**Author details**

**6.8. Comparison between biomarker of sepsis**

72 Biomarker - Indicator of Abnormal Physiological Process

Lactate should be evaluated at least within 24 h after emergency admission, the decrease of lactate after 24 h related to poor prognosis of the patients [94]. CRP can increase within 24–48 h duration to 1000 folds during the acute phase and decrease to low normal value after the acute phase [95]. Procalcitonin start to rise 3–6 h after infection occur and reach its peak on 6–8 h, then remained in the blood until 12–48 h [96]. Meanwhile presepsin increase faster within 2–3 h after sepsis developed and rapidly decreased after symptoms resolved [97] so it

Several conditions can increase lactate in any person, such condition as inadequate oxygen delivery oxygen demands mismatch and inadequate oxygen utilization [94]. CRP increase in bacterial infection as part of innate immune response [95, 98]. It can also increase in condition of inflammation even can predict the cardiovascular event such as the sign of atherogenesis and pathogenesis of myocardial injury and used as predictor in healthy individuals [99, 100]. It also can be a predictor of mortality in hemodialysis patient [101, 102]. Procalcitonin will rise in the event of sepsis, systemic infection and severe inflammation. Procalcitonin will not rise in the event of viral infection, autoimmune and neoplasma, but it can rise in some people with some neuroendocrine tumor such as medullare carcinoma of thyroid, small cell lung carcinoma and renal failure [96, 103]. Procalcitonin is also known to rise in person with trauma [97]. Some inflammation can trigger the rise of procalcitonin are pancreatitis [104], appendicitis [105], burns [106], heat stroke [107], multitrauma [108] and extensive surgery [109]. Presepsin do not increase in patient with trauma without associated infection, thus make it specific in patient with sepsis [97]. Presepsin also reliable in patient with sepsis and both acute kidney injury and those who do not, but it has caveats in patient with advanced kidney injury and end stage renal disease [110]. Head to head study by cochrane comparing procalcitonin, presepsin and CRP is still ongoing [111]. Several data about sensitivity and specificity of these parameters are already covered by some journal. The study about diagnostic value of lactate in cancer patient with sepsis showed for the cutoff value of lactate more than 1 mmol/L could predict sepsis with sensitivity of 86.36% and specificity of 28.12%, with additional data that the value were not different in patient with and without cancer [112]. Another study showed 34.0% sensitivity and 82.0% specificity at the cutoff point of 2.0 mmol/L that emphasized the low sensitivity but high specificity in diagnosing sepsis [113]. While other study measures prognostic value of lactate showed that lactate value over 4.0 mmol/L have increased mortality with sensitivity and specificity of 36 and 92%, respectively [114]. CRP found to be useful as part of screening in sepsis patient with sensitivity and specificity 98.5 and 75%, respectively, for cutoff value 5 mg/dL or more [115]. Another study use CRP as parameter for successful treatment in ICU patient showed that decreasing level of CRP by 25% or more are good indicator with sensitivity of 97% and specificity of 95% [116]. A study showed that sensitivity and specificity of procalcitonin were 75 and 79%, respectively [117]. While another study in patient with renal impairment proposed different cutoff to determine if patient is in septic condition, due to the caveats of procalcitonin in renal failure patient [118]. Another study comparing CRP, procalcitonin and presepsin showed advantage of presepsin, with AUC of presepsin was 0.845, compared to PCT (0.652), and CRP (0.815). With sensitivity and specificity of presepsin with

can be used to determine whether the treatment is successful in patient with sepsis.

cutoff value 600 pg./mL was 87.8 and 81.4%, respectively [84].

Agustin Iskandar<sup>1</sup> , Hani Susianti1 , Muhammad Anshory<sup>2</sup> and Salvatore Di Somma3 \*

\*Address all correspondence to: salvatore.disomma@uniroma1.it

1 Clinical Pathology Department, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia

2 Internal Medicine Department, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia

3 Department of Medical-Surgery Sciences and Translational Medicine, Sapienza University of Rome, Italy
