Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Acute Pancreatitis II: Pathophysiology

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...

Acute Pancreatitis I: Introduction

Acute Pancreatitis I: Introduction

Acute pancreatitis is the sudden inflammation of the pancreas caused by the early activation of digestive enzymes, leading to the autodigestion of pancreatic tissue. This results in local inflammation and, in severe cases, systemic complications.EtiologyUnderstanding the underlying causes is crucial, as identifying the etiology guides treatment and anticipates complications. Acute pancreatitis can be triggered by various factors, typically grouped into the following clinical categories.Biliary...

Acute Pancreatitis I: Introduction

Acute Pancreatitis I: Introduction

Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:

Acute Pancreatitis II: Clinical Manifestations and Management

Acute Pancreatitis II: Clinical Manifestations and Management

Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...

Chronic Pancreatitis I: Introduction

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...

Chronic Pancreatitis I: Introduction

Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Development of a predictive model for postoperative body mass index and diabetes outcomes after metabolic bariatric surgery: retrospective cohort study.

BJS open·2026

Same author

Sleeve gastrectomy versus Roux-en-Y-gastric bypass in patients with body mass index over 50 kg/m2: international multicentre cohort.

BJS open·2026

Same author

Reversal of Roux-en-Y Gastric Bypass: A Swedish National Cohort Study.

Annals of surgery·2026

Same author

Factors associated with anemia after bariatric surgery.

Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery·2026

Same author

Best achievable benchmarks in bariatric surgery: a nationwide registry study.

Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery·2026

Same author

Survival After Pancreatic Resection for Intraductal Papillary Mucinous Neoplasm: Supporting Selective Surgery.

United European gastroenterology journal·2026

Search research articles

Related Experiment Video

Updated: Jun 5, 2026

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection

Published on: May 10, 2024

Tissue factor in predicted severe acute pancreatitis.

Ellen Andersson¹, Jakob Axelsson, Gunilla Eckerwall

¹Department of Surgery, Clinical Sciences Lund, Lund University and Lund University Hospital, SE-221 85 Lund, Sweden. ellen.andersson@med.lu.se

World Journal of Gastroenterology

|December 25, 2010

Summary

Tissue Factor (TF) levels are elevated early in severe acute pancreatitis (AP). While TF is a better predictor of AP severity than C-reactive protein (CRP), it is less effective than Interleukin-6 (IL-6).

More Related Videos

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice

Published on: June 28, 2021

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Published on: April 1, 2022

Related Experiment Videos

Last Updated: Jun 5, 2026

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection

Published on: May 10, 2024

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice

Published on: June 28, 2021

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Published on: April 1, 2022

Area of Science:

Biochemistry
Clinical Medicine
Pathophysiology

Background:

Acute pancreatitis (AP) is a serious condition with varying severity.
Identifying early markers for severe AP is crucial for timely intervention.
Tissue Factor (TF) plays a role in coagulation and inflammation.

Purpose of the Study:

To investigate Tissue Factor (TF) levels in patients with acute pancreatitis.
To assess the potential of TF as an early predictive marker for AP severity.

Main Methods:

Prospective study of 49 patients with predicted severe acute pancreatitis.
Blood samples collected at baseline, 12 hours, 1 day, and 3 days for TF analysis.
Comparison of TF levels with Interleukin-6 (IL-6) and C-reactive protein (CRP) as severity markers.

Main Results:

Higher TF levels were observed in the severe AP group at baseline and 12 hours (P = 0.035 and P = 0.049).
TF showed an Area Under the Curve (AUC) of 0.679 for predicting severe AP.
Interleukin-6 (IL-6) demonstrated superior predictive value (AUC = 0.775) compared to TF and CRP.

Conclusions:

Tissue Factor (TF) levels are elevated early in severe acute pancreatitis.
TF serves as an early predictive marker for severe AP, outperforming CRP.
TF's predictive capability for severe AP is less than that of IL-6.