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Recent Advances in Inflammation & Allergy Drug Discovery

Editor-in-Chief

ISSN (Print): 2772-2708
ISSN (Online): 2772-2716

Research Article

The Role of Inflammatory and Hemostatic Markers in the Prediction of Severe Acute Pancreatitis: An Observational Cohort Study

Author(s): Liudmila Orbelian*, Nikita Trembach and Vladimir Durleshter

Volume 19, Issue 3, 2025

Published on: 17 December, 2024

Page: [428 - 440] Pages: 13

DOI: 10.2174/0127722708356543241209060544

open_access

Abstract

Introduction: Acute pancreatitis (AP) is a serious inflammatory disease of the pancreas that can lead to significant morbidity and increased mortality. The special role of inflammation and disruption of the hemostatic system in the development of severe forms of the disease is known, however, the relationship between inflammatory and anti-inflammatory cytokines and thromboelastogram parameters has not been sufficiently studied.

Aim: The aim of this study is to assess the prognostic significance of thromboelastogram parameters, interleukin-6, and interleukin-22 levels in assessing the risk for developing severe forms of acute pancreatitis.

Materials and Methods: Data from 149 patients with acute pancreatitis were included in the analysis. The classification of AP was performed according to the 2012 Revision of the Atlanta Classification. Data including gender, age, lab tests, radiological information, and prognosis were included. The following scales were used to assess severity: SOFA scale and BISAP scale. IL-6 and IL-22 were analyzed at 24 h and 48 h after the onset of symptoms. The collected TEG parameters included K-time, R-value, and Maximum amplitude value at admission. All patients were divided into three groups: mild, moderate-severe, and severe pancreatitis.

Results: Statistically significant differences were found between the groups in the IL-6 level at the first measurement and on day 2 of the study. IL-22 values were also higher in the group with severe pancreatitis, however, on day 2, its level became lower compared to the group of patients with moderate and mild pancreatitis. Statistically significant differences were found in the level of K-time, R-value, Maximum amplitude, fibrinogen concentration, and platelets count, demonstrating a hypercoagulation state in severe pancreatitis at admission. The conducted logistic regression showed that the factors associated with the development of severe forms are the number of points on the BISAP scale, the level of interleukin-6 in the first 24 hours of the disease, delta IL-22, and K-time. (AUC = 0.948).

Conclusion: The study highlights that both IL-6 and IL-22 play crucial roles in the inflammatory cascade of severe acute pancreatitis. Their levels, along with specific hemostasis parameters like K-time and BISAP score, serve as reliable early predictors of disease severity.

Keywords: Acute pancreatitis, hypercoagulation, thromboelastogram, pancreatitis, BISAP scale, SOFA scale.

Graphical Abstract
[1]
Fidan S, Erkut M, Coşar AM, et al. Higher thrombin-antithrombin III complex levels may indicate severe acute pancreatitis. Dig Dis 2018; 36(3): 244-51.
[http://dx.doi.org/10.1159/000485613] [PMID: 29332096]
[2]
Dumnicka P, Maduzia D, Ceranowicz P, Olszanecki R, Drożdż R, Kuśnierz-Cabala B. The interplay between inflammation, coagulation and endothelial injury in the early phase of acute pancreatitis: Clinical implications. Int J Mol Sci 2017; 18(2): 354.
[http://dx.doi.org/10.3390/ijms18020354] [PMID: 28208708]
[3]
Liang W, Liu T, Gong M. The role of thromboelastogram (TEG) and routine coagulation indexes in evaluating the severity of acute pancreatitis in the early stage of onset. Signa Vitae 2023; 19(3): 132-6.
[4]
Li L, Tan Q, Wu X, et al. Coagulopathy and acute pancreatitis: pathophysiology and clinical treatment. Front Immunol 2024; 15: 1477160.
[http://dx.doi.org/10.3389/fimmu.2024.1477160] [PMID: 39544925]
[5]
Rafaqat S, Patoulias D, Behnoush AH, Sharif S, Klisic A. Interleukins: pathophysiological role in acute pancreatitis. Arch Med Sci 2024; 20(1): 138-56.
[http://dx.doi.org/10.5114/aoms/178183] [PMID: 38414463]
[6]
Venkatesh K, Glenn H, Delaney A, Andersen CR, Sasson SC. Fire in the belly: A scoping review of the immunopathological mechanisms of acute pancreatitis. Front Immunol 2023; 13: 1077414.
[http://dx.doi.org/10.3389/fimmu.2022.1077414] [PMID: 36713404]
[7]
Sternby H, Hartman H, Thorlacius H, Regnér S. The initial course of IL1β, IL-6, IL-8, IL-10, IL-12, IFN-γ and TNF-α with regard to severity grade in acute pancreatitis. Biomolecules 2021; 11(4): 591.
[http://dx.doi.org/10.3390/biom11040591] [PMID: 33920566]
[8]
Kolber W, Dumnicka P, Maraj M, et al. Does the automatic measurement of interleukin 6 allow for prediction of complications during the first 48 h of acute pancreatitis? Int J Mol Sci 2018; 19(6): 1820.
[http://dx.doi.org/10.3390/ijms19061820] [PMID: 29925813]
[9]
Mititelu A, Grama A, Colceriu MC, Benţa G, Popoviciu MS, Pop TL. Role of interleukin 6 in acute pancreatitis: A possible marker for disease prognosis. Int J Mol Sci 2024; 25(15): 8283.
[http://dx.doi.org/10.3390/ijms25158283] [PMID: 39125854]
[10]
Xu Q, Fu X, Xiu Z, et al. Interleukin‑22 alleviates arginine‑induced pancreatic acinar cell injury via the regulation of intracellular vesicle transport system: Evidence from proteomic analysis. Exp Ther Med 2023; 26(6): 578.
[http://dx.doi.org/10.3892/etm.2023.12277] [PMID: 38023358]
[11]
Fu X, Xiu Z, Xu Q, Yue R, Xu H. Interleukin-22 alleviates caerulein-induced acute pancreatitis by activating AKT/mTOR pathway. Dig Dis Sci 2024; 69(5): 1691-700.
[http://dx.doi.org/10.1007/s10620-024-08360-6] [PMID: 38466463]
[12]
Song J, Park D, Moon S, et al. Diagnostic and prognostic value of interleukin-6, pentraxin 3, and procalcitonin levels among sepsis and septic shock patients: a prospective controlled study according to the Sepsis-3 definitions. BMC Infect Dis 2019; 19(1): 968.
[http://dx.doi.org/10.1186/s12879-019-4618-7] [PMID: 31718563]
[13]
Qiao Z, Wang W, Yin L, et al. Using IL-6 concentrations in the first 24 h following trauma to predict immunological complications and mortality in trauma patients: a meta-analysis. Eur J Trauma Emerg Surg 2018; 44(5): 679-87.
[http://dx.doi.org/10.1007/s00068-017-0880-9] [PMID: 29138874]
[14]
Cuzzocrea S, Mazzon E, Dugo L, et al. Absence of endogenous interleukin-6 enhances the inflammatory response during acute pancreatitis induced by cerulein in mice. Cytokine 2002; 18(5): 274-85.
[http://dx.doi.org/10.1006/cyto.2002.0883] [PMID: 12161103]
[15]
Lesina M, Wörmann SM, Neuhöfer P, Song L, Algül H. Interleukin-6 in inflammatory and malignant diseases of the pancreas. Semin Immunol 2014; 26(1): 80-7.
[http://dx.doi.org/10.1016/j.smim.2014.01.002] [PMID: 24572992]
[16]
Li J, Chen Z, Li L, et al. Interleukin-6 is better than C-reactive protein for the prediction of infected pancreatic necrosis and mortality in patients with acute pancreatitis. Front Cell Infect Microbiol 2022; 12: 933221.
[http://dx.doi.org/10.3389/fcimb.2022.933221] [PMID: 36467730]
[17]
Rodriguez-Nicolas A, Martínez-Chamorro A, Jiménez P, Matas-Cobos AM, Redondo-Cerezo E, Ruiz-Cabello F. TH1 and TH2 cytokine profiles as predictors of severity in acute pancreatitis. Pancreas 2018; 47(4): 400-5.
[http://dx.doi.org/10.1097/MPA.0000000000001006] [PMID: 29517628]
[18]
Rao SA, Kunte AR. Interleukin-6: An early predictive marker for severity of acute pancreatitis. Indian J Crit Care Med 2017; 21(7): 424-8.
[http://dx.doi.org/10.4103/ijccm.IJCCM_478_16] [PMID: 28808361]
[19]
Jin M, Zhang H, Wu M, et al. Colonic interleukin‐22 protects intestinal mucosal barrier and microbiota abundance in severe acute pancreatitis. FASEB J 2022; 36(3): e22174.
[http://dx.doi.org/10.1096/fj.202101371R] [PMID: 35137988]
[20]
Mareninova OA, Hermann K, French SW, et al. Impaired autophagic flux mediates acinar cell vacuole formation and trypsinogen activation in rodent models of acute pancreatitis. J Clin Invest 2009; 119(11): 3340-55.
[http://dx.doi.org/10.1172/JCI38674] [PMID: 19805911]
[21]
Garg PK, Singh VP. Organ failure due to systemic injury in acute pancreatitis. Gastroenterology 2019; 156(7): 2008-23.
[http://dx.doi.org/10.1053/j.gastro.2018.12.041] [PMID: 30768987]
[22]
Bai J, Bai J, Yang M. Interleukin-22 attenuates acute pancreatitis-associated intestinal mucosa injury in mice via STAT3 activation. Gut Liver 2021; 15(5): 771-81.
[http://dx.doi.org/10.5009/gnl20210] [PMID: 33495423]
[23]
Xu F, Chen X, Li C, et al. Prediction of multiple organ failure complicated by moderately severe or severe acute pancreatitis based on machine learning: A multicenter cohort study. Mediators Inflamm 2021; 2021: 1-11.
[http://dx.doi.org/10.1155/2021/5525118] [PMID: 34054342]
[24]
Fan C, Song Y, Wang X, Mao C, Xiong Y. Identification of early derangements of coagulation, hematological and biochemical profiles in patients with acute pancreatitis. Clin Biochem 2022; 109-110: 37-43.
[http://dx.doi.org/10.1016/j.clinbiochem.2022.08.005] [PMID: 35964680]
[25]
Rao P, Niemann B, Szeligo B, et al. Acute pancreatitis induces a transient hypercoagulable state in murine models. Pancreatology 2023; 23(3): 306-13.
[http://dx.doi.org/10.1016/j.pan.2023.02.007] [PMID: 36898897]
[26]
Gou Y, Yao L, Cao J. Changes in coagulation indices and D-dimer levels in hypertriglyceridemic acute pancreatitis and their value in predicting disease severity. Zhong Nan Da Xue Xue Bao Yi Xue Ban 2023; 48(7): 1050-8.
[http://dx.doi.org/10.11817/j.issn.1672-7347.2023.230155] [PMID: 37724408]
[27]
Saif MW. DIC secondary to acute pancreatitis. Clin Lab Haematol 2005; 27(4): 278-82.
[http://dx.doi.org/10.1111/j.1365-2257.2005.00697.x] [PMID: 16048498]
[28]
Akbal E, Demirci S, Koçak E, Köklü S, Başar Ö, Tuna Y. Alterations of platelet function and coagulation parameters during acute pancreatitis. Blood Coagul Fibrinolysis 2013; 24(3): 243-6.
[http://dx.doi.org/10.1097/MBC.0b013e32835aef51] [PMID: 23425662]

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