Since presepsin was first discovered as a novel biomarker for sepsis in 2002 , a number of studies have demonstrated the significance of presepsin for identifying sepsis or predicting mortality. Although the diagnostic and prognostic values of presepsin for sepsis have been demonstrated in various studies [14–17], the complementary utility and applicability of presepsin in clinical practice still need further research.
Sepsis, a life-threatening organ dysfunction caused by infection, continues to be a major cause of death globally . Multiple studies have established the advantage of prompt intervention, such as rapid antibiotics administration, in reducing mortality [19, 20]. Early recognition of high-risk patients is crucial to improving patient outcomes. Nonetheless, it is often challenging to sort out high-risk patients in real-life clinical practice.
In this study, our data showed a significant difference in presepsin levels among the non-sepsis, sepsis, and septic shock patients, when categorized by the Sepsis-3 criteria. In addition, presepsin levels demonstrated a statistically significant difference between survivors and non-survivors in both sepsis and non-sepsis groups. It is noteworthy that presepsin was able to predict mortality even in the non-sepsis group. Moreover, combining presepsin with other well-known markers such as the Sepsis-3 definition by SOFA score and lactate provided greater predictive power. When presepsin was combined with the delta SOFA score, the predictive power for mortality was greater than using SOFA score alone, advocating the benefit of ancillary use of presepsin along with other markers. The results are in line with previous notions addressing the prognostic value of presepsin. Thus, with the help of presepsin, the chance of identifying high-risk patients could be improved.
Although the biological function of presepsin itself has yet to be elucidated, the primary source of presepsin secretion is CD14-positive monocyte/macrophage lineages which are triggered by bacterial phagocytosis . Presepsin is currently known to rise faster than PCT and CRP [6, 7, 10]. It is also speculated that presepsin rises faster than lactate, considering the fact that increases in lactate level result from tissue hypoperfusion. Besides, presepsin shows excellent correlation between sample types including whole blood, and the result can be obtained within 17 minutes . Hence, presepsin is a feasible marker for predicting survival in sepsis, especially at an early stage before progression of organ failure. Utilization of presepsin may assist in identifying patients with potentially unfavorable outcomes and could improve mortality rates by facilitating prompt treatment.
Although other markers such as CRP and PCT have been widely used, those markers have their own limitations in terms of predicting prognosis . Lactate levels could be also increased by hepatic dysfunction, renal dysfunction, or catecholamine, as well as sepsis-induced tissue hypoxia . Compared with those biomarkers, presepsin might have some advantages in that it could be more specific for sepsis and could have an earlier increase. On the other hand, presepsin may be elevated in renal or hepatic dysfunction without infection [3, 24] so further research would be needed for clinical interpretation.
There are several limitations to our study that deserve to be acknowledged. First, while the subjects were enrolled in a prospective manner, the selection criteria included procalcitonin and blood culture, which could cause selection bias. However, since procalcitonin and blood culture are generally ordered for almost all suspected sepsis patients, the chance of selection bias is relatively low. Besides, to the best of our knowledge, the number of reviewed subjects in this study is the largest among studies evaluating presepsin under the Sepsis-3 criteria, to date. Second, this study was conducted in a single institution, and approximately two-thirds of the enrolled subjects had a malignancy. Third, we were unable to obtain follow-up presepsin level changes over time. Since we only retrieved the presepsin level from a single time point at presentation, the actual onset of sepsis and whether the measured presepsin level represents the peak level are uncertain. Nonetheless, the characteristics of our data may in actuality better reflect the real-world clinical setting. Further research regarding the underlying mechanism of presepsin secretion, the biological role of presepsin, and the serial kinetics of presepsin according to the patient status are warranted.