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Review
. 2023 Jan 9:10:1019825.
doi: 10.3389/fped.2022.1019825. eCollection 2022.

Evaluation of presepsin as a diagnostic tool in newborns with risk of early-onset neonatal sepsis

Iva Pospisilova  1   2 , Helena L Brodska  3 , Marketa Bloomfield  2   4 , Klara Borecka  1 , Jan Janota  5   6   7
Affiliations
Review

Evaluation of presepsin as a diagnostic tool in newborns with risk of early-onset neonatal sepsis

Iva Pospisilova et al. Front Pediatr. .

Abstract

Objectives: To evaluate the efficacy of presepsin (P-SEP) as a potential biomarker of early-onset neonatal sepsis (EOS) and compare it to other routinely used markers of inflammation. To establish the cut-off values of P-SEP for EOS.

Study design: 184 newborns were prospectively recruited between January 2018 to December 2020. Newborns >34th gestational week with suspected infection were included up to 72 h after delivery, and divided into three categories (i.e., unlikely, possible, and probable infection) based on risk factors, clinical symptoms and laboratory results. Values of plasma P-SEP were sequentially analyzed.

Results: Median values of P-SEP in newborns with probable infection were significantly higher compared to healthy newborns (p = 0.0000013) and unlikely infection group (p = 0.0000025). The AUC for discriminating the probable infection group from the unlikely infection group was 0.845 (95% Cl: 0.708-0.921). The diagnostic efficacy of P-SEP was highest when used in combination with IL-6 and CRP (0.97; 95% CI: 0.911-0.990). The optimal cut-off value of P-SEP was determined to be 695 ng/L.

Conclusion: P-SEP, when combined with IL-6 and CRP, may be utilized as a negative predictive marker of EOS (NPV 97.2%, 95% CI: 93.3-101), especially in newborns at low to medium risk of infection.

Keywords: biomarker; inflammation; neonatal sepsis; newborns; presepsin.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Representation of newborns in the study.
Figure 2
Figure 2
Presepsin (P-SEP) levels at T0 (onset of symptoms) in the 3 subgroups (low [1], medium [2], high-risk [3]) of enrolled neonates and healthy controls [0]. Kruskal-Wallis test followed by robust Dunn's multiple comparisons with Bonferroni correction was used to evaluate between group differences. Vertical lines symbolize medians, boxes indicate interquartile range, whiskers indicate the limits for data homogeneity, and crosses with rhombs symbolize means with SDs. ***p < 0.001, *p < 0.05.
Figure 3
Figure 3
CRP levels at T0 (onset of symptoms) in the 3 subgroups (low [1], medium [2], high-risk [3]) of enrolled neonates and healthy controls [0]. Kruskal-Wallis test followed by robust Dunn's multiple comparisons with Bonferroni correction was used to evaluate between group differences. Vertical lines symbolize medians, boxes indicate interquartile range, whiskers indicate the limits for data homogeneity, and crosses with rhombs symbolize means with SDs. ***p < 0.001.
Figure 4
Figure 4
Time-dependent dynamics of presepsin and other biomarkers in the 3 subgroups of neonates. Triangles, squares, and circles with error bars symbolize re-transformed means with their 95% confidence intervals after Bonferroni correction for low-risk, medium-risk and high-risk group, respectively as evaluated by ANOVA model consisting of between subject factor Risk of infection, within-subject factor Hour, and Subject factor (explaining inter-individual variance) followed by Bonferroni multiple comparisons. Presepsin-Risk: F = 113.9, p < 0.001, ηp2 = 0.37; Hour: F = 5.5, p = 0.013, ηp2 = 0.0276; Risk × Hour: F = 1.6, p = 0.209, ηp2 = 0.0165; Subj(Risk): F = 8.9, p < 0.001, ηp2 = 0.186; IL-6-Risk: F = 2.8, p = 0.088, ηp2 = 0.0362; Hour: F = 13.7, p < 0.001, ηp2 = 0.157; Risk × Hour: F = 1.9, p = 0.147, ηp2 = 0.0498; Subj(Risk): F = 3, p = 0.018, ηp2 = 0.171; PCT-Risk: F = 1.7, p = 0.214, ηp2 = 0.0388; Hour: F = 5.7, p = 0.011, ηp2 = 0.121; Risk × Hour: F = 0.4, p = 0.836, ηp2 = 0.017; Subj(Risk): F = 3.9, p = 0.005, ηp2 = 0.321; CRP-Risk: F = 7.9, p = 0.003, ηp2 = 0.169; Hour: F = 2.7, p = 0.091, ηp2 = 0.0653; Risk × Hour: F = 0.5, p = 0.733, ηp2 = 0.0254; Subj(Risk): F = 2.4, p = 0.05, ηp2 = 0.233; F, p, and ηp2 represent F-statistic, p-value, and effect size, respectively; ηp2 = 0.01, 0.06, and >0.14 are small, medium, and large effect size.
Figure 4
Figure 4
Risk, hour and both variables of individual inflammatory markers is in the text of Figure 4.
Figure 5
Figure 5
ROC curves for P-SEP, CRP at T0 (onset of symptoms) in healthy controls, and in the group low-risk extra PCT and IL-6 at T0 (onset of symptoms) in the group low-risk.
Figure 6
Figure 6
ROC curve depicting the diagnostic power of combined use of P-SEP with IL-6 and CRP in between-group comparison of low-risk vs. high-risk group.
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