Rosuvastatin may play a neuroprotective role due to its protective effects on the vascular endothelium and its anti-inflammatory functions. Our study aimed to explore the potential protective function of rosuvastatin against SAE.
METHODS
METHODS
Sepsis patients without any neurological dysfunction on admission were prospectively enrolled in the "Rosuvastatin for Sepsis-Associated Acute Respiratory Distress Syndrome" study (SAILS trial, ClinicalTrials.gov number: NCT00979121). Patients were divided into rosuvastatin and placebo groups. This is a secondary analysis of the SAILS dataset. Baseline characteristics, therapy outcomes, and adverse drug events were compared between groups.
RESULTS
RESULTS
A total of 86 patients were eligible for our study. Of these patients, 51 were treated with rosuvastatin. There were significantly fewer cases of SAE in the rosuvastatin group than in the placebo group (32.1% vs. 57.1%, P=0.028). However, creatine kinase levels were significantly higher in the rosuvastatin group than in the placebo group (233 [22-689] U/L vs. 79 [12-206] U/L, P=0.034).
CONCLUSION
CONCLUSIONS
Rosuvastatin appears to have a protective role against SAE but may result in a higher incidence of adverse events.
Identifiants
pubmed: 36119770
doi: 10.5847/wjem.j.1920-8642.2022.072
pii: WJEM-13-367
pmc: PMC9420670
doi:
Banques de données
ClinicalTrials.gov
['NCT00979121']
Types de publication
Journal Article
Langues
eng
Pagination
367-372Informations de copyright
Copyright: © World Journal of Emergency Medicine.
Déclaration de conflit d'intérêts
Conflicts of interest: The authors declare that they have no competing interests.
Références
JAMA. 2010 Oct 27;304(16):1787-94
pubmed: 20978258
Anesth Analg. 2009 Aug;109(2):572-84
pubmed: 19608834
Neurol India. 2018 Mar-Apr;66(2):352-361
pubmed: 29547154
Infect Immun. 2014 Sep;82(9):3555-66
pubmed: 24914219
Pharmacol Res. 2016 May;107:1-18
pubmed: 26930419
Intensive Care Med. 2006 Jan;32(1):75-9
pubmed: 16283159
Crit Care Med. 2006 Apr;34(4):1080-6
pubmed: 16484926
Br J Anaesth. 2007 Feb;98(2):163-75
pubmed: 17251210
Cardiovasc Ther. 2015 Dec;33(6):338-46
pubmed: 26280110
Burns. 2012 Mar;38(2):208-13
pubmed: 22079540
N Engl J Med. 2013 Oct 3;369(14):1306-16
pubmed: 24088092
Antioxid Redox Signal. 2012 Jun 1;16(11):1295-322
pubmed: 22117137
Crit Care Med. 2015 Jun;43(6):1213-22
pubmed: 25760659
Lancet Respir Med. 2013 Sep;1(7):515-23
pubmed: 24461612
Front Immunol. 2017 Jun 16;8:597
pubmed: 28670310
Pharmacol Res. 2019 Nov;149:104469
pubmed: 31577918
Int J Mol Sci. 2022 Feb 13;23(4):
pubmed: 35216180
JAMA. 2016 Feb 23;315(8):801-10
pubmed: 26903338
N Engl J Med. 2014 Jun 5;370(23):2191-200
pubmed: 24835849
Cell Physiol Biochem. 2018;49(6):2163-2173
pubmed: 30286467
Am J Respir Crit Care Med. 2014 Mar 15;189(6):666-73
pubmed: 24417431
Crit Care. 2013 Sep 18;17(5):R204
pubmed: 24047502
Circulation. 2004 Aug 17;110(7):880-5
pubmed: 15289367
Mol Aspects Med. 2014 Aug;38:1-53
pubmed: 24813475
Crit Care Med. 2014 Aug;42(8):1899-909
pubmed: 24810528
Pharmacol Ther. 2006 Oct;112(1):71-105
pubmed: 16714062
Front Cardiovasc Med. 2021 Nov 15;8:674248
pubmed: 34869619
Intensive Care Med. 2006 Jan;32(1):160-4
pubmed: 16086178
Cardiovasc Drugs Ther. 2005 Jan;19(1):13-21
pubmed: 15883752
Curr Atheroscler Rep. 2019 May 20;21(8):28
pubmed: 31111235
JAMA. 1996 Feb 14;275(6):470-3
pubmed: 8627969
J Crit Care. 2010 Dec;25(4):656.e7-22
pubmed: 20413251
Chest. 2018 Apr;153(4):805-815
pubmed: 28962887
Intensive Care Med. 2009 Jun;35(6):1039-46
pubmed: 19183945
Clin Microbiol Infect. 2009 Apr;15(4):325-34
pubmed: 19416304
Front Microbiol. 2019 Sep 04;10:1947
pubmed: 31551944
J Neuroinflammation. 2020 Jan 10;17(1):14
pubmed: 31924221
Crit Care. 2005 Feb;9(1):37-44
pubmed: 15693982
J Int Med Res. 2018 Jun;46(6):2410-2422
pubmed: 29644918
Nat Rev Immunol. 2006 May;6(5):358-70
pubmed: 16639429
Cardiovasc Diabetol. 2017 Apr 4;16(1):44
pubmed: 28376896
Lancet. 2007 Nov 24;370(9601):1781-90
pubmed: 17559928
Lancet Respir Med. 2016 Mar;4(3):203-12
pubmed: 26832963