Pathophysiology, classification and available guidelines of acute pancreatitis

Abstract

Acute pancreatitis (AP) constitutes the majority of cases requiring hospital admission in gastroenterology. We are yet to know many things about its pathophysiology which is a certain drawback for the progress in its treatment. Prediction of severity is necessary for the plan of the management. The existing scoring systems are yet to be satisfactory. However our progress in the field was significant in the recent decade and a leap forward is expected in this cumbersome-to-manage condition which has many unmet needs. In this review, we are going to summarize the hitherto data in pathogenesis and would weigh the usefulnes and weaknes of each of existing scoring systems in the management of AP. Keywords: Acute pancreatitis, guideline, pathophysiology, scoring systems, classifications, insights Pancreas was first discovered by Herophilus, a Greek anatomist and surgeon, in Chalcedon (now Kadıkoy, Istanbul) in 336 BC. Despite the many years since its discovery, a lot remains unknown about pancreas. The coming decade would, probably, witness several advances in our understanding of pancreas and its diseases.This review aims to describe the hitherto knowledge in pancreas pathophysiology and classification systems of severity scoring. PATHOPHYSIOLOGYThe main reason for the lack of successful treatment in acute pancreatitis (AP) is that many aspects of this condition regarding the pathophysiology are still unknown. AP has a severe course in 20% of the cases and may be associated with high morbidity and mortality in 2-3%. Pancreatic autodigestion (trypsinogen-centered) theory has been in use in the AP pathogenesis for over a hundred year. In this theory, premature activation of pancreatic proenzymes (zymogens) induces autolysis, which triggers inflammatory events followed by continued damage to the pancreas and/or non-pancreatic tissues in some way.Experimental models (1,2) have demonstrated the involvement of trypsin activation in hereditary pancreatitis (3). Along with zymogen activation, natural factor kappa beta (NFkB) activation is also important in the development of AP. Whether both are involved or are independently-acting parallel factors in AP is controversial. It was shown, in vitro, that trypsinogen expression did not activate NFkB (4

A Chinese Herbal Decoction, Huoxue Qingyi Decoction, Promotes Rehabilitation of Patients with Severe Acute Pancreatitis: A Retrospective Study

“…Severe acute pancreatitis (SAP), a life-threatening condition characterized by edema, inflammation, hemorrhage, and necrosis of the pancreas, still remains an important surgical problem with high morbidity and mortality [ 12 , 13 ]. Traditional Chinese Medicine active ingredients, such as emodin, magnolol, naringin, ginkgolide B, sanchinoside, taxol, resveratrol, rutoside, tetramethylpyrazine, and breviscapine, being used in treating SAP have advantages in not only acting on the pancreas, stomach, and intestines, but also having marked treatment effects on other visceral injuries arising from systemic inflammatory responses accompanying pancreatitis and blocking the disease progression [ 14 ].…”

Validation of the Revised Atlanta Criteria in determining the severity of acute pancreatitis

“…Severity assessment was also made according to the Determinant Based Classification (DBC) [11]. HAPS (Harmless Acute Pancreatitis Score), Ranson, BISAP (Bedside Index of Severity in Acute Pancreatitis), SIRS (Systemic Inflammatory Response Syndrome), Modified Glasgow, Panc 3, and Computer Tomography Severity Index (CTSI) scores were calculated [11][12][13][14][15][16][17]. APACHE II score was calculated with Qx Calculate.…”

CD177 Inhibits Neutrophil Extracellular Trap Formation and Protects against Acute Pancreatitis in Mice

“…However, in severe acute pancreatitis (SAP), injured acinar cells activate digestive enzymes and release factors that lead to the recruitment of inflammatory cells, along with the generation of multiple mediators, such as reactive oxygen species (ROS) and cytokines [ 4 ], resulting in systemic inflammatory response syndrome (SIRS) and even multiple-organ dysfunction (MODS) [ 5 ]. Therefore, the treatment of MAP patients is relatively conservative and requires only a short hospitalization, whereas that of SAP patients typically involves intensive care [ 6 ]. In recent years, SAP patients have incurred high health care costs, and the disease has shown a high mortality and great severity [ 7 , 8 , 9 ].…”