Shi PN, Song ZZ, He XN, Hong JM. Evaluation of scoring systems and hematological parameters in the severity stratification of early-phase acute pancreatitis. World J Gastroenterol 2025; 31(15): 105236 [DOI: 10.3748/wjg.v31.i15.105236]
Corresponding Author of This Article
Jie-Ming Hong, MD, Chief Physician, Department of Gastroenterology, Ningbo Yinzhou No. 2 Hospital, No. 998 Qianhe North Road, Yinzhou District, Ningbo 315000, Zhejiang Province, China. jm_hong@126.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Clinical Trials Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Author contributions: Shi PN and Hong JM designed the research; Song ZZ and He XN contributed to the data collection; Shi PN and He XN analyzed the data; Shi PN, Song ZZ, and Hong JM wrote the paper. All authors reviewed the manuscript.
Institutional review board statement: The study was approved by the Human Ethics Committee of the Yinzhou No. 2 Hospital (approval number: Y2024-50).
Clinical trial registration statement: This clinical trial was registered at ClinicalTrials.gov, No. ChiCTR2500098956.
Informed consent statement: Informed consent statement has been applied for exemption for this study.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
CONSORT 2010 statement: The authors have read the CONSORT 2010 Statement, and the manuscript was prepared and revised according to the CONSORT 2010 Statement.
Data sharing statement: No additional data are available.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Jie-Ming Hong, MD, Chief Physician, Department of Gastroenterology, Ningbo Yinzhou No. 2 Hospital, No. 998 Qianhe North Road, Yinzhou District, Ningbo 315000, Zhejiang Province, China. jm_hong@126.com
Received: January 18, 2025 Revised: February 24, 2025 Accepted: March 25, 2025 Published online: April 21, 2025 Processing time: 92 Days and 4.5 Hours
Abstract
BACKGROUND
Acute pancreatitis (AP) is an emergency gastrointestinal disease that requires immediate diagnosis and urgent clinical treatment. An accurate assessment and precise staging of severity are essential in initial intensive therapy.
AIM
To explore the prognostic value of inflammatory markers and several scoring systems [Acute Physiology and Chronic Health Evaluation II, the bedside index of severity in AP (BISAP), Ranson’s score, the computed tomography severity index (CTSI) and sequential organ failure assessment] in severity stratification of early-phase AP.
METHODS
A total of 463 patients with AP admitted to our hospital between 1 January 2021 and 30 June 2024 were retrospectively enrolled in this study. Inflammation marker and scoring system levels were calculated and compared between different severity groups. Relationships between severity and several predictors were evaluated using univariate and multivariate logistic regression models. Predictive ability was estimated using receiver operating characteristic curves.
RESULTS
Of the 463 patients, 50 (10.80%) were classified as having severe AP (SAP). The results revealed that the white cell count significantly increased, whereas the prognostic nutritional index measured within 48 hours (PNI48) and calcium (Ca2+) were decreased as the severity of AP increased (P < 0.001). According to multivariate logistic regression, C-reactive protein measured within 48 hours (CRP48), Ca2+ levels, and PNI48 were independent risk factors for predicting SAP. The area under the curve (AUC) values for the CRP48, Ca2+, PNI48, Acute Physiology and Chronic Health Evaluation II, sequential organ failure assessment, BISAP, CTSI, and Ranson scores for the prediction of SAP were 0.802, 0.736, 0.871, 0.799, 0.783, 0.895, 0.931 and 0.914, respectively. The AUC for the combined CRP48 + Ca2+ + PNI48 model was 0.892. The combination of PNI48 and Ranson achieved an AUC of 0.936.
CONCLUSION
Independent risk factors for developing SAP include CRP48, Ca2+, and PNI48. CTSI, BISAP, and the combination of PNI48 and the Ranson score can act as reliable predictors of SAP.
Core Tip: Acute pancreatitis (AP) is an emergency gastrointestinal disease that requires immediate diagnosis and urgent clinical treatment. An accurate assessment and staging of severity are essential in initial intensive therapy. This study systematically explored the prognostic value of inflammatory markers and several scoring systems in severity stratification of early-phase AP. 463 patients with AP were enrolled in this study. The results revealed that C-reactive protein measured within 48 hours, calcium and prognostic nutritional index measured within 48 hours were independent risk factors for predicting severe AP. Computed tomography severity index, bedside index of severity in AP, and the combination of prognostic nutritional index measured within 48 hours and the Ranson score can act as reliable predictor of severity AP.
Citation: Shi PN, Song ZZ, He XN, Hong JM. Evaluation of scoring systems and hematological parameters in the severity stratification of early-phase acute pancreatitis. World J Gastroenterol 2025; 31(15): 105236
Acute pancreatitis (AP), a serious and rapidly developing inflammatory process of the pancreas, is one of the leading gastrointestinal diseases requiring immediate diagnosis and urgent clinical treatment[1-3]. Biliary sludge and/or gallstones, alcohol consumption, and hypertriglyceridemia, are the most common causes of AP, whereas drugs, obesity, diabetes, autoimmune disease, and infection are also potential causes[4,5]. AP can be classified into three categories based on severity: Mild AP (MAP), moderately severe AP (MSAP), and severe AP (SAP), according to the Atlanta’s criteria in 2012. Most cases of AP are self-limited and resolve spontaneously with a favorable clinical recovery. However, the remaining approximately 20%-30% of patients may develop severe forms of AP and serious local and/or systemic complications with deterioration[6]. Severe cases may deteriorate rapidly for a brief period of time in the early stages of disease, resulting in systemic inflammatory response syndrome and even multiple organ dysfunction syndrome[7]. An accurate assessment and precise staging of severity are essential in the initial intensive therapy, thereby improving the prognosis.
Currently, numerous risk scoring systems have been proposed and applied to identify the severity of AP. Acute Physiology and Chronic Health Evaluation II (APACHE II), the bedside index of severity in AP (BISAP), Ranson’s score, and the computed tomography (CT) severity index (CTSI) are commonly used scoring systems in the clinic[8]. The APACHE II score is helpful for intensive care unit outcome prediction; however, its use is complex and prone to mistakes[9]. CTSI can be used to evaluate pancreatic inflammation and necrosis to predict the severity of AP and is usually used after 48-72 hours post-presentation[10,11]. Other recent scores, such as the BISAP score, have been proposed as simple and accurate tools for the early identification of in-hospital mortality[12]. The sequential organ failure assessment (SOFA) score has also been applied to stratify risk and monitor responses to treatment in recent years[9]. However, these scoring systems have been criticized at times due to limitations such as low sensitivity, unnecessary complexity, an overly restrictive process, high cost, and too many parameters limiting widespread use[13]. Concurrently, a number of hematological and biochemical parameters have been used to predict the prognosis of AP at an early stage, such as C-reactive protein (CRP), blood urea nitrogen, and D-dimer[8]. However, most of these parameters cannot be used to comprehensively and systematically assess the severity of AP. Previous studies have suggested a potential clinical relationship between some combined hematological parameters and systemic inflammation, including the neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), lymphocyte-monocyte ratio (LMR), and red cell distribution width[14,15]. The prognostic nutritional index (PNI), which is calculated by the ratio of the albumin concentration and lymphocyte count, has attracted attention as an easily accessible biomarker reflecting inflammation and nutritional status[16]. These inflammation-based laboratory markers have also been investigated to predict illness severity in AP[17-19]. However, although scoring systems and hematological parameters have been previously explored to identify the adverse outcomes associated with AP, previous studies have revealed inconsistencies in their predictive ability. Few systematic studies have focused on the combination of these values in AP. Thus, this study systematically explored the prognostic value of these inflammatory markers (NLR, LMR, PLR, PNI, and CRP) and several scoring systems (APACHE II, SOFA, BISAP, CTSI, and Ranson) in the severity stratification of AP in the early phase.
MATERIALS AND METHODS
Patient selection
This study consecutively analyzed patients with AP admitted to Ningbo Yinzhou No. 2 Hospital between January 1, 2021, and June 30, 2024. The study was approved by the Human Ethics Committee of the Yinzhou No. 2 Hospital (approval number: Y2024-50) and the study was conducted with the patients’ informed consent. The diagnosis and severity stratification of AP were performed according to the 2012 revised Atlanta classification. The diagnosis of AP was based on two or more of the following features: (1) Abdominal pain characteristic of AP; (2) Threefold elevation of serum amylase and/or lipase levels above the upper limit of normal; and (3) Characteristic findings of AP on abdominal ultrasonography, magnetic resonance imaging or CT scan[1]. MAP was defined as an absence of organ failure and local complications; MSAP was defined as the presence of local or systemic complications and/or organ failure relieved within 48 hours; and SAP was defined as persistent organ failure for more than 48 hours[1]. The definition of organ failure included respiratory, renal, and cardiovascular failure, which was based on a score of 2 or more using the modified Marshall scoring system[20]. Biliary AP was defined as the existence of gallstones or biliary sludge on ultrasonography, CT, or magnetic resonance imaging. Hypertriglyceridemia-induced AP was defined as a serum triglyceride (TG) level reaching 11.3 mmol/L or TG levels between 5.65 and 11.3 mmol/L with chylous serum. Alcoholic AP was defined as a history of alcohol abuse within 48 hours before the onset of illness. Other possible causes of AP should be excluded when the above etiological diagnosis is made. Patients who met the following criteria were excluded: Age < 16 years, short hospital stay of less than 48 hours, pregnancy, chronic pancreatitis or pancreatic carcinoma, metastatic tumor, or severe infectious and immunosuppressive conditions.
Data collection
A detailed history and physical examinations of all enrolled patients, including age, gender, and body mass index (BMI), were conducted after admission. Laboratory parameters were collected upon arrival at the hospital, including complete blood counts, blood gas analyses, serum amylase, electrolytes, D dimer, and renal and hepatic function. The calcium (Ca2+) level was measured within 48 hours after admission. The worst value of all the laboratory parameters and vital signs were selected during the collection period. Additional outcome measures included length of hospital stay, the interval between medical attention and symptom onset, the presence of organ failure, and local complications. Contrast-enhanced CT was performed in all patients on days 2-5 after admission. Two senior radiologists calculated the CTSI score after contrast-enhanced CT. The radiologists who participated were blinded to all the clinical data and the scoring results of the other evaluators. The APACHE II, BISAP, and SOFA scores in the first 24 hours and the Ranson score at 48 hours after admission were recorded. Markers of inflammation (NLR, LMR, and PLR) levels were calculated at admission. PNI and CRP levels were measured at admission (PNIi; CRPi) and within 48 hours (PNI48; CRP48). There were no missing data during the research process.
Statistical analysis
Statistical analysis was performed with Statistical Product and Service Solutions software 27.0 (SPSS, Chicago, IL, United States) and GraphPad Prism (GraphPad Software, La Jolla, CA, United States). Sample size calculation was performed using Power Analysis and Sample Size (PASS, Kaysville, UT, United States) at the study design stage. The calculation was based on a predefined type I error of 0.05 (α = 0.05) and a test power of 0.9 (β = 0.1). Categorical variables were statistically compared using the χ2 test or Fisher’s exact test and are presented as numbers and percentages. Continuous variables were verified by the Kolmogorov-Smirnov test for the normality test. Variables that were normally distributed are presented as the means with standard deviations and were compared by one-way analysis of variance (ANOVA). Variables with skewed distributions are presented as medians with interquartile ranges and were compared using Kruskal-Wallis H test. Multiple variables were further evaluated and adjusted using the Bonferroni method for multiple comparisons. All parameters were tested by univariate logistic regression and P values < 0.05 were considered potentially significant. The clinical significance of each parameter was also considered for selection. The potential independent predictive variables were subsequently evaluated using forward stepwise multivariate logistic regression analyses. Multivariate models were established after eliminating the factors with collinearity. Receiver operating characteristic (ROC) analysis was used, and the area under the curve (AUC) was compared to evaluate the predictive accuracy of each scoring system and the laboratory predictive variables. The sensitivity, specificity, positive predictive value, and negative predictive value were assessed for severity prediction. A P value < 0.05 was considered to indicate statistical significance.
RESULTS
A total of 463 patients with AP were enrolled and categorized into three groups: MAP (n = 319, 68.90%), MSAP (n = 94, 20.30%), and SAP (n = 50, 10.80%). Tables 1 and 2 show the clinical profiles and basic characteristics of the patients. There were 309 (66.7%) males and 154 (33.3%) females with a median age of 49.0 (37.0-63.0) years and a mean BMI of 25.27 ± 4.01 kg/m2. There were no differences in respect to age (P = 0.057), gender (P = 0.683), or BMI (P = 0.700) among the three groups. The majority of etiologies included hypertriglyceridemia (n = 162, 35.0%) and gallstone (n = 156, 33.7%). With regard to comorbidities, 121 patients (26.1%) had diabetes mellitus, 154 patients (33.3%) had hypertension, 24 patients (5.2%) had coronary artery disease, 10 patients (2.2%) had chronic kidney disease, and 184 patients (39.7%) had biliary tract disease. As the disease worsened, the length of hospital stays significantly increased (P < 0.001). However, the duration of medical attention from symptom onset among the three groups was not significantly different (P = 0.182).
Table 1 Demographics and clinical profile in patients with acute pancreatitis, n (%).
Compared with the MAP group, the MSAP group presented significantly higher levels of CRPi, CRP48, D dimer, lactate dehydrogenase (LDH), and glucose (P < 0.001). However, they did not differ between the MSAP and SAP groups. The Ca2+ level significantly decreased as the severity of AP increased (P < 0.001), whereas the white cell count increased (P < 0.001). The serum platelet and hematocrit levels did not differ significantly among the different severity groups. The NLR of the MSAP group was significantly greater than that of the MAP group (P < 0.001), whereas the LMR was lower (P = 0.003). However, the NLR and LMR did not differ between the MSAP and SAP groups (P = 0.546; P = 1.000). There was no statistically significant difference in PLR between the different severity groups. The PNI48 was lower in the SAP group than in the MAP group (P < 0.001). APACHE II, BISAP, CTSI, SOFA, and Ranson scores all were significantly higher in the SAP group than in the MSAP group than in the MAP group (P < 0.001).
Univariate logistic regression analyses were used to evaluate all the predictors. The results revealed that etiology, diabetes mellitus status, white cell count, CRPi, CRP48, red cell distribution width, Ca2+, LDH, D dimer, TG, NLR, and PNI48 were potentially significant variables. Multivariate logistic regression revealed that CRP48 [adjusted odds ratio (OR) = 1.007, 95% confidence interval (CI): 1.002-1.011, P = 0.010], Ca2+ (adjusted OR = 0.125, 95%CI: 0.022-0.700, P = 0.007) and PNI48 (adjusted OR = 0.800, 95%CI: 0.720-0.880 P < 0.001) were independent risk factors for predicting SAP (Table 3). The combined CRP48 + Ca2+ + PNI48 model was constructed using the formula = 8.825 + 0.008 × CRP48 (mg/L) - 2.286 × Ca2+ (mmol/L) - 0.185 × PNI48.
Table 3 Results of univariate and multivariate logistic regression analysis for predicting severe acute pancreatitis.
Table 4 and Figure 1 showed the comparisons of the ROC curves for SAP among CRP48, Ca2+, and PNI48, the combined CRP48 + Ca2+ + PNI48 model, and all the scoring systems. The AUC values for CRP48, Ca2+, PNI48, APACHE II, SOFA, BISAP, CTSI, and Ranson scores for the prediction of SAP were 0.802, 0.736, 0.871, 0.799, 0.783, 0.895, 0.931 and 0.914, respectively. The sensitivity, specificity, positive predictive value, and negative predictive value for the above parameters were determined with optimal cutoff values of 118.25, 2.045, 38.53, 7.50, 1.50, 1.50, 4.50, and 2.50, respectively. The AUC for the combined CRP48 + Ca2+ + PNI48 model was 0.892, which was superior to those obtained for CRP48 (Z = 2.771, P = 0.006) and Ca2+ (Z = 4.625, P < 0.001). However, a comparison between the PNI48 model and the combined CRP48 + Ca2+ + PNI48 model revealed no difference (Z = 1.610, P = 0.107). Among the single parameters, CTSI demonstrated the highest accuracy for predicting SAP. However, there was no significant difference between pairwise comparisons among CTSI, BISAP, and Ranson (CTSI vs BISAP, Z = 1.640, P = 0.101; CTSI vs Ranson, Z = 0.793, P = 0.428; Ranson vs BISAP, Z = 0.836, P = 0.403). Among the scoring systems evaluated in the first 24 hours, the BISAP score was superior to the APACHE II score (Z = 3.124, P = 0.002) and the SOFA score (Z = 3.084, P = 0.002). When both PNI48 and Ranson were measured within 48 hours, the combination of PNI48 and Ranson achieved an AUC of 0.936.
Figure 1 Receiver operating characteristic curve analysis for predicting severe acute pancreatitis by different parameters.
ROC: Receiver operating characteristic; CRP48: C-reactive protein measured within 48 hours; PNI48: Prognostic nutritional index measured within 48 hours; APACHE II: Acute Physiology and Chronic Health Evaluation II; SOFA: Sequential organ failure assessment; BISAP: Bedside index of severity in acute pancreatitis; CTSI: Computed tomography severity index; AUC: Area under the curve.
Table 4 Statistical data of receiver-operating characteristics curve analysis for predicting severe acute pancreatitis by different parameters.
Variables
AUC (95%CI)
P value
Cut-off value
Sensitivity, %
Specificity, %
PPV, %
NPV, %
CRP48
0.802 (0.734-0.870)
< 0.001
118.25
76.00
76.51
28.15
96.34
Ca2+
0.736 (0.643-0.828)
< 0.001
2.045
60.00
84.99
32.61
94.61
PNI48
0.871 (0.826-0.916)
< 0.001
38.53
90.00
74.33
29.80
98.40
CRP48 + Ca2+ + PNI48
0.892 (0.843-0.940)
< 0.001
0.15
78.00
86.68
40.86
96.76
APACHE II
0.799 (0.735-0.864)
< 0.001
7.50
72.00
77.97
28.35
95.83
SOFA
0.783 (0.711-0.856)
< 0.001
1.50
72.00
74.09
25.17
95.63
BISAP
0.895 (0.862-0.929)
< 0.001
1.50
94.00
79.18
35.34
99.09
CTSI
0.931 (0.900-0.962)
< 0.001
4.50
80.00
89.83
48.78
97.38
Ranson
0.914 (0.878-0.949)
< 0.001
2.50
88.00
77.97
32.59
98.17
PNI48 + Ranson
0.936 (0.909-0.962)
< 0.001
0.07
94.00
81.11
37.60
99.11
DISCUSSION
AP is an inflammatory disease of the pancreas, with significant morbidity and mortality in severe cases. In this study, we compared the predictive value of hematological parameters and several scoring systems (APACHE II, SOFA, BISAP, CTSI, and Ranson) for the onset of AP. We identified three independent risk factors: CRP48, Ca2+, and PNI48. Our data also suggested that, among the comorbidities, diabetes mellitus was significantly associated with MSAP and SAP.
The mechanisms and progressions of SAP are still poorly understood and may be associated with many factors. Some simple hematological parameters in the clinic, such as CRP and Ca2+, are widely used to evaluate the condition of AP patients. CRP is an essential indicator of inflammatory reactions. The localization and deposition of CRP appear to be key mediators of serious disease process, including AP[21]. CRP enhances the inflammatory cascade by stimulating the complement system and inducing the secretion of pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-1β, thereby aggravating pancreatic tissue damage[22,23]. Prior studies have shown the poor predictive value of CRP levels at an early stage[24]. However, after 24-48 hours, the CRP level has good prognostic accuracy for SAP, mortality, and pancreatic necrosis[25,26]. Our studies revealed that CRPi and CRP48 were significantly higher in MSAP compared with MAP, but no difference was detected between MSAP and SAP. CRP48 can be regarded as an independently predictive factor with the AUC value of 0.802. Therefore, continuous monitoring of CRP levels reliable for predicting severity.
Ca2+ is a versatile signal carrier that regulates various cellular functions[27]. Ca2+ overload and premature trypsinogen activation sabotage crucial cellular defense mechanisms, leading to pancreatic necrosis[28-30]. Previous studies have identified low Ca2+ levels as a risk factor for pancreatic necrosis, persistent organ failure, and SAP[31-33]. Similarly, in our study, the concentration of Ca2+ was negatively and significantly correlated with the severity of AP. PNI is regarded as a simple and effective parameter reflecting the nutritional and immunological status of the body. Prior studies confirmed the function of PNI as a predictive indicator for the prognosis of many cancers and inflammatory diseases[16,34]. Li et al[35] reported that PNI was independently associated with the development of SAP and mortality in AP patients. Despite this evidence, very few studies have reported a relationship between PNI and the severity of AP. In our study, we estimated the prognostic value of PNI for predicting the severity of AP. Multivariate regression analyses indicated that PNI48 was independently associated with the occurrence of SAP. ROC curve analysis revealed that the ability of PNI48 to predict SAP was preferable, with an AUC value of 0.871. We found that the PNI48 level significantly decreased as the severity of AP increased, whereas the PNIi level did not significantly change. The reason for this phenomenon may be inflammatory cascade and nutrient expenditure during the development of AP. Therefore, variations in the nutritional status of patients may be related to the severity of AP. As PNI may be affected by nutritional support, patients with a low PNI after nutritional treatment need more attention due to the possibility of AP aggravation.
Three inflammatory markers, CRP48, Ca2+, and PNI48, were combined to construct a logistic regression model, including. Previous studies have also explored the use of combined indicators to predict AP. For instance, Li et al[36] utilized a combination of fatty liver, procalcitonin, and the CRP-to-lymphocyte ratio to diagnose SAP, achieving an AUC of 0.795, which also reflects a high level of diagnostic performance. Similarly, Kong et al[37] identified heparin-binding protein, procalcitonin, and CRP as risk factors for SAP and combined these three markers to predict the severity of AP. Yi et al[38] reported the independent predictive value of CRP, LDH, Ca2+, and ascites in hypertriglyceridemia-induced AP. This combined diagnostic model demonstrated high accuracy, with an AUC of 0.960[38]. In our study, the AUC of the CRP48 + Ca2+ + PNI48 model reached 0.892, indicating strong predictive ability. To the best of our knowledge, we are the first to apply these three inflammatory markers to evaluate SAP. Our findings suggest that the combination of multiple hematological parameters can effectively predict SAP, highlighting the broader clinical practicability of integrated inflammatory parameters.
We found that the scores of several scoring systems (APACHE II, SOFA, BISAP, CTSI, and Ranson) significantly increased with the increasing severity of AP. The ROC curve indicated that CTSI achieved the highest AUC for the prediction of SAP among the single parameters, whereas the BISAP and Ranson scores presented similar results. The abilities of APACHE II and SOFA were fair, with AUC values of 0.799 and 0.783, respectively. The CTSI, a scoring system derived by Balthazar et al[39], has been widely used as a standard assessment to describe CT findings in AP[40]. Prior studies have confirmed that CTSI is significantly correlated with clinical outcome parameters, consistent with the revised Atlanta criteria grading of severity[11,41]. However, a CT scan is usually recommended after 48-72 hours to determine the exact extent of pancreatic necrosis[41]. Therefore, the CTSI obtained from CT scans in the early stage of the disease may not confirm the exact severity of AP. The evaluation of CTSI may emphasize local complications but not the systemic inflammatory response. Ranson and APACHE II have been used since the 1970s to assess the severity of AP. The main limitation of Ranson is the need for a 48-hour duration to complete the calculation. As PNI48 was also measured within 48 hours with good prognostic accuracy, we found that the combination of PNI48 and the Ranson score reached an AUC of 0.936, reflecting superior prognostic value. The BISAP was designed to construct a simple scoring system that provides an early estimation of AP risk based on five variables collected within 24 hours[12]. Our data showed BISAP performed better than APACHE II and SOFA in predicting SAP in patients during the first 24 hours. Therefore, BISAP is superior to other predictors in the prediction of SAP during the first 24 hours. As AP progresses to within 48 hours, the combination of PNI48 and the Ranson score could improve the prediction performance. CTSI can be a useful predictor of local complications.
There were several limitations in this study. Selection bias was inevitable since this was a retrospective single-center study with a limited sample size. Multicenter research with a large sample size could be conducted to confirm the value of the present analysis in further research. Second, laboratory parameters were collected upon arrival at the hospital and within 48 hours. Considering these variables change with time, they should be studied at additional time points. Using more detection methods and studying more relevant laboratory parameters may reveal other pertinent factors. Then, the common and classical scoring systems for AP were studied in this study. Some of the novel scoring systems are yet to be adopted and can be verified in future studies. Moreover, the mechanisms underlying the relationships between the predictors and severity of AP need to be investigated.
CONCLUSION
In conclusion, CRP48, Ca2+, and PNI48 were independent risk factors for AP in our study. The combination of CRP48, Ca2+, and PNI48 could be helpful tools as hematological parameters in evaluating SAP. CTSI was the best single parameter in predicting severity, but it had the shortcomings of assessing too later. BISAP can act as a simple and excellent predictor of SAP during the first 24 hours. As AP progresses to within 48 hours, the combination of PNI48 and the Ranson score could be a superior predictor of adverse outcomes in SAP.
Footnotes
Provenance and peer review: Unsolicited article; Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Gastroenterology and hepatology
Country of origin: China
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P-Reviewer: Wu YM; Xu DH; Zhou X S-Editor: Wang JJ L-Editor: A P-Editor: Zhao S
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