Acute pancreatitis (AP) is a non-bacterial inflammation of the pancreas. Based on the development of local complications and/or organ failures, its severity is classified into mild, moderately severe, and severe according to the revised Atlanta classification.¹ Moderately severe and severe AP comprise approximately 15% to 25% of all cases. The mortality rate differs according to severity; mild AP has a very low mortality, whereas severe AP has a mortality as high as 36% to 50%.¹

Early recognition of severity of AP is crucial for management of AP and predictors of severity of AP reported in previous studies include clinical features, laboratory tests, radiologic findings, and various scoring systems. Hematocrit, blood urea nitrogen, C-reactive protein (CRP), and serum creatinine are routinely performed laboratory tests that can predict the severity of AP. Other markers include interleukin (IL)-1, 6, and 8, procalcitonin, trypsinogen activation peptide, polymorphonuclear elastase, pancreatic-associated protein, procarboxypeptidase-B, carboxypepsidase-B activation peptide, trypsinogen-2, phospholipase A-2, substance P, antithrombin III, and platelet activating factor. The scoring systems include the Ranson score, Glasgow score, Acute Physiology and Chronic Health Evaluation II score, bedside index of severity in AP, and harmless AP score. Balthazar score and computed tomography severity index (CTSI) score using radiologic images were also used to predict severity of AP. The targets of these predictors varied among studies, including only severe AP, both moderately severe and severe AP, organ failure, and local or systemic complications.²

Cho et al.³ conducted a retrospective study to investigate the role of inflammatory markers, including IL-6, procalcitonin, and CRP, and various scoring systems including CTSI, in differentiating mild from moderately severe and severe AP. Total 103 patients including 42 (40.8%) with mild AP were included. The area under the receiver operating characteristic curve for IL-6 at admission and CRP measured 24 hours after admission, and CTSI, were 0.775, 0.787, and 0.851, respectively; these markers were identified as useful predictors of mild AP. The diagnostic accuracy of IL-6 at admission (<50 pg/mL) and CRP levels at 24 hours after admission (<50 mg/L), for mild AP, were 70.9% and 69.9%, respectively. Among the scoring systems, CTSI showed an area under the receiver operating characteristic curve similar to that of IL-6 and CRP2.

CRP is produced by the liver in response to IL-1 and IL-6 stimulation. Previously, severe AP was suspected if the level of CRP was ≥150 mg/L at 48 hours from symptom onset.⁴ A CRP level ≥190 mg/L at 48 hours after admission or an increase in CRP level to >90 mg/L in the 48 hours interval from admission predicts severe AP.⁵ In this study, CRP levels <50 mg/L at 24 hours after admission predicted mild AP. Monitoring changes in CRP levels up to 48 hours should be considered when observing the severity of AP. IL-6 is a proinflammatory cytokine released during the early course of AP as an acute-phase response. A meta-analysis of 181 studies reported that the sensitivity and specificity of IL-6 in predicting moderately severe AP/severe AP is 87% and 88%, respectively.⁶ Although Cho et al. showed that the level of IL-6 at admission predicted mild AP earlier than the CRP level at 24 hours after admission, IL-6 is not a routinely performed laboratory test for AP in real world settings. Procalcitonin is released during bacterial infection and sepsis and acts as an acute-phase reactant. It can also be elevated in non-infectious conditions such as severe AP, and can predict the severity of AP with an accuracy of 86%.⁷ In a study by Cho et al.,³ the procalcitonin level failed to predict mild AP, but had a high area under the receiver operating characteristic curve value for predicting severe AP, consistent with the results of previous studies. Although computed tomography scans obtained less than 72 hours after symptom onset might underestimate the severity of AP, the study by Cho et al. showed that CTSI was predictive for mild AP. CTSI has shown to predict the severity of AP and the development of organ failure in previous studies.^8,9

For optimal predictors of the severity of AP, the acquisition of prediction result should be simple, prediction result should be available early, ideally identified at the time of admission, and cost-effective. Several parameters have shown promising results in predicting the severity of AP, but applying a single parameter is not sufficient. Further, predicting the severity and planning treatment strategy should be based on the incorporation of clinical, laboratory, and radiologic findings. Further large-scale prospective studies are required to validate the usefulness of IL-6, CRP2, and CTSI in predicting mild AP.

No potential conflict of interest relevant to this article was reported.