Subject characteristics
During the study period, 69 consecutive patients with predicted SAP were admitted
to ICU: 3 patients were excluded because of prior history of acute pancreatitis, and
66 patients were enrolled in this investigation. Table 1 lists the patients’ demographic data and clinical characteristics. Overall, the in-hospital
mortality for the entire group was 19.7%. Compared to hospital survivors, the hospital
non-survivors had higher disease severity as evidenced by higher Ranson, APACHE II,
SOFA, and modified Marshall scores.
Table 1. Patients’ demographic data and clinical characteristics
Lipid profile and mortality
The levels of HDL, and APO-A-I were significantly higher in those who survived (Table 1), while the levels of TNF-? and IL-6 were higher in those who died. Although weak,
HDL and APO A-I were inversely correlated with Ranson, APACHE II, SOFA and modified
Marshall scores (Table 2). Among these, HDL had the strongest negative correlation with the modified Marshall
score. Inflammatory cytokines were also negatively correlated with HDL, and APO A-I.
Of these, HDL had the strongest inverse relationship with serum IL-6 levels. The concentrations
of APO A-I and HDL decreased progressively and significantly with the number of organ
failures as defined by the modified Marshall score (Figure 1). The discriminating power of APO A-I and HDL to predict 28-day mortality was tested
using the AUROC. The AUROC for APO A-I and HDL to predict 28-day mortality was 0.869?±?0.047
(mean?±?standard error of the mean (SEM)), 95% CI 0.764 to 0.940, and 0.791?±?0.059,
95% CI 0.673 to 0.881, respectively.
Table 2. Correlation between serum lipid, disease severity scores, and serum inflammatory cytokines
Figure 1. Association among apolipoprotein A-I (APO A-1), high-density lipoprotein (HDL) and
organ failure. The levels of apolipoprotein A-I and HDL decrease progressively and significantly
with the number of organ failures. *P 0.05 compared to the group with no organ system failure; **P 0.001 compared to the group with no organ system failure (Kruskall-Wallis test followed
by Dunn’s post hoc test). Results are expressed as median, with error bars representing
the IQR.
Lipid profile and organ failure
Table 3 lists the demographic data, clinical characteristics and lipid profiles in patient
subgroups stratified by the presence of OF. The levels of total cholesterol, HDL,
LDL and APO A-I were significantly lower in patients with OF, while the levels of
TNF-?, IL-6 and CRP were lower in those without OF. When persistency of organ failure
was not taken into account, there was no difference in mortality rates between patient
with OF and those without OF (Table 3).
Table 3. Patients’ demographic data and clinical characteristics stratified by early organ
failure
HDL and APO A-I as markers to predict persistent organ failure
To further demonstrate the association among lipid profile, persistent OF and mortality,
those patients with OF were sub-grouped into transient OF and persistent OF. Table 4 shows the clinical characteristics and outcomes in patient subgroups stratified by
persistency of OF. The levels of total cholesterol, HDL, LDL and APO A-I were significantly
lower in patients with persistent OF, while the levels of TNF-?, and IL-6 were higher
in those with persistent OF. The mortality rates were significantly higher in patients
with persistent OF, while ICU stay was shorter in patients with transient OF. The
discriminating power of APO A-I and HDL to predict persistent OF was also tested using
AUROC. When all patients with predicted SAP were analyzed, the AUROC for APO A-I and
HDL to predict persistent OF was 0.898?±?0.043 (mean?±?SEM), 95% CI 0.813 to 0.983,
and 0.912?±?0.036, 95% CI: 0.842 to 0.982, respectively. There was no significant
difference in discriminating power between HDL and APO A-I (P?=?0.587). When those patients with OF were analyzed, the AUROC for APO A-I and HDL
to predict persistent OF was 0.895?±?0.045 (mean?±?SEM), 95% CI 0.808 to 0.983, and
0.904?±?0.037, 95% CI 0.832 to 0.976 respectively (P?=?0.838). These results indicate that both HDL and APO A-I are good markers in this
clinical setting. Meanwhile, we also evaluated the discriminating ability of CRP because
it has been used as a biomarker to predict severity 1]. The area under ROC curve for CRP obtained by analyzing all patients or patients
with OF was 0.603?±?0.061, and 0.568?±?0.076, respectively. Pair-wise comparisons
of AUROC showed that both HDL and APO A-I gave significantly higher AUROC and thus,
better predictive accuracy than CRP when analyzing all patients (P 0.001 relative to both HDL and APO A-I) or patients with OF (P 0.001 relative to both HDL and APO A-I). The best cutoff points of HDL and APO A-I
to predict persistent OF remained the same when analyzing all patients or patients
with OF. Table 5 shows the predictive values of the chosen cutoff points (16.5 mg/dl for HDL, 64 mg/dl
for APO A-I), which gave the best Youden index, for prediction of persistent OF.
Table 4. Patients’ demographic data and clinical characteristics stratified by persistent organ
failure
Table 5. HDL and APO A-I for prediction of persistent organ failure
We also evaluated the performance of different scores. We found that there is no difference
in discriminating power of predicting persistent OF among HDL, APO A-I and different
scores (Additional file 1: Table S1).