Abstract
Rapidly identifying acute pancreatitis (AP) patients at higher risk of developing severe AP (SAP) can help clinicians better direct medical treatment and management. Therefore, we examined clinical parameters and laboratory markers in patients with different etiologies and severities of AP. Demographic, clinical characteristics, and laboratory data were collected from electronic medical records of adult patients with AP and admitted to 1 healthcare system between 2015 and 2021. AP severity was determined using the revised Atlanta classification. The association between biomarkers and outcomes was assessed using exploratory data analyses. Patients with SAP were older than those with mild AP (58.3 (20.2) vs 48.1 (17.5) years, P = .002). Acute biliary pancreatitis predominantly affected women (66%) and Hispanic individuals (51%). Acute alcoholic pancreatitis predominantly affected men (72%) and Black individuals (53%). For patients with acute biliary pancreatitis and pancreatitis of other etiologies, creatinine was the most significant predictor of pancreatitis severity. Patients with hypertriglyceridemia-associated AP were younger (mean (SD): 41.1 (11.9) years, P < .001) and had a higher white blood cell count (14.2 × 103 cells/µL, P < .001). Distinct clinical features and indicators are indicative of mild AP and SAP. Etiology-specific patterns can aid in identifying individuals at high risk of SAP.
Keywords: acute disease, biomarkers, pancreas, pancreatitis, retrospective studies
1. Introduction
Acute pancreatitis (AP) is an inflammatory disease characterized by trypsinogen activation and subsequent conversion of trypsinogen to the enzyme trypsin within the pancreatic acinar cell. Trypsin digests proteins and activates other digestive enzymes, causing inflammation and destruction of secretory cells. AP can also be caused by hypercalcemia, which results in pancreatic secretory block and pancreatic injury. Ductal obstruction, which causes a blockage of pancreatic enzymes leading to accumulation and inflammation in the pancreas, can also lead to AP.[1–3] The main AP etiologic factors in the United States are gallstones and alcohol consumption. Other causes include hypertriglyceridemia (HTG), drugs, endoscopic procedures, and diabetes.[1]
Nearly 220,000 people are diagnosed with AP in the United States every year, with an approximate incidence of 65 cases per 100,000 person-years.[4,5] The mortality rate is 0.4 to 1 deaths per 100,000 person-years.[5] AP generates more than 600,000 annual visits to the emergency department (ED) per year, and the age-standardized disability-adjusted life year (years of life lost due to premature mortality and years of life lived with disability) in the United States for 2018 was 27.1 to 34.5 per 100,000 person-years. In 2018, the annual cost of AP hospitalization was almost 5 billion dollars (USD).[6]
Several clinical and biochemical parameters have been used to develop scoring systems to predict AP severity. However, these systems have some drawbacks. Ranson criteria and Glasgow Coma Scale are limited by an inability to complete the score before 48 hours of illness initiation. Acute Physiology and Chronic Health Evaluation is limited by its complexity.[7] Bedside index for severity in AP (BISAP) was initially developed to prognosticate mortality in AP; however, the score has only a ~51% sensitivity in diagnosing AP severity.[8] The biomarker C-reactive protein (CRP) exhibits a delayed peak, typically 72 hours after the onset of symptoms.[7] Recently, a new score using baseline laboratory values of creatinine (Cr), white blood cell (WBC) count, procalcitonin (PCT), and the systemic inflammatory response system (SIRS) was developed.[9] Identifying these clinical and biochemical parameters at the beginning of AP presentation helps to identify patients who are at higher risk of developing SAP. This allows for direct medical treatment and management, limiting the morbidity and mortality of AP.
The objective of this study was to examine variations in baseline clinical parameters and biochemical laboratory markers among patients with different AP severities upon presentation to the emergency department (ED). Specifically, we emphasized the distinctions between patients with moderately severe AP (MSAP) experiencing transient organ failure (TOF) and those with acute pancreatic fluid collections (APFC). Furthermore, we explored how these parameters differ according to AP etiology.
2. Methods
2.1. Study design and setting
This retrospective descriptive exploratory data analysis (EDA) investigated patterns between laboratory parameters and the severity and etiology of AP. The study included patients from 3 hospitals affiliated with 1 healthcare system in Dallas, TX, United States, between January 2015 and December 2021. All patients received standardized early medical management following the Methodist AP Protocol.[10] The WCG Institutional Review Board approved the study (Study Number: 1270067), confirming that it met the criteria for a consent waiver under 45 CFR 46 116 (f) (2018 requirements).
2.2. Participants
Baseline data were extracted from electronic medical records. Patients were selected if they were ≥ 18 years of age, admitted to the hospital within 48 hours of symptom onset, and met the diagnostic criteria for AP based on at least 2 of the following 3 features: abdominal pain consistent with a diagnosis of AP; serum amylase and/or lipase levels elevated to at least 3 times the upper limit of normal; or characteristic imaging findings on enhanced computed tomography scans.[11] Patients were excluded if they had end-stage renal disease and were on dialysis, post-endoscopic retrograde cholangiopancreatography pancreatitis, trauma-related pancreatitis, or pancreatic cancer.
2.3. Independent variables and outcomes
Demographic characteristics of the patients, including age, body mass index (BMI), and race/ethnicity were collected from the electronic medical records. Baseline laboratory values obtained upon admission to the ED included Cr level, hematocrit (HCT), and WBC, neutrophil, lymphocyte, and platelet counts. Additionally, systemic immune-inflammatory markers, such as the neutrophil to lymphocyte ratio (NLR), the systemic immune-inflammation index (SII), and the platelet-to-lymphocyte ratio (PLR), were collected; calculations of NLR, SII, and PLR are described elsewhere.[12] Additional marker data collected included CRP, PCT, albumin, bilirubin, albumin–bilirubin (ALBI) score, and CRP/albumin ratio. Calculation of the ALBI score was according to the formula described elsewhere.[13] The CRP/albumin ratio was calculated by dividing the CRP level (mg/dL) by the serum albumin level (g/dL). Clinical indicators, such as the BISAP score, SIRS, and harmless AP score (HAPS), were gathered at admission.
AP severity was determined according to the revised Atlanta classification, which defines AP into 3 categories: mild AP (MAP), characterized by a lack of organ failure and the absence of local or systemic complications; MSAP, defined by the presence of TOF or APFC, local complications, or exacerbation of comorbidities; and SAP, defined by persistent (>48 hours) organ failure.[11,14] Organ failure included failure in at least 1 system (i.e., respiratory, renal, or cardiovascular), with a modified Marshall score ≥ 2.[11] In the patients with MSAP, TOF was defined as organ failure that resolves in < 48 hours,[11] and APFC was defined as those collections identified with computed tomography scans if abdominal pain persisted 24 hours after admission.[15]
AP etiologies were grouped into 4 categories: acute biliary pancreatitis (ABP), acute alcoholic pancreatitis (AAP), HTG-AP, and other causes of AP. ABP was diagnosed based on identification of gallbladder stones with ultrasound, other diagnostic images, or previous episodes of biliary colic.[3] AAP was diagnosed when there was a history of chronic alcohol consumption and an increased aspartate aminotransferase to alanine aminotransferase ratio.[16] HTG-AP was diagnosed when serum triglyceride levels were > 1000 mg/dL.[3] Patients with other etiologies or idiopathic pancreatitis where included in the other causes group.
2.4. Statistical analysis
The distribution and pattern of continuous variables were examined through EDA using histograms, box plots, and bar charts. These variables were described with mean and standard deviation when normally distributed or with median and minimum to maximum values (min–max) when non-normally distributed. T tests or analysis of variance with Bonferroni correction were used to compare differences between means, and the non-parametric Kruskal–Wallis test was applied when dealing with non-normal distributions. Pairwise comparisons were conducted between the subgroups for each outcome. Categorical variables were summarized as percentages and compared using the Pearson chi-square test. Additionally, pairwise comparisons were made for contingency tables (2 × 2). The data contained 6% of missing values for PCT, which were imputed using the median for the variable. P-values < .05 were considered statistically significant. The EDA was performed using Python version 3.9 (Python Software Foundation, Wilmington), and the statistical analysis was conducted with the Statistical Analysis System OnDemand for Academics (SAS) 9.4 (SAS Institute, Cary).
3. Results
In total, 779 patients met the diagnostic criteria for AP. The mean age of patients with AP was 48.9 (18) years and 52% were female (Table 1). The patients were racially diverse: 36% were Black, 39% were Hispanic, and 25% were White. ABP (39%) and AAP (27%) were the most common etiologies of AP. The mortality rate during hospital stay was 0.6%.
Table 1.
Baseline and demographic characteristics of patients with acute pancreatitis stratified by severity.
| Variable | Overall (N = 779) |
MAP (N = 670) |
MSAP (N = 81) |
SAP (N = 28) |
P value* | Pa value† | Pb value‡ | Pc value§ |
|---|---|---|---|---|---|---|---|---|
| Age (yr), mean (SD) | 48.9 (18) | 48.1 (17.5) | 52.6 (19.3) | 58.3 (20.2) | .0019 | .0317 | .0031 | .1451 |
| BMI (kg/m2), mean (SD) | 29.8 (7.7) | 29.7 (7.9) | 29.6 (5.9) | 31.5 (7.6) | .4723 | .9105 | .2266 | .2609 |
| Gender, n (%) | ||||||||
| Female | 404 (52%) | 358 (53%) | 38 (47%) | 8 (29%) | .023 | .267 | .0099 | .0902 |
| Male | 375 (48%) | 312 (47%) | 43 (53%) | 20 (72%) | ||||
| Race/ethnicity, n (%) | ||||||||
| White | 197 (25%) | 164 (24%) | 26 (32%) | 7 (25%) | .5501 | .3072 | .7253 | .5048 |
| Black | 281 (36%) | 244 (36%) | 25 (31%) | 12 (43%) | ||||
| Hispanic | 301 (39%) | 262 (39%) | 30 (37%) | 9 (32%) | ||||
| Etiology, n (%) | ||||||||
| Biliary | 303 (39%) | 267 (40%) | 27 (33%) | 9 (32%) | .0006 | .0075 | .0012 | .4823 |
| Alcoholic | 208 (27%) | 182 (27%) | 18 (22%) | 8 (29%) | ||||
| Hypertriglyceridemia | 48 (6%) | 31 (5%) | 11 (14%) | 6 (21%) | ||||
| Other causes of AP | 220 (28%) | 190 (28%) | 25 (31%) | 5 (18%) | ||||
| HAPS, n (%) | ||||||||
| Not harmless | 423 (54%) | 348 (52%) | 52 (64%) | 23 (82%) | .0012 | .0368 | .0017 | .0772 |
| Harmless | 356 (46%) | 322 (48%) | 29 (36%) | 5 (18%) | ||||
| SIRS, n (%) | ||||||||
| No | 514 (66%) | 468 (70%) | 38 (47%) | 8 (29%) | <.0001 | <.0001 | <.0001 | .0902 |
| Yes | 265 (34%) | 202 (30%) | 43 (53%) | 20 (71%) | ||||
| BISAP, n (%) | ||||||||
| 0 | 345 (86%) | 327 (49%) | 18 (22%) | 0 (0%) | <.0001 | <.0001 | <.0001 | .0001 |
| 1 | 302 (39%) | 249 (37%) | 42 (52%) | 11 (39%) | ||||
| 2 | 105 (13%) | 81 (12%) | 15 (19%) | 9 (32%) | ||||
| 3 | 22 (3%) | 13 (2) | 6 (7%) | 3 (10%) | ||||
| 4 | 5 (4%) | 0 (0%) | 0 (0%) | 5 (18%) | ||||
| Laboratory values, mean (SD), median (min–max) | ||||||||
| CR (mg/dL) | 0.8 (0.3–6.2) | 0.7 (0.3–3.1) | 0.9 ((0.3–4.1) | 1.7 (0.5–6.2) | <.0001 | .0001 | <.0001 | .0005 |
| HCT (%) | 41 (5.9) | 40.9 (5.7) | 41.5 (6.8) | 42 (7.9) | .4496 | .3705 | .3425 | .7227 |
| WBC (×103/µL) | 10.9 (4.4) | 10.5 (4.1) | 12.8 (5.2) | 14.7 (4.7) | <.0001 | <.0001 | <.0001 | .0396 |
| Neutrophils (×103/µL) | 8.3 (4.3) | 7.9 (4.1) | 10.1 (4.8) | 11.6 (4.4) | <.0001 | <.0001 | <.0001 | .091 |
| Lymphocytes (×103/µL) | 1.4 (0.1–19.1) | 1.5 (0.1–19.1) | 1.2 ((0.1–6) | 0.9 (0.2–4.9) | .012 | .2069 | .0055 | .0961 |
| Platelets (×103/µL) | 251 (117) | 248 (105) | 283 (192) | 243 (92) | .0366 | .0109 | .8507 | .1251 |
| CRP (mg/dL) | 14 (3–380) | 13 (3–260) | 18 (5–355) | 23.5 (5–380) | <.0001 | <.0001 | .0035 | .6049 |
| PCT (ng/mL) | 0.1 (0–100) | 0.1 (0–100) | 0.2 (0–65.5) | 0.5 (01–40.3) | <.0001 | <.0001 | <.0001 | .0035 |
| Albumin (g/dL) | 4.2 (0.6) | 4.2 (0.6) | 4 (0.8) | 4.1 (0.8) | .0183 | .0086 | .2206 | .7385 |
| Bilirubin (mg/dL) | 1.1 (0.2–20.8) | 1.1 (0.2–19) | 1 (0.3–20.8) | 1.9 (0.3–11.5) | .0099 | .3881 | .0028 | .0554 |
| ALBI score | -2.7 (-4.2 to 1.3) | -2.8 (-4.1 to 1.3) | -2.7 (-3.9 to 0.3) | -2.5 (-3.8 to 1) | .0057 | .019 | .0186 | .4815 |
| CRP/albumin | 3 (1–127) | 3 (1–65) | 5 (1–127) | 5 (1–101) | <.0001 | <.0001 | .0044 | .7288 |
| SII | 1261 (44.9–28,350) | 1178 (45–28,350) | 1973 (128–20,536) | 3076 (433–10,535) | <.0001 | .0002 | <.0001 | .0736 |
| NLR | 8.1 (0.2–86) | 5.3 (0.2–86) | 7.8 (0.5–49) | 11.7 (1.5–35) | <.0001 | .0005 | <.0001 | .0302 |
| PLR | 164 (23–2800) | 161 (23–2800) | 187 (40–1297) | 236 (75–1003) | .012 | .0598 | .0155 | .2525 |
ANOVA = analysis of variance, AP = acute pancreatitis, CR = creatinine, CRP = C-reactive protein, CRP/albumin = CRP/albumin ratio, HCT = hematocrit, MAP = mild acute pancreatitis, max = maximum values, min = minimum, MSAP = moderately severe acute pancreatitis, n = number, NLR = neutrophil to lymphocyte ratio, PCT = procalcitonin, % = percentage, PLR = platelets to lymphocyte ratio, SAP = severe acute pancreatitis, SD = standard deviation, SII = systemic immune index.
Overall ANOVA P value.
Pairwise comparison between MAP and MSAP.
Pairwise comparison between MAP and SAP.
Pairwise comparison between MSAP and SAP.
EDA revealed that the age distribution of patients with AP exhibited a bimodal pattern, with 1 peak at 40 years and the other at 60 years (see Figure S1, Supplemental Digital Content, https://links.lww.com/MD/P882 which illustrates the normality or non-normality of the predictors and biomarkers included in the analysis).
3.1. Severity of AP
The most common severity grade was MAP followed by MSAP and SAP (86%, 10.4%, and 3.6%, respectively; Table 1). As the severity of AP increased, so did the mean age of the patients (MAP: 48.1 (17.5); MSAP: 52.6 (19.3); and SAP: 58.3 (20.2), P = .002; see Figure S2, Supplemental Digital Content, https://links.lww.com/MD/P882 which shows patients with AP stratified by severity). Females were more commonly affected by AP than males (52% vs 48%, P = .02). However, a higher proportion of males had SAP than females (72% vs 29%, P = .02; see Figure S2, Supplemental Digital Content, https://links.lww.com/MD/P882 which shows patients with AP stratified by severity). AP severity was comparable between the different racial and ethnic groups (P = .55). Patients with HTG-AP were at an increased risk of developing SAP compared to other causes (P < .001). As the severity of AP increased, the percentage of patients with positive clinical indicators of severity (e.g., HAPS, SIRS, and BISAP) also increased. Most laboratory biomarkers differed significantly between patients with MAP and SAP, except for HCT (P = .45; Table 1 and see Figure S2, Supplemental Digital Content, https://links.lww.com/MD/P882 which shows patients with AP stratified by severity).
3.2. MSAP
Of the patients diagnosed with MSAP, 51 (63%) had APFC, and 29 (37%) had TOF (Table 2 and see Figure S3, Supplemental Digital Content, https://links.lww.com/MD/P882 which shows laboratory data of patients with MSAP). One patient had both and was subsequently removed from the analysis. Patients with TOF were older (61 (19.7) vs 47.4 (17.4) years, P = .002) and more often had a BISAP score ≥ 2 (52% vs 10%, P < .001) compared to those with APFC. Additionally, patients with TOF had higher median Cr (1.6 (0.5–4.1) vs 0.8 (0.3–2.5) mg/dL, P < .001) and PCT (0.1–65.5) vs 0.1 (0.1 (0–2.18) ng/dL, P = .017) levels indicative of an initial acute inflammatory response. In contrast, patients with APFC had higher median lymphocyte (1.6 (0.4–6) vs 0.9 (0.1–2.7) × 103 cells/µL, P = .005) and platelet (295 (228–866) vs 266 (52–1566) × 103 cells/µL, P = .03) counts reflecting a prolonged inflammatory response. The remaining biomarkers were comparable between patients with TOF and APFC (see Table S1, Supplemental Digital Content, https://links.lww.com/MD/P883 which shows differences in data for AP, classified according to MAP, APFC, and OF).
Table 2.
Baseline characteristics in the moderately severe acute pancreatitis group stratified by those that experienced total organ failure and acute pancreatic fluid collections.
| Variable | APFC (N = 51) |
TOF (N = 29) |
P value |
|---|---|---|---|
| Age (yr), mean (SD) | 47.4 (17.4) | 61 (19.7) | .0019 |
| BMI (kg/m2), mean (SD) | 29.3 (5.7) | 30.4 (6) | .4219 |
| Gender, n (%) | |||
| Female | 22 (43%) | 16 (55%) | .3001 |
| Male | 29 (57%) | 13 (45%) | |
| Race/ethnicity, n (%) | |||
| White | 17 (33%) | 9 (31%) | .976 |
| Black | 15 (30%) | 9 (31%) | |
| Hispanic | 19 (37%) | 11 (38%) | |
| Etiology, n (%) | |||
| Biliary | 17 (33%) | 10 (34%) | .21 |
| Alcoholic | 11 (22%) | 7 (24%) | |
| Hypertriglyceridemia | 10 (20%) | 1 (3%) | |
| Other causes of AP | 13 (25%) | 11 (38%) | |
| HAPS, n (%) | |||
| Not harmless | 31 (61%) | 21 (72%) | .2945 |
| Harmless | 20 (39%) | 8 (28%) | |
| SIRS, n (%) | |||
| No | 26 (51) | 12 (41%) | .4084 |
| Yes | 25 (49%) | 17 (59%) | |
| BISAP, n (%) | |||
| 0 | 16 (31%) | 2 (7%) | .0001 |
| 1 | 30 (59%) | 12 (41%) | |
| 2 | 5 (10%) | 10 (35%) | |
| 3 | 0 (0%) | 5 (17%) | |
| 4 | 0 (0%) | 0 (0%) | |
| Laboratory values, mean (SD) or median (min–max) | |||
| CR (mg/dL) | 0.8 (0.3–2.5) | 1.6 (0.5–4.1) | <.0001 |
| HCT (%) | 41.8 (6.4) | 41.1 (7.7) | .6471 |
| WBCs (×103/µL) | 13.4 (5.0) | 11.7 (5.5) | .1798 |
| Neutrophils (×103/µL) | 10.5 (4.7) | 9.3 (5.1) | .2843 |
| Lymphocytes (×103/µL) | 1.6 (0.4–6) | 0.9 (0.1–2.7) | .0047 |
| Platelets (×103/µL) | 295 (228–866) | 266 (52–1556) | .0277 |
| CRP (mg/dL) | 16 (5–355) | 31 (5–228) | .397 |
| PCT (ng/mL) | 0.1 (0–18) | 0.2 (0.1–65.5) | .0172 |
| Albumin (g/dL) | 4.0 (0.7) | 4.1 (0.8) | .4869 |
| Bilirubin | 1.0 (0.3–20.8) | 1.5 (0.3–8) | .3943 |
| ALBI score | -2.7 (-3.6 to 1.0) | -2.7 (-3.9 to -0.3) | .8102 |
| CRP/albumin | 4 (1–127) | 16 (1–54) | .4589 |
| SII | 1459 (128–20,536) | 2579 (190–7181) | .2644 |
| NLR | 6.6 (0.5–25) | 10.8 (1.5–49) | .1399 |
| PLR | 164 (40–1237) | 226 (57–1297) | .0599 |
| LOS | 6.8 (1–21.9) | 4 (1.2–13.1) | .0264 |
AP = acute pancreatitis, APFC = acute pancreatic fluid collections, BMI = body mass index, CR = creatinine, CRP = C-reactive protein, CRP/Albumin = CRP/albumin ratio, HCT = hematocrit, MSAP = moderately severe acute pancreatitis, NLR = neutrophil to lymphocyte ratio, PCT = procalcitonin, PLR = platelets to lymphocyte ratio, SAP = severe acute pancreatitis, SII = systemic immune index, TOF = transient organ failure, WBC = white blood cells.
3.3. AP according to etiology
Patients with ABP were predominantly women (66%) and Hispanic (51%) (Table 3). Compared to other etiological groups, ABP patients had higher median levels of PCT (0.1 (0.03–54) ng/mL), bilirubin (1.6 (0.2–20.8) mg/dL), NLRs (6.7 (0.8–86)), and PLRs (190 (44–1235)). In contrast, AAP patients had a lower mean BMI (26.8 (6.4) kg/m²) and were primarily men (72%) and Black (53%). The mean age of HTG-AP patients was significantly lower than that of ABP patients (41.1 (11.9) vs 51.7 (20.4) years; P < .001) and those with AP from other etiologies (41.1 (11.9) vs 51.5 (17.7) years; P < .001; see Figure S4 Supplemental Digital Content, https://links.lww.com/MD/P882 which presents laboratory data and patient characteristics by etiology). HTG-AP patients also had a higher percentage of positive SIRS criteria (65%), BISAP scores ≥ 1 (69%), SII index (1621 (66–9353) pg/mL), and ALBI scores (-2.4 (-3.7 to -1.1)). They exhibited elevated inflammatory markers, including WBC, neutrophils, lymphocytes, and CRP compared to other groups (Table 3).
Table 3.
Baseline demographics and clinical characteristics of patients with acute pancreatitis according to the etiology.
| Variable | ABP (N = 303) |
AAP (N = 208) |
HTG-AP (N = 48) |
Other AP (N = 220) |
P value* | P value† | P value‡ | P value§ | P valueǁ | P value¶ | P value# |
|---|---|---|---|---|---|---|---|---|---|---|---|
| Age (yr), mean (SD) | 51.7 (20.4) | 43.9 (13.6) | 41.1 (11.9) | 51.5 (17.7) | <.0001 | <.0001 | .0001 | .9002 | .3172 | <.0001 | .0002 |
| BMI, (kg/m2), mean (SD) | 31.4 (7.8) | 26.8 (6.4) | 31.7 (5.2) | 29.9 (8.1) | <.0001 | <.0001 | .7981 | .0236 | <.0001 | <.0001 | .1314 |
| Gender, n (%) | |||||||||||
| Female | 199 (66%) | 59 (28%) | 19 (40%) | 127 (58%) | <.0001 | <.0001 | .0005 | .064 | .128 | <.0001 | .0222 |
| Male | 104 (34%) | 149 (72%) | 29 (60%) | 93 (42%) | |||||||
| Race/ethnicity, n (%) | |||||||||||
| White | 68 (22%) | 50 (24%) | 17 (35%) | 62 (28%) | <.0001 | <.0001 | .0663 | .0013 | <.0001 | .0034 | .0094 |
| Black | 82 (27%) | 110 (53%) | 7 (15%) | 82 (37%) | |||||||
| Hispanic | 153 (51%) | 48 (23%) | 24 (50%) | 76 (35%) | |||||||
| HAPS, n (%) | |||||||||||
| Not harmless | 166 (55%) | 122 (59%) | 25 (52%) | 110 (50%) | .3405 | .3864 | .7269 | .2792 | .4066 | .0725 | .7937 |
| Harmless | 137 (45%) | 86 (41%) | 23 (48%) | 110 (50%) | |||||||
| SIRS, n (%) | |||||||||||
| No | 206 (68%) | 121 (58%) | 17 (35%) | 170 (77%) | <.0001 | .0232 | <.0001 | .0197 | .0044 | <.0001 | <.0001 |
| Yes | 97 (32%) | 87 (42%) | 31 (65%) | 50 (23%) | |||||||
| BISAP, n (%) | |||||||||||
| 0 | 124 (41%) | 107 (51%) | 15 (31%) | 99 (45%) | <.0001 | .0028 | .0006 | .0844 | .0077 | .1542 | .0008 |
| 1 | 107 (35%) | 80 (38%) | 29 (61%) | 86 (39%) | |||||||
| 2 | 55 (18%) | 16 (8%) | 2 (4%) | 32 (15%) | |||||||
| 3 | 15 (5%) | 4 (2%) | 0 (0%) | 3 (15%) | |||||||
| 4 | 2 (1%) | 1 (1%) | 2 (4%) | 0 (0%) | |||||||
| Laboratory values, mean (SD), median (min–max) | |||||||||||
| CR (mg/dL) | 0.8 (0.3–4.6) | 0.8 (0.4–2.9) | 0.6 (0.3–5.2) | 0.8 (0.3–6.2) | <.0001 | .6511 | <.0001 | .1635 | <.0001 | .0949 | <.0001 |
| HCT (%) | 40.5 (5.2) | 42.5 (6.4) | 40.8 (6.6) | 40.3 (6.0) | .0004 | .0002 | .7943 | .6218 | .069 | .0001 | .5971 |
| WBC (×103/µL) | 11.2 (4.3) | 10.2 (4.1) | 14.2 (4.7) | 10.6 (4.3) | <.0001 | .0079 | <.0001 | .0924 | <.0001 | .3485 | <.0001 |
| Neutrophils (×103/µL) | 8.7 (4.3) | 7.7 (3.9) | 11.2 (4.5) | 7.6 (4.2) | <.0001 | .0087 | .0002 | .0017 | <.0001 | .6674 | <.0001 |
| Lymphocytes (×103/µL) | 1.2 (0.1–4.9) | 1.3 (0.2–7.9) | 1.8 (0.6–3.8) | 1.8 (0.1–19.1) | <.0001 | .0823 | <.0001 | <.0001 | .0003 | <.0001 | .7741 |
| Platelets (×103/µL) | 247 (104) | 232 (127) | 276 (103) | 270 (123) | <.0001 | .1455 | .108 | .0289 | .0175 | .0008 | .725 |
| CRP (mg/dL) | 14 (3.0–332) | 14 (5–380) | 19 (5–335) | 13 (5–252) | .0019 | .9471 | .0255 | .0692 | .0011 | .7136 | .001 |
| PCT (ng/mL) | 0.1 (0.03–54) | 0.07 (0.05–66) | 0.08 (0.05–40.3) | 0.05 (0.03–100) | <.0001 | .0045 | .3259 | <.0001 | .5461 | .0001 | .0069 |
| Albumin (g/dL) | 4.2 (0.6) | 4.4 (0.6) | 3.9 (0.7) | 4.2 (0.5) | <.0001 | .001 | .0018 | .6061 | <.0001 | .0004 | .0057 |
| Bilirubin (mg/dL) | 1.6 (0.2–20.8) | 1.1 (0.2–19) | 1.2 (0.4–11.5) | 0.7 (0.1–7.1) | <.0001 | <.0001 | .0377 | <.0001 | .4215 | <.0001 | <.0001 |
| ALBI score | -2.6 (-3.8 to 1.3) | -2.9 (-4.2 to 0.4) | -2.4 (-3.7 to 1.1) | -2.8 (-3.9 to 0.4) | <.0001 | <.0001 | .0064 | <.0001 | <.0001 | .2439 | <.0001 |
| CRP/albumin | 4 (1–101) | 3 (1–75) | 5 (1–127) | 3 (1–79) | .0003 | .0099 | .0108 | .0851 | .0002 | .3294 | .0005 |
| SII | 1600 (74–12,734) | 1145 (45–9922) | 1621 (66–9353) | 1009 (1106–28,350) | <.0001 | .0006 | .8819 | <.0001 | .0253 | .0915 | .0013 |
| NLR | 6.7 (0.8–86) | 5.7 (0.2 (30.3) | 6.0 (1–33) | 3.7 (0.5–40) | <.0001 | .0079 | .4002 | <.0001 | .4889 | .0001 | .0018 |
| PLR | 190 (44–1235) | 157 (23–1297) | 153 (30–470) | 145 (29–2800) | <.0001 | .0011 | .0171 | <.0001 | <.0001 | .1062 | .6175 |
| LOS | 4 (1–46.1) | 2.6 (1–51.8) | 4 (1–71) | 2.2 (0.3–34) | <.0001 | <.0001 | .3741 | <.0001 | <.0001 | .8116 | <.0001 |
| Severity, n(%) | |||||||||||
| MAP | 267 (88%) | 182 (86%) | 31 (65%) | 190 (86%) | .0006 | .8611 | <.0001 | .5922 | .0006 | .4341 | .0003 |
| MSAP | 27 (9%) | 18 (9%) | 11 (23%) | 25 (11%) | |||||||
| SAP | 9 (3%) | 8 (4%) | 6 (13%) | 5 (2%) |
AAP = acute alcoholic pancreatitis, ABP = acute biliary pancreatitis, AP = acute pancreatitis, BMI = body mass index, CR = creatinine, CRP = C-reactive protein, CRP/albumin = CRP/albumin ratio, HCT = hematocrit, HTG-AP = hypertriglyceridemia acute pancreatitis, MAP = mild acute pancreatitis, MSAP = moderately severe acute pancreatitis, NLR = neutrophil to lymphocyte ratio, other AP = other acute pancreatitis, PCT = procalcitonin, PLR = platelets to lymphocyte ratio, SAP = severe acute pancreatitis, SII = systemic immune index, WBC = white blood cells.
Overall ANOVA P value.
Pairwise comparison between ABP and AAP.
Pairwise comparison between ABP versus HTG-AP.
Pairwise comparison between ABP versus other AP.
Pairwise comparison between AAP and HTG-AP.
Pairwise comparison between AAP and other AP.
Pairwise comparison between HTG-AP and other AP.
The EDA highlighted differences among the etiologic groups and associations with AP severity (Table 4 and see Figure S5, Supplemental Digital Content, https://links.lww.com/MD/P882 which shows laboratory data and patient characteristics stratified by etiology and severity of AP). Notably, within the HTG-AP subgroup the mean ages were 43.1 (11.3) years for MAP, 39.6 (13.3) years for MSAP, and 33.5 (10.8) years for SAP (P = .18). A pairwise comparison between MAP and SAP yielded a P value of .07. Although not statistically significant, these results suggest a trend: younger patients may face a higher risk of SAP in the context of HTG-AP.
Table 4.
Etiology subgroup analysis, comparative means according to severity of acute pancreatitis.
| Acute biliary pancreatitis | Acute alcoholic pancreatitis | Hypertriglyceridemia acute pancreatitis | Other etiologies | |||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Predictors, mean (SD) or median (min–max) | MAP (N = 267) |
MSAP (N = 27) |
SAP (N = 9) |
P value | MAP (N = 182) |
MSAP (N = 18) |
SAP (N = 8) |
P value | MAP (N = 31) | MSAP (N = 11) | SAP (N = 6) |
P value | MAP (N = 190) | MSAP (N = 25) | SAP (N = 5) |
P value |
| Age (yr) | 50.4 (20) | 57.3 (21.7) | 73.1 (11.7) | .0014 | 43.7 (13.6) | 43.2 (12.6) | 49.9 (15.20 | .4464 | 43.1 (11.3) | 39.6 (13.3) | 33.5 (10.8) | .1776 | 49.8 (17.1) | 60 (18.1) | 75 (3.7) | .0002 |
| Cr (mg/dL) | 0.7 (0.3–3.1) | 1 (0.5–3.5) | 2.1 (1.1–4.6) | <.0001 | 0.8 (0.4–2.4) | 0.9 (0.4–2.9) | 1.4 (0.7–2.5) | .0012 | 0.6 (0.3–1.1) | 0.6 (0.3–1.6) | 0.7 (0.5–5.2) | .2556 | 0.8 (0.3–2.0) | 1 (0.5–4.1) | 2.2 (1.1–6.2) | <.0001 |
| HCT (%) | 40.5 (5.2) | 41.4 (6) | 40.1 (5.9) | .6772 | 41.9 (6.2) | 45.6 (6.6) | 47.7 (6.4) | .0037 | 41.4 (5.7) | 37.1 (7.3) | 44.1 (8.2) | .0725 | 40.4 (5.9) | 40.7 (6.5) | 33.6 (5.1) | .0407 |
| WBCs (×103/µL) | 10.9 (4) | 12.2 (6.4) | 15.4 (3.9) | .0038 | 9.8 (3.8) | 12.5 (4.8) | 13.8 (5..1) | .0007 | 13.4 (4.5) | 15.8 (10.7–21.5) | 15.5 (79–26.5) | .2866 | 10.2 (4.3) | 12.3 (4.2) | 13.9 (4.2) | .0174 |
| Neutrophils (×103/µL) | 8.5 (4.1) | 9.9 (5.2) | 11.2 (14.9) | .0535 | 7.3 (3.6) | 10.2 (4.7) | 11.1 (4.9) | .0004 | 10.4 (4.6) | 12.2 (7.5–17.7) | 13.1 (4.3) | .3045 | 7.2 (4.1) | 9.2 (4.6) | 11.6 (3.4) | .0096 |
| Lymphocytes (×103/µL) | 1.3 (0.1–4) | 0.9 (0.1–3.9) | 1.4 (0.2–4.9) | .0171 | 1.4 (0.2–7.9) | 0.9 (0.4–2.4) | 1.1 (0.5–1.6) | .0201 | 1.8 (0–3.5) | 2.1 (0.6–3.8) | 1.7 (0.7–2.1) | .1835 | 1.8 (0.1–19.1) | 1.8 (0.6–6) | 1.2 (0.6–2.2) | .3208 |
| Platelets (×103/µL) | 249 (103) | 225 (112) | 259 (113) | .5026 | 228 (90) | 301 (319) | 184 (60.8) | .0342 | 256 (93.1) | 345 (124) | 254 (202–348) | .0365 | 264 (118) | 304 (158) | 297 (103) | .2781 |
| CRP (mg/dL) | 14 (3–260) | 18 (5–251) | 34 (5–332) | .0176 | 13 (5–254) | 14 (5–166) | 13 (5–380) | .5085 | 15 (5–185) | 33 (12–355) | 23 (12–64) | .0661 | 12 (5–159) | 18 (5–252) | 63 (7–90) | .0023 |
| PCT (ng/mL) | 0.1 (0.03–54) | 0.3 (0–34) | 5.6 (0.5–33.1) | <.0001 | 0.1 (0.1–50) | 0.1 (0.1–66) | 0.3 (0.1–9.8) | .0084 | 0.1 (0.1–1) | 0.1 (0.1–0.6) | 0.3 (0.2–40.3) | .0149 | 0.1 (0–100) | 0.1 (0–48) | 0.2 (0.1–0.5) | .0409 |
| Albumin (g/dL) | 4.2 (0.6) | 4.1 (0.7) | 4.1 (0.7) | .5426 | 4.4 (0.6) | 4.3 (0.9) | 4.4 (1) | .9535 | 4 (0.6) | 3.6 (0.7) | 4 (0.9) | .199 | 4.2 (0.5) | 4 (1.4) | 3.8 (0.3) | .0717 |
| Bilirubin (mg/dL) | 1.5 (0.2–10.2) | 2.3 (0.3–20.8) | 2.4 (1.1–5) | .055 | 1 (0.2–19) | 1.4 (0.3–4.7) | 1.8 (1.1–5.3) | .0169 | 1.5 (0.4–3.4) | 1.1 (0.5–3.1) | 1.7 (0.7–11.5) | .2659 | 0.7 (0.2–4) | 0.7 (0.3–7.1) | 0.9 (0.3–0.9) | .7942 |
| ALBI score | -2.6 (0.6) | -2.4 (0.7) | -2.4 (0.7) | .3917 | -2.9 (0.5) | -2.8 (0.8) | -2.7 (-3.8--1.2) | .9394 | -2.5 (0.5) | -2.2 (0.5) | -2.4 (0.8) | .3184 | -2.8 (0.5) | -2.6 (0.6) | -2.5 (0.2) | .0624 |
| CRP/albumin | 3 (1–65) | 4 (1–60) | 8 (1–101) | .022 | 3 (1–62) | 3 (1–40) | 3 (1–75) | .4454 | 4 (1–50) | 7 (3–127) | 6 (03–21) | .0684 | 5.3 (1–43) | 5 (01–79) | 19 (2–24) | .002 |
| SII | 1505 (74–12,734) | 2227 (190–9648) | 3823 (564–10,535) | .036 | 1046 (45–9922) | 2410 (585–7182) | 1727 (433–5325) | .0009 | 1295 (66–9353) | 2081 (491–7050) | 2395 (1164–4068) | .334 | 975 (1006–28,350) | 1546 (128–20,536) | 3448 (1244–4841) | .004 |
| NLR | 6.5 (0.8–86) | 9.8 (2.1–49) | 15.5 (1.5–35) | .0024 | 5.4 (0.2–31) | 10.1 (2.3–25) | 9.8 (3.7_26) | .0003 | 5.4 (1–33.2) | 4.3 (2.2–25) | 9.3 (4.3–16.1) | .2015 | 3.5 (0.9–39) | 4.2 (0.5–24) | 9.1 (5.5–21) | .0201 |
| PLR | 187 (44–1235) | 176 (57–1035) | 398 (75–1003) | .0798 | 149 (23–1270) | 262 (97–1297) | 168 (77–416) | .0096 | 158 (30_470) | 142 (62–470) | 151 (126_360) | .5165 | 141 (292,800) | 168 (40.2–1237) | 338 (76–467) | .0893 |
AP = acute pancreatitis, Cr = creatinine, CRP = C-reactive protein, CRP/albumin = CRP/albumin ratio, HCT = hematocrit, MAP = mild acute pancreatitis, MSAP = moderately severe acute pancreatitis, NLR = neutrophil to lymphocyte ratio, PCT = procalcitonin, PLR = platelets to lymphocyte ratio, SAP = severe acute pancreatitis, SII = systemic immune index, WBC = white blood cells.
Patients with HTG-AP had the lowest median Cr levels among the etiologies. However, Cr was not a reliable indicator of severity, as its median values were similar across MAP, MSAP, and SAP (P = .26).
Higher WBC counts were associated with SAP in ABP, AAP, and AP from other etiologies, indicating a strong correlation with disease severity. However, in HTG-AP, this association was not statistically significant (P = .29), likely due to the small sample size in this subgroup, limiting the ability to detect a clear relationship. Although bilirubin levels were higher in ABP, the differences between severity groups were not statistically significant (P = .06). In AAP, however, higher total bilirubin levels were significantly associated with increased severity (P = .02).
4. Discussion
AP severity is correlated with age, sex, and etiology in this cohort. As severity increases, patients tend to be older, and men face a higher risk of developing SAP than women. Patients with HTG-AP more frequently have SAP. Clinical severity indicators (i.e., HAPS, SIRS, and BISAP) become more prevalent, and most laboratory biomarkers differ significantly between MAP and SAP. These results are supported by previous studies.[9] However, this population tends to be younger when the etiology is ABP, especially when compared with the Asian population.[17]
This study investigated patients diagnosed with MSAP and classified them into 2 distinct groups: APFC and TOF. Notable differences emerged between these groups. APFC patients were typically younger and exhibited a distinct inflammatory response (i.e., an increase in lymphocytes and platelets) compared to TOF patients. APFC results from a subacute or delayed process, typically presenting between 2 to 4 weeks after AP onset.[11] Approximately 20% of APFC patients had documented hospitalization for AP 4 weeks before the ongoing episode of AP. TOF patients had higher median values for Cr and PCT, which reflect an early phase of the acute process. The observed differences in inflammatory markers (specifically lymphocytes, platelets, CRP, and PCT) between patients with APFC and those with TOF reflect the distinction between a persistent local inflammatory response (seen in APFC) and an acute-phase systemic response (seen in TOF). These differences may be explained by the compensatory immune response that occurs during AP, exemplified by an increase in regulatory T cells (a subtype of lymphocytes) commonly observed in patients with APFC.[3] Additionally, these differences in the APFC and TOF subgroups can explain the decrease in accuracy of some models that attempt to predict severity when using variables such as age, Cr, CRP, and PCT.
During examination of the AP etiologies, this study found that ABP predominantly affected women and the Hispanic population. Patients in this group had higher median values of PCT, bilirubin, NLR, and PLR compared to other etiological groups. AAP predominantly affected men and the Black population. They had a lower mean BMI and exhibited a higher mean HCT value. The HTG-AP group was characterized by a younger patient population with a higher percentage of patients with positive SIRS criteria and BISAP scores. Additionally, they had elevated inflammatory cell counts (WBC, neutrophils, and lymphocytes) and CRP levels. Similar results were reported by Zhang et al for ABP and HTG-AP regarding PCT and WBC counts.[17] Cr and other inflammatory biomarkers do not exhibit a significant association with severity, specifically in HTG-AP. The small sample size of the HTG-AP subgroup limits statistical power, preventing us from confidently demonstrating the associations observed in other etiologic groups.
The current study included several inflammatory prognostic indicators, such as SII, NLR, and PLR, which have been associated with AP severity and mortality.[18,19] However, these biomarkers, specifically SII and PLR, do not demonstrate a distinct superiority in our cohort when compared with WBC or neutrophil counts. Similarly, bilirubin level and the ALBI score can be associated with SAP, but their use does not offer any specific advantage over other biomarkers in this study. A recent study compared the CRP/albumin ratio with CRP alone, showing a similar capacity to predict the severity of AP.[20] The current study shows that CRP/albumin ratio behaves similarly to CRP and does not provide an advantage over the latter.
This study has limitations. EDA cannot establish causality and cannot definitively conclude that changes in biomarkers directly influence disease outcomes. Retrospective studies are susceptible to selection bias. Patients who are present to the ED may not represent the entire population with AP. Comorbidities and medications can act as confounders and may influence both biomarker levels and severity. Cautious interpretation and generalization are necessary due to inherent limitations.
In conclusion, this study demonstrates that age, sex, and etiology significantly influence the severity of AP. By examining biomarkers, such as Cr, PCT, and WBC count, physicians can identify potential associations between with biomarker level and AP severity, as well as specific biomarker differences based on etiology. This retrospective descriptive analysis of biomarkers in patients with AP in our sample offers valuable insights into real-world clinical practice and patient outcomes, enabling the exploration of trends and patterns without imposing predefined hypotheses.
Acknowledgments
The authors thank Anne Murray, PhD, MWC of the Clinical Research Institute at Methodist Health System, Dallas for providing editorial support.
Author contributions
Conceptualization: Paul R. Tarnasky.
Data curation: Jimmy Shah.
Formal analysis: Jimmy Shah.
Methodology: Juana Valentina Barrera, Jimmy Shah.
Project administration: Elaina Vivian, Paul R. Tarnasky.
Supervision: Paul R. Tarnasky.
Writing – original draft: Juana Valentina Barrera, Elaina Vivian.
Writing – review & editing: Jimmy Shah, Elaina Vivian, Paul R. Tarnasky.
Supplementary Material
Abbreviations:
- AAP
- acute alcoholic pancreatitis
- ABP
- acute biliary pancreatitis
- ALBI
- albumin–bilirubin
- AP
- acute pancreatitis
- APFC
- acute pancreatic fluid collections
- BISAP
- bedside index for severity in acute pancreatitis
- BMI
- body mass index
- Cr
- creatinine
- CRP
- C-reactive protein
- ED
- emergency department
- EDA
- exploratory data analysis
- HAPS
- harmless acute pancreatitis score
- HCT
- hematocrit
- HTG
- hypertriglyceridemia
- MAP
- mild acute pancreatitis
- MSAP
- moderately severe acute pancreatitis
- NLR
- neutrophil to lymphocyte ratio
- PCT
- procalcitonin
- PLR
- platelet-to-lymphocyte ratio
- SII
- systemic immune-inflammation index
- SIRS
- systemic inflammatory response system
- TOF
- transient organ failure
- WBC
- white blood cell.
The authors have no funding and conflicts of interest to disclose.
The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.
Supplemental Digital Content is available for this article.
How to cite this article: Barrera JV, Shah J, Vivian E, Tarnasky PR. Baseline severity and etiology parameters in acute pancreatitis: A descriptive cross-sectional analysis. Medicine 2025;104:36(e43738).
Contributor Information
Juana Valentina Barrera, Email: juanavbarrera1@gmail.com.
Jimmy Shah, Email: JimmyShah@mhd.com.
Elaina Vivian, Email: ElainaVivian@mhd.com.
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