Journal of Critical Care 38 (2017) 289294

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Journal of Critical Care

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Decreased high-density lipoprotein cholesterol level is an early prognostic

marker for organ dysfunction and death in patients with suspected sepsis
Mihai Cirstea, BSc , Keith R. Walley, MD, James A. Russell, MD, Liam R. Brunham, MD, PhD,
Kelly R. Genga, MD, John H. Boyd, MD
Centre for Heart Lung Innovation, University of British Columbia, Vancouver, British Columbia, Canada

a r t i c l e i n f o a b s t r a c t

Keywords: Purpose: We sought to determine whether an early high-density lipoprotein cholesterol (HDL-C) measurement
Suspected sepsis at emergency department (ED) admission is prognostic of multiorgan dysfunction syndrome (MODS) and
Emergency department death in a suspected sepsis cohort.
Sepsis biomarkers Materials and Methods: Two hundred patients with clinically suspected sepsis were recruited at admission to our
Cholesterol tertiary care hospital's ED. Lipids were measured at the time of rst ED blood draw. Clinical data were collected
High-density lipoprotein via chart review. Primary outcomes of interest were development of MODS and 28-day mortality. Secondary out-
Multiorgan dysfunction syndrome
comes included need for critical care, single-organ failures, days alive and free of vasopressor and ventilator sup-
port, and 90-day mortality.
Results: High-density lipoprotein cholesterol was greatly decreased in patients who developed MODS and/or died
and remained stable over the rst week of admission. Receiver operator characteristic analysis demonstrated
that HDL-C had superior predictive ability compared with all routine clinical markers for both development of
MODS and 28-day mortality, and identied an HDL-C cutoff of 25.1 mg/dL below which patients were at signif-
icantly greater risk for development of all adverse outcomes.
Conclusions: Plasma HDL-C level was characterized by early decrease and high stability, and was the best prog-
nostic marker for adverse outcomes in a suspected sepsis cohort.
2016 Elsevier Inc. All rights reserved.

1. Introduction
Sepsis is a serious complication of a microbial infection characterized
by a dysregulated inammatory response and altered metabolic state,
leading to tissue injury, organ failure, and sometimes death. During sep-
sis, lipopolysaccharide (LPS) and other pathogen lipids are sequestered
within high- (HDL-C), low- (LDL) and very low-density lipoproteins [1]
and are then cleared from circulation via the liver through receptors
such as the LDL receptor [2] and the HDL-C receptor SR-BI [3]. High-
density lipoprotein in particular has the highest afnity for both
LPS [4] and the gram-positive toxin lipoteichoic acid [5], making it
especially benecial in reducing their ability to trigger an innate im-
mune response. High-density lipoprotein is also important in healthy
endothelial function and repair [6]. Thus, HDL-C plays an important
role in modulating the septic inammatory response.
High-density lipoprotein cholesterol levels are known to be low in
established septic shock [7-10]. In patients admitted to a critical care
unit for organ failure(s), an HDL-C level lower than 20 mg/dL is associ-
ated with increased 30-day mortality, prolonged (N7 days) intensive
Corresponding author.
E-mail address: mihai.cirstea@hli.ubc.ca (M. Cirstea).
care unit (ICU) stay, and greater hospital-acquired infection rate [11];
pediatric nonsurvivors of severe meningococcal sepsis have lower
HDL-C than do survivors [12]; and low HDL-C during septic shock is
generally associated with increased hospital mortality [13-16].
Despite this extensive literature, lipid proles are rarely measured or
interpreted in clinical management of sepsis [17] and are not even men-
tioned in the Surviving Sepsis Campaign guidelines [18]. However, pre-
vious studies of lipoproteins during sepsis focus exclusively on patients
already receiving critical care for established septic shock and therefore
may have missed the opportunity to assess the prognostic value of an
early HDL-C measurement at triage. To date (to our knowledge), no
studies have measured HDL-C level in a suspected sepsis cohort at the
time of emergency department (ED) presentation and assessed its asso-
ciation with outcomes of sepsis.
Accordingly, we sought to determine whether low HDL-C levels pre-
cede the development of organ dysfunction and could therefore be of
utility as an early prognostic biomarker in the ED setting. To do this,
we recruited patients with clinically suspected sepsis at the time of pre-
sentation to the ED and measured a full lipid panel on plasma collected
at the time of rst blood draw for routine testing. We tested the associ-
ation of early plasma HDL-C levels with the subsequent development of
single or multiple-organ dysfunction and mortality. The prognostic

http://dx.doi.org/10.1016/j.jcrc.2016.11.041
0883-9441/ 2016 Elsevier Inc. All rights reserved.
290 M. Cirstea et al. / Journal of Critical Care 38 (2017) 289294

value of HDL-C level was compared with other lipid panel components R statistical software (https://www.r-project.org/), and a Youden index
(LDL-C, non-HDL-C, and triglycerides) as well as several other routinely (Sensitivity + Specicity 1) HDL-C cutoff threshold for 28-day mortal-
measured biomarkers, namely, lactate, platelets, white blood cell (WBC) ity was calculated using the OptimalCutpoints (https://cran.r-project.org/
count, creatinine, and hemoglobin. web/packages/OptimalCutpoints/index.html) package. Univariate logistic
regression was performed for the association of baseline demographics,
2. Methods underlying conditions, Acute Physiology and Chronic Health Evaluation
(APACHE) II score, lactate, platelets, hemoglobin, creatinine, and WBC
2.1. Design, setting, and patient eligibility count with 28-day mortality and development of MODS using R's gener-
alized linear model function. Variables were included in multivariate lo-
In this blinded, observational cohort study, we recruited 200 adult gistic regression if they achieved P b .1 in the univariate analysis;
patients with suspected sepsis at the time of admission to the ED of St creatinine and WBC count were excluded due to high redundancy with
Paul's Hospital (SPH), a tertiary care teaching hospital in Vancouver, APACHE II; and sex, body mass index (BMI) and statin use were prospec-
Canada. Patients were identied when the attending physician activat- tively included due to potential inuence on HDL-C cholesterol. Univari-
ed our Institutional Suspected Sepsis Protocol; this requires a clinically ate analysis results are available in Supplementary Table 1. The
suspected infection and at least 2 of the following: (i) temperature N 38 following covariates were included in the nal multivariate analysis: he-
C or b36 C, (ii) heart rate N90 beats/min, (iii) WBC count N12 000 or moglobin, lactate, platelets, sex, statin use, BMI, hepatitis, cirrhosis, and
b4000 per mm3. Recruitment occurred from January 2011 to June APACHE II. All lipids were analyzed separately in multivariate analysis
2014. Study identication numbers were assigned to the secured enroll- with the above covariates. Correlation between septic and nonseptic
ment forms, and clinical data were stored in an ORACLE-based database HDL-C levels was assessed using Spearman rank test.
on a rewalled, RSS-encrypted server at SPH. No patients were retro-
spectively excluded. All studies were approved by University of British 3. Results
Columbia and SPH ethics boards.
3.1. Baseline characteristics
2.2. Blood collection and lipid measurements
Of the 200 enrolled patients, 96 required ICU admission, 112 had at
A 6-mL EDTA tube of blood was collected at the time of the rst clin- least 1 organ dysfunction over the course of their hospital stay, 74 devel-
ical blood draw in ED. Where available (48% of patients), another sam- oped MODS, 14 patients died within 28 days (7%), and 28 died within 90
ple was taken on day 7 3 of admission to track changes in lipid days (14%). There were no signicant differences in baseline demo-
levels over the course of their admission. Blood was spun at 1800 * g graphics or underlying conditions, with the exception of conditions af-
for 12 minutes and a complete lipid panel (total cholesterol, HDL-C cho- fecting the liver (hepatitis and cirrhosis) between patients who did or
lesterol, LDL cholesterol, non-HDL-C cholesterol, and triglycerides) was did not develop MODS (Table 1). As expected, patients who developed
measured in plasma on the SPH clinical laboratory's ADVIA 1800 MODS had signicantly higher APACHE II, lower hemoglobin, and
Chemistry System (Siemens, Erlangen, Germany). Technicians handling
blood processing and lipid measurements received tubes labeled with a Table 1
randomized numerical ID and were blinded to patient demographics Baseline patient demographics and characteristics
and outcomes. Separate investigators performed chart reviews and
Variables No MODS (n = 126) MODS (n = 74) P
were blinded to patient lipid proles.
Age (y), mean (SD) 56.5 (17.9) 55.9 (15.7) .815
APACHE II, mean (SD) 7.67 (5.58) 14.2 (6.2) b.001
2.3. Denitions of organ dysfunction Male, no. (%) 83 (65.9) 47 (63.5) .736
Underlying conditions, no. (%)
The standard denition of multiorgan dysfunction syndrome Hypertension 45 (35.7) 28 (37.8) .763
(MODS) was used, namely, the development of potentially reversible Diabetes mellitus 33 (26.2) 19 (25.7) .936
COPD 24 (19.0) 19 (25.7) .271
physiologic derangement involving two or more organ systems not in-
Chronic renal failure 11 (8.7) 12 (16.2) .109
volved in the disorder that resulted in ICU admission, and arising in Hepatitis 16 (12.7) 21 (28.4) .006
the wake of a potentially life-threatening physiologic insult [19]. As HIV 11 (8.7) 11 (14.9) .181
per this denition, only the development of new (not preexisting) Malignancy 5 (4.0) 3 (4.1) .976
organ dysfunctions were counted. A Sequential Organ Failure Assess- CHF 9 (7.1) 11 (14.9) .079
Cirrhosis 3 (2.4) 9 (12.2) .005
ment score of 2 or higher [20] was used to determine individual organ Statin use 32 (25.4) 25 (33.8) .205
dysfunction. In addition, we calculated a composite outcome of days Chronic steroids 9 (7.1) 5 (6.8) .855
alive and free of vasopressors/ventilator (DAF Vaso/Vent) as is used in Pathogen type in culture, no. (%)
an ongoing randomized controlled trial of selepressin in septic shock Gram-positive alone 26 (20.6) 26 (35.1) .037
Gram-negative alone 10 (7.9) 11 (14.9) .192
(https://clinicaltrials.gov/ct2/show/NCT02508649?term=selepressin&
Mixed organisms 12 (9.5) 12 (16.2) .238
rank=1). DAF Vaso/Vent is dened as the number of days, from admis- Fungal 3 (2.4) 4 (5.4) .468
sion to day 28, in which a patient is both alive and free of vasopressor No pathogen in culture 75 (59.5) 21 (28.4) b.001
treatment and mechanical ventilation. Twenty-day-nonsurvivors are Clinical measures, mean (SD)
assigned a value of zero. Hemoglobin 120.9 (26.4) 107.4 (22.6) b.001
WBCs 10.6 (7.9) 13.8 (9.3) .017
Lactate 2.1 (2.06) 3.13 (3.0) .022
2.4. Statistical analyses Creatinine 119.2 (145.9) 176.5 (173.2) .015
Platelets 237.8 (116.4) 205.9 (128.6) .088
Differences in quantitative variables were assessed using Pearson 2 tests Plasma lipids, mean (SD)
Total cholesterol 129.9 (43.7) 91.4 (45.0) b.001
for categorical variables and Mann-Whitney U tests for continuous
HDL-C 39.9 (17.2) 25.7 (16.1) b.001
variables. Kaplan-Meyer time to death analysis was performed LDL-C 66.7 (32.1) 43.5 (33.1) b.001
using GraphPad (La Jolla, CA, USA) Prism software, and differences in Non-HDL-C 90.1 (34.1) 65.7 (35.6) b.001
survival curves were assessed via Mantel-Cox log-rank test. Receiver Triglycerides 119.4 (78.3) 111.3 (69.5) .459
operator characteristic (ROC) analysis was performed using the pROC Patients were grouped based on development of MODS. Values are presented as mean and
package (https://cran.r-project.org/web/packages/pROC/index.html) in SD, or number and percent.
 M. Cirstea et al. / Journal of Critical Care 38 (2017) 289294
elevated leukocyte, creatinine and lactate levels at admission. Platelet
count did not differ signicantly. Plasma lipid levels with the exception
of triglycerides were signicantly lower in patients who developed
MODS compared with those who did not. Levels of HDL-C at ED admis-
sion ranged from 3.8 to 104.4 mg/dL, with a mean (SD) of 34.6 (18.1)
and a median of 32.2 mg/dL.
3.2. Receiver operator characteristic analysis of lipoproteins and clinical
variables
Receiver operator characteristic analysis was performed on 5 routinely
measured clinical markers (lactate, hemoglobin, creatinine, platelets, and
WBC count) and 3 lipid panel components (HDL-C, LDL-C, and triglycer-
ides) to assess the sensitivity/specicity predictive value of each for the de-
velopment of MODS and 28-day mortality. High-density lipoprotein
cholesterol was the best predictor of both development of MODS (area
under the curve [AUC] = 0.749, Youden index threshold = 30.9 mg/dL,
sensitivity = 0.716, specicity = 0.690, positive predictive power =
0.576, negative predictive power = 0.806), and 28-day mortality (AUC =
0.818, Youden index threshold = 25.1 mg/dL, sensitivity = 0.857,
specicity = 0.699, positive predictive power = 0.176, negative predictive
power = 0.985) (Table 2). Receiver operator characteristic curves for HDL-
C and lactate, a common biomarker for severe shock, are shown for
reference for both outcomes of interest (Fig. 1). The ROC-informed thresh-
old for short-term mortality (25.1 mg/dL) is used as a patient subgroup
cutoff for subsequent analyses of mortality and adverse outcome.
3.3. Low HDL-C is associated with increased mortality rate and adverse
hospital events
Kaplan-Meyer survival analysis showed a signicantly higher mor-
tality rate for patients with an ED triage HDL-C level lower than 25.1
mg/dL (P b .0001 at 28 days and P = .0007 at 90 days; Fig. 2). Patients
above and below this cutoff value were also compared for propensity
to progress to adverse hospital outcomes, including need for ICU care,
single- and multiple-organ dysfunctions, death, and composite days
alive and free of both ventilation and vasopressor support (Table 3). In
every case, the proportion of patients progressing to adverse outcome
was signicantly higher in the low-HDL-C group. For instance, 74% of
patients below the 25.1 mg/dL HDL-C cutoff required ICU care compared
with only 35% above the cutoff; the proportion developing serious acute
kidney dysfunction (acute kidney injury score N 2) was 47% vs 21%, re-
spectively; the incidence of multiple organ dysfunction was 60% vs 25%;
and the requirement for mechanical ventilation was 53% vs 21%. There
were also more than 10-fold higher 28-day mortality (17.6% vs 1.5%)
and a mean of 6.2 fewer days free of mechanical ventilation and vaso-
pressor support in the low-HDL-C group.
Table 2
ROC AUC scores for development of MODS and 28-day mortality
Variable AUC: MODS AUC: 28-d mortality
HDL-C 0.749 0.818
LDL-C 0.742 0.674
Triglycerides 0.541 0.606
Hemoglobin 0.645 0.668
WBC count 0.613 0.642
Lactate 0.624 0.595
Creatinine 0.660 0.761
Platelets 0.606 0.645
HDL-C had the highest ROC AUC for both outcomes of interest, when compared with other
lipid panel components and 5 additional clinical measures.
291
3.4. Low HDL-C is independently associated with development of MODS
and 28-day mortality
To test whether HDL-C was independently associated with develop-
ment of MODS and 28-day mortality, multivariate logistic regression
was performed controlling for all relevant patient demographics
and preexisting comorbidities. This analysis showed that only plasma
HDL-C level was signicantly associated with development of MODS
and 28-day mortality after multiple adjustments (Table 4). For every in-
cremental 1-mg/dL decrease in HDL-C, there was a 3.10% increase in the
odds of developing MODS, an impressive effect given that HDL-C ranged
from 3.8 to 104.4 mg/dL. A modest 10-mg/dL decrease in HDL-C
increased the odds of developing MODS by 26.6%. Neither LDL (P =
.078) nor triglycerides (P = .290) achieved statistical signicance
in the analysis. Likewise, HDL-C was the best prognostic marker of
28-day mortality, predicting a 6.90% increase in odds of death for
every 1-mg/dL decrease in HDL-C, or a 51.2% increase for a 10-mg/dL
HDL-C decrease. Again, neither LDL-C nor triglycerides were predictive
(P = .469 and .727, respectively).
3.5. HDL-C is stable during sepsis admission
We sought to determine whether baseline plasma HDL-C levels
remained constant or recovered during hospital admission. A second
blood sample was available in 94 patients at 7 3 days after admission.
These patients were grouped based on development MODS (n = 49) or
not (n = 45), and for each group, baseline HDL-C was compared with
the follow-up measurement. In both groups, HDL-C remained virtually
unchanged over hospital admission: 38.2 19.7 baseline vs 38.8
18.6 follow-up in patients without MODS, and 23.7 16.1 baseline vs
25.5 13.3 follow-up in patients with MODS (mean SD; all values
in mg/dL), showing a remarkable stability.
3.6. Additional chart reviews
We performed a retrospective review in our cohort for any lipid
panel ordered outside their current sepsis encounter, from 5 years be-
fore 2 years after their sepsis admission. Using this window, we obtain-
ed lipid panels from 116 of the 200 patients. Although the nonseptic
HDL-C of this group was normal (mean, 44.1 mg/dL), there was a highly
signicant positive correlation between nonseptic and septic plasma
HDL-C levels (r = 0.457, P = 2.43E7 by Spearman rank test).
Finally, we reviewed patient charts to query the extent to which
serum lipid levels were used in the clinical management of this cohort.
In agreement with the observation that lipid levels are very rarely used
during the diagnosis and treatment of sepsis, only 1 (0.5%) of 200 pa-
tients in our cohort had a lipid panel ordered at any time during their
hospital admission.
4. Discussion
We make the novel observation that the decrease in HDL-C precedes
the onset of single- and multiple-organ failure by measuring plasma li-
poprotein levels at the time of ED admission in a suspected sepsis pop-
ulation. Low HDL-C was independently and uniquely associated with
development of MODS and 28-day mortality, and in ROC analysis, the
predictive value of HDL-C level surpassed that of all other measured var-
iables for both events. An HDL-C level lower than 25.1 mg/dL at admis-
sion was highly prognostic for every adverse outcome examined, which
may suggest a clinically relevant threshold to dene patients at highest
risk for serious adverse events including death. In both patients who did
and did not develop MODS, HDL-C remained virtually unchanged at
about 1 week after admission, suggesting that a single measurement
at ED triage is likely adequate to dene those at risk for developing
MODS as a result of an infection.
292 M. Cirstea et al. / Journal of Critical Care 38 (2017) 289294

Fig. 1. Receiver operator characteristic analysis for HDL-C and lactate. High-density lipoprotein cholesterol was the single best predictor of both development of MODS and 28-day
mortality, with an AUC of 0.749 and 0.818, respectively; lactate, a criterion standard biomarker for severe shock, was a relatively poor predictor of both outcomes in this less severely
ill cohort with an AUC of 0.624 and 0.595, respectively.

100
Percent survival

90 HDL> 25.1 mg/dL

HDL < 25.1 mg/dL

80

70
60
0
0 15 30 45 60 75 90
Days
At-risk patients:
HDL > 25.1mg/dL 132 131 130 125 124 123 121
HDL < 25.1mg/dL 68 62 57 54 52 52 51

Fig. 2. Kaplan-Meier time-to-death analysis. Ninety-day time-to-death curves were generated by stratifying patients above and below an HDL-C cutoff of 25.1 mg/dL. Lower HDL-C was
strongly associated with increased mortality (P b .0001 at 28 days and P = .0007 at 90 days).
 M. Cirstea et al. / Journal of Critical Care 38 (2017) 289294 293

Table 3 or both. We speculate that patients with dangerously low HDL-C may
Hospital outcomes by HDL-C cutoff then be particularly poorly equipped to deal with the progression of
Outcomes Baseline HDL-C level P their infection, due to an impaired ability to neutralize pathogenic
b25.1 mg/dL N25.1 mg/dL
toxins and preserve normal vascular function. In combination, this
(n = 68) (n = 132) leads to a prolonged and uncontrolled immune response even after
the live organisms that cause infection are controlled by antibiotics.
Need for ICU care 50 (73.5%) 46 (34.8%) b.001
N2 organ failures 41 (60.3%) 33 (25.0%) b.001 High-density lipoprotein cholesterol promises many advantages
Mechanical ventilation 36 (52.9%) 27 (20.5%) b.001 over other sepsis biomarkers and diagnostic tools. Blood cultures in-
Vasopressor support 21 (30.9%) 15 (11.4%) .001 volve long waits for results and are very prone to both false negatives
Liver failure 18 (26.5%) 14 (10.6%) .007 and false positives [39,40]. Microbial nucleic acid testing is expensive
AKI score N 2 32 (47.1%) 28 (21.2%) b.001
28-d mortality 12 (17.6%) 2 (1.5%) b.001
and technically complex, and interpretation remains challenging [39].
90-d mortality 17 (25.0%) 11 (8.3%) .003 Traditional acute-phase markers such as C-reactive protein,
DAF Vaso/Vent, mean SD 20.2 10.0 26.4 4.0 b.001 procalcitonin, and other cytokines are short-lived and only briey corre-
Patients were divided into groups above or below an ROC-informed HDL-C cutoff of 25.1 late with disease severity [7,41]. Lactate is one of the most useful bio-
mg/dL, and the proportion who went on to require ICU care and develop multiple- or sin- markers for differentiating sepsis from more severe septic shock [20,
gle- (respiratory, circulatory, liver, kidney%) organ dysfunctions was compared, as was 42]; however, its lack of prognostic ability in our study highlights its
mortality and the average ( SD) composite vasopressor/ventilator-free days. Values limitations at the time of admission in a heterogeneous cohort of early
are presented as number (percent) unless noted.
AKI indicates acute kidney injury
suspected sepsis. In contrast to all these, HDL-C measurement is rapid,
inexpensive, routinely available in clinical settings, and its immediate
drop and prolonged stability gives it more robust predictive value com-
Animal model studies consistently show that HDL-C mitigates the pared with markers with short half-lives and unpredictable peaks.
adverse consequences of sepsis. Animals with elevated HDL that are Some limitations to this study should be noted. First, this was a
subjected to LPS injection or live infection show reduced cytokine levels, single-center study and the results may not be directly applicable to
less organ dysfunction, increased LPS clearance, and improved survival other patient populations. Second, presepsis and postsepsis lipid levels
[21-26]. Human studies of low-dose LPS challenge in healthy volunteers were determined by chart review over a period of 7 years and we did
align with these ndings [27,28]. There are several hypotheses for the not assess the reason for the tests being ordered (eg, we cannot rule
protective effects of HDL-C during infection and acute inammation. out that some may have been during another acute infection). Finally,
As mentioned, HDL-C is central in the neutralization and clearance of for some clinical markers, there were small proportions of patients
bacterial pathogen lipids. In addition, HDL-C protects LDL against oxida- without measurements at ED admission, as follows (variable and per-
tion [29], helps preserve normal microvascular structure and endotheli- cent missing): hemoglobin 4.5%, WBC count 5%, lactate 13.5%, creatinine
al integrity during infection [30,31], and promotes the removal of LPS 5%, and platelets 8%. Patient demographics, outcomes, and lipid proles
from activated monocytes [32]. Interestingly, reduced HDL-C levels are were available for 100% of patients.
observed in a variety of nonacute conditions such as cancer [33,34],
HIV [35], diabetes [36], Alzheimer disease and dementia [37], and car-
diovascular disease [38]. This is signicant in that individuals with con- 5. Conclusion
ditions associated with chronically below-average HDL-C may be
especially predisposed to fall below a dangerous HDL-C threshold dur- The results of our study suggest that a low plasma HDL-C level at the
ing acute infection. time of ED admission for suspected sepsis is strongly and independently
To our knowledge, prior studies have not examined whether low prognostic of subsequent multiple-organ dysfunction and death, with a
HDL-C levels contribute to poor outcomes (MODS and death), or con- predictive value surpassing that of all other clinical variables routinely
versely whether septic shock decreases HDL-C levels. Our very early de- measured at triage in this patient population. High-density lipoprotein
tection of decreased HDL-C before the development of organ cholesterol level may therefore provide valuable and easily accessible
dysfunctions and the high correlation between paired septic and prognostic information for clinicians when encountering patients with
nonseptic HDL-C levels supports the former hypothesis. We surmise suspected sepsis, and facilitate more rapid intervention for those at
that initial infection may decrease the HDL-C levels of some patients highest risk for progression to multiorgan dysfunction. Although our
below a critical threshold, either due to underlying factor(s) (e.- data suggest a causal relationship between an early drop in HDL-C and
g., genetics or preexisting conditions associated with low HDL-C) or subsequent deterioration of organ function, supported in part by knowl-
due to some early effect of bacterial toxins on lipoprotein metabolism, edge of HDL-C's importance in pathogen toxin clearance and endotheli-
al preservation, further studies are needed to establish denite
Table 4
mechanisms by which HDL-C protects organ integrity during sepsis, as
Multivariate logistic regression well as to establish the mechanisms by which HDL-C levels are de-
creased in the rst place.
MODS 28-d mortality
Supplementary data to this article can be found online at http://dx.
Variable Odds Odds
95% CI P 95% CI P doi.org/10.1016/j.jcrc.2016.11.041.
ratio ratio

HDL-C 0.969 0.944-0.994 .0166 0.931 0.858-0.991 .0489

Sex (male) 0.592 0.249-1.365 .2237 11.37 0.841-500.2 .1273 Acknowledgments
BMI 0.990 0.925-1.056 .7522 1.101 0.96-1.27 .1655
Lactate 1.076 0.923-1.272 .3552 0.909 0.608-1.17 .5302
Hemoglobin 0.999 0.982-1.015 .8745 0.990 0.951-1.025 .597 The authors would like to thank the Centre for Heart Lung
Platelets 0.999 0.996-1.002 .5413 0.999 0.991-1.005 .7535 Innovation's clinical research team for facilitating patient recruitment
Statin use 1.038 0.419-2.542 .9358 0.836 0.144-4.701 .8358 and data collection. This research was supported by Grant No.
Hepatitis 1.604 0.499-5.237 .4265 8.599 0.57-149.837 .1133 1368896 from the Canadian Institutes of Health Research.
Cirrhosis 4.152 0.614-43.047 .1739 0.158 0.004-4.327 .2918
APACHE II 1.118 1.048-1.199 .0011 1.253 1.087-1.505 .0054
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