Abstract

Acute pancreatitis (AP) is a severe inflammation of the pancreas presented with sudden onset and severe abdominal pain with a high morbidity and mortality rate, if accompanied by severe local and systemic complications. Numerous studies have been published about the pathogenesis of AP; however, the precise mechanism behind this pathology remains unclear. Extensive research conducted over the last decades has demonstrated that the first 24 h after symptom onset are critical for the identification of patients who are at risk of developing complications or death. The identification of these subgroups of patients is crucial in order to start an aggressive approach to prevent mortality. In this sense and to avoid unnecessary overtreatment, thereby reducing the financial implications, the proper identification of mild disease is also important and necessary. A large number of multifactorial scoring systems and biochemical markers are described to predict the severity. Despite recent progress in understanding the pathophysiology of AP, more research is needed to enable a faster and more accurate prediction of severe AP. This review provides an overview of the available multifactorial scoring systems and biochemical markers for predicting severe AP with a special focus on their advantages and limitations.

Highlights

  • Acute pancreatitis (AP) is a severe inflammation of the pancreas presented with sudden onset and severe abdominal pain with a high morbidity and mortality rate, if accompanied by severe local and systemic complications

  • The Ranson score was published in 1974 as the first specific multifactorial scoring system for AP [34]. It was primarily designed for patients with acute alcoholic pancreatitis, consisting of 11 parameters identified as significant prognostic factors: Five parameters measured at admission and six during the 48 h

  • Ke et al [63] showed that the admission Pancreatitis Activity Score System (PASS) score was strongly associated with infected pancreatic necrosis (IPN), with an area under the receiver-operating curve (AUC) of 0.813, which is was to the APACHE-II score of 0.791, blood urea nitrogen (BUN) of 0.740, and c-reactive protein (CRP) of 0.619

Read more

Summary

Introduction

Acute pancreatitis (AP) is a severe inflammation of the pancreas presented with sudden onset and severe abdominal pain with a high morbidity and mortality rate, if accompanied by severe local and systemic complications It is the most common gastrointestinal cause of hospitalization [1], associated with high financial burdens [2]. The remaining may suffer from severe attacks, with a high morbidity and mortality This subgroup of patients need to be identified early in the course of the disease and need to be aggressively treated to prevent mortality [25]. In this sense and in order to avoid unnecessary overtreatment, thereby reducing the financial implications, proper identification of the mild disease is important and necessary. An overview of the multifactorial scoring systems and biochemical markers for predicting severe AP will be discussed, with a special focus on their advantages and limitations

Clinical Assessment
Ranson Score
Glasgow Score
Acute Physiology and Chronic Health Evaluation II Score
Bedside Index of Severity in Acute Pancreatitis Score
Systemic Inflammatory Response Syndrome
Pancreatitis Activity Scoring System
Contrast-Enhanced Computed Tomography
Transabdominal Ultrasonography
Endoscopic Ultrasonography
Metabolic Syndrome
Increased Body Mass Index
Hyperlipidemia
Hypertension
Fatty Liver
Diabetes Mellitus
Genetic Predisposition
Tumor Necrosis Factor-Alpha
Interleukin-1
Interleukin-6
Interleukin-8
C-Reactive Protein
Procalcitonin
Polymorphonuclear Elastase
Tissue Factor
Hepcidin
7.10. Copeptin
7.11. Soluble E-Selectin and Soluble Thrombomodulin
7.12. Endothelin I
7.13. Matrix Metalloproteinase-9
7.14. Albumin
7.16. Pancreatic Protease Activation Peptides
7.17. Red Blood Cell Distribution Width
7.18. Blood Urea Nitrogen
7.19. Hematocrit
7.20. Creatinine
7.21. Proteinuria
7.22. Angiopoietin 2
7.23. Oleic Acid Chlorohydrin
7.24. D-Dimer
7.25. Histones
7.26. Inter-Cellular Adhesion Molecule 1
Proteomic Profiling
Metabolomic Profiling
10. Clinical Relevance and Future Directions
Findings
11. Conclusions
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call