High-density lipoprotein (HDL) particle size and concentration changes in septic shock patients.
High-density lipoproteins
Inflammation
Intensive care unit
Lipid profile
Lipoprint
Sepsis
Size
Journal
Annals of intensive care
ISSN: 2110-5820
Titre abrégé: Ann Intensive Care
Pays: Germany
ID NLM: 101562873
Informations de publication
Date de publication:
13 Jun 2019
13 Jun 2019
Historique:
received:
26
02
2019
accepted:
30
05
2019
entrez:
15
6
2019
pubmed:
15
6
2019
medline:
15
6
2019
Statut:
epublish
Résumé
Sepsis is associated with systemic inflammation that may impact lipoprotein function. In particular, high-density lipoproteins (HDLs) that display pleiotropic protective roles may be dysfunctional in septic conditions. The aim of this study was to evaluate the HDL profile and the inflammatory context in septic shock patients admitted to our intensive care unit (ICU). In this study, 20 septic shock patients and 20 controls (ICU patients without septic shock) were included. Plasma samples were collected on days 1, 2 and 7. Total cholesterol and lipoprotein concentrations were determined. HDL profiles were obtained using the Lipoprint HDL concentration was statistically lower in septic shock patients than in controls. At days 1 and 2, septic patients had significantly more large-sized HDL than control patients. Patients recovered a normal lipid profile at day 7. Our results emphasize that HDL levels are dramatically decreased in the acute phase of septic shock and that there is a shift toward large HDL particles, which may reflect a major dysfunction of these lipoproteins. Further mechanistic studies are required to explore this shift observed during sepsis.
Sections du résumé
BACKGROUND
BACKGROUND
Sepsis is associated with systemic inflammation that may impact lipoprotein function. In particular, high-density lipoproteins (HDLs) that display pleiotropic protective roles may be dysfunctional in septic conditions. The aim of this study was to evaluate the HDL profile and the inflammatory context in septic shock patients admitted to our intensive care unit (ICU).
METHODS
METHODS
In this study, 20 septic shock patients and 20 controls (ICU patients without septic shock) were included. Plasma samples were collected on days 1, 2 and 7. Total cholesterol and lipoprotein concentrations were determined. HDL profiles were obtained using the Lipoprint
RESULTS
RESULTS
HDL concentration was statistically lower in septic shock patients than in controls. At days 1 and 2, septic patients had significantly more large-sized HDL than control patients. Patients recovered a normal lipid profile at day 7.
CONCLUSIONS
CONCLUSIONS
Our results emphasize that HDL levels are dramatically decreased in the acute phase of septic shock and that there is a shift toward large HDL particles, which may reflect a major dysfunction of these lipoproteins. Further mechanistic studies are required to explore this shift observed during sepsis.
Identifiants
pubmed: 31197574
doi: 10.1186/s13613-019-0541-8
pii: 10.1186/s13613-019-0541-8
pmc: PMC6565796
doi:
Types de publication
Journal Article
Langues
eng
Pagination
68Subventions
Organisme : European Regional Development Funds
ID : RE0001897
Références
Atherosclerosis. 2002 Mar;161(1):1-16
pubmed: 11882312
Crit Care Med. 2002 May;30(5 Suppl):S294-301
pubmed: 12004251
Crit Care Med. 2003 May;31(5):1359-66
pubmed: 12771603
Trends Cardiovasc Med. 2003 Aug;13(6):226-31
pubmed: 12922018
Shock. 2003 Dec;20(6):551-7
pubmed: 14625480
Crit Care Med. 2004 Mar;32(3):632-7
pubmed: 15090939
Lancet. 2005 Jan 1-7;365(9453):63-78
pubmed: 15639681
Circ Res. 2005 Aug 5;97(3):236-43
pubmed: 16002747
Crit Care Med. 2005 Aug;33(8):1688-93
pubmed: 16096442
Immunol Res. 2006;34(2):133-41
pubmed: 16760573
Atherosclerosis. 2007 Mar;191(1):63-72
pubmed: 16806233
Intensive Care Med. 2007 Jan;33(1):13-24
pubmed: 17093985
Nat Rev Microbiol. 2007 Aug;5(8):577-82
pubmed: 17632569
Ann Intern Med. 2009 Jan 20;150(2):84-93
pubmed: 19153411
Atherosclerosis. 2009 Oct;206(2):611-6
pubmed: 19375079
Intensive Care Med. 2009 Nov;35(11):1877-85
pubmed: 19669126
Crit Care. 2010;14(1):R15
pubmed: 20144219
Intensive Care Med. 2010 Aug;36(8):1286-98
pubmed: 20443110
J Lipid Res. 2010 Sep;51(9):2695-705
pubmed: 20495214
Arterioscler Thromb Vasc Biol. 2011 Jun;31(6):1333-41
pubmed: 21474825
PLoS One. 2011 Apr 13;6(4):e18679
pubmed: 21533243
Atherosclerosis. 2012 Jun;222(2):390-4
pubmed: 22456230
J Clin Exp Cardiolog. 2011 Dec 22;2(172):null
pubmed: 23227448
Br J Pharmacol. 2013 Jun;169(3):493-511
pubmed: 23488589
JAMA. 2013 Mar 20;309(11):1154-62
pubmed: 23512062
Circulation. 2014 Feb 11;129(6):635-42
pubmed: 24243886
N Engl J Med. 2013 Nov 21;369(21):2063
pubmed: 24256390
Am J Physiol Regul Integr Comp Physiol. 2014 Sep 1;307(5):R514-24
pubmed: 24920733
Biol Chem. 2015 Jan;396(1):53-60
pubmed: 25205725
J Surg Res. 2015 Mar;194(1):248-54
pubmed: 25438956
Handb Exp Pharmacol. 2015;224:483-508
pubmed: 25522999
Medicine (Baltimore). 2016 Jan;95(4):e2600
pubmed: 26825910
JAMA. 2016 Feb 23;315(8):801-10
pubmed: 26903338
Cell Physiol Biochem. 2016;38(5):1906-14
pubmed: 27160732
Crit Care Med. 2017 Mar;45(3):486-552
pubmed: 28098591
Ann Intensive Care. 2017 Dec;7(1):60
pubmed: 28589535
Am J Respir Crit Care Med. 2019 Apr 1;199(7):854-862
pubmed: 30321485
J Am Coll Cardiol. 2019 Jun 25;73(24):e285-e350
pubmed: 30423393
Curr Opin Lipidol. 2019 Apr;30(2):108-116
pubmed: 30649022
J Biol Chem. 1988 Sep 25;263(27):13479-81
pubmed: 3138236
Clin Chem. 1986 Jan;32(1 Pt 1):142-5
pubmed: 3940695
J Clin Invest. 1981 Mar;67(3):827-37
pubmed: 7204557
Infect Immun. 1980 May;28(2):373-80
pubmed: 7399668
Am Surg. 1996 May;62(5):350-5
pubmed: 8615560
J Exp Med. 1996 Nov 1;184(5):1601-8
pubmed: 8920850
Thromb Haemost. 1998 Aug;80(2):316-20
pubmed: 9716159