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Activation of the Inflammasome Is Not Associated With Multiorgan Failure in Bacteremic Patients With Severe Sepsis FREE TO VIEW

Sheila Habib, MD; Mandeep Mangat, MD; Bravein Amalakuhan, MD; Felipe Reyes, MD; Antonio Anzueto, MD; Stephanie Levine, MD; Jay Peters, MD; Carlos Orihuela, PhD; Marcos Restrepo, MD
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The University of Texas Health Science Center at San Antonio, San Antonio, TX

Chest. 2015;148(4_MeetingAbstracts):351A. doi:10.1378/chest.2261126
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SESSION TITLE: Sepsis and Shock Posters

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 28, 2015 at 01:30 PM - 02:30 PM

PURPOSE: Severe sepsis is a frequent cause of admission to intensive care units that is associated with significant health care cost and mortality. The host immune response to infection is multifaceted including activation of the inflammasome, a multiprotein complex that assembles in response to invading microorganisms and tissue injury. It functions as a potent activator of the inflammatory cascade by means of two pro-inflammatory cytokines, interleukin (IL)-1β and IL-18. Limited data are available regarding the effect of inflammasome activation in severe infections causing bacteremia. The aim of this study was to determine if the activation of the inflammasome is associated with multi-organ failure (MOF) in bacteremic patients with severe sepsis.

METHODS: We performed a secondary data analysis on a prospectively collected cohort of adult subjects with severe sepsis at two academic ICUs between 2007 and 2012. The cohort was stratified according to the presence or absence of bacteremia. Inflammasome activation was measured by the expression of serum IL-1β and IL-18 levels obtained within 48 hours of initial organ failure in subjects with severe sepsis. The primary outcome was MOF and secondary outcomes were ICU and hospital mortality.

RESULTS: Forty-eight subjects were enrolled in this study, of which 26 (54%) were bacteremic. Three (12%) bacteremic subjects died in the ICU and in the hospital. There was no significant difference in IL-1β and IL-18 levels between bacteremic and non-bacteremic subjects (IL-1β: median [IQR] 1.9[1.2-2.5] v. 1.95[1.2-3.4], p=0.9; IL-18: 392[299-938] v. 376[227-641], p=0.5). In bacteremic subjects, there were no significant differences in IL-1β (1.95[1.9-3.1] v. 1.89[1.2-1.9]; p=0.1) and IL-18 (519[266-1151] v. 335[31-587]; p=0.4) levels with respect to development of MOF. There were also no significant differences in IL-1β and IL-18 levels with respect to ICU and hospital mortality (IL-1β: 4.2[3.1-10.1 v. 1.9[1.2-2.3], p=0.1; IL-18: 1340[758-1475] v. 343[305-674]; p=0.4).

CONCLUSIONS: Activation of the inflammasome (defined as expression of serum IL-1β and IL-18 levels) was not associated with the development of MOF and ICU or hospital mortality in bacteremic subjects with severe sepsis.

CLINICAL IMPLICATIONS: Further prospective studies are needed to clarify the association between markers of inflammasome activity and outcomes in bacteremic subjects with severe sepsis.

DISCLOSURE: The following authors have nothing to disclose: Sheila Habib, Mandeep Mangat, Bravein Amalakuhan, Felipe Reyes, Antonio Anzueto, Stephanie Levine, Jay Peters, Carlos Orihuela, Marcos Restrepo

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