ArticleInternational journal of inflammation2012
The clinical course of acute pancreatitis and the inflammatory mediators that drive it.
Article in International journal of inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02602574 (Endoscopic Retrograde Cholangiopancreatography), which is not on this map. Cited by 46 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Endoscopic Retrograde Cholangiopancreatography (ERCP)-Induced and Non-ERCP Induced Acute Pancreatitis: Two Distinct Clinical and Immunological Entities?
Who cites it
46 citing papers in PubMed, 104 citations in OpenAlex.
- Prevention of Severe Acute Pancreatitis With Cyclooxygenase-2 Inhibitors: A Randomized Controlled Clinical Trial.The American journal of gastroenterology · 2020Trial
- Integrated Transcriptomics and Lipidomics Identify CES1-Mediated Maladaptive Lipolysis as a Key Target of Hyperlipidemic Acute Pancreatitis.Metabolites · 2026Article
- Mapping the vascular complications of acute pancreatitis: focus on splanchnic vein thrombosis.BMC gastroenterology · 2026Article
- Natural Course of Asymptomatic Walled-off Necrosis due to Acute Pancreatitis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026Article
- Integrating Bayesian Inference and Machine Learning to Evaluate TAP and Trypsin-2 as Early Biomarkers of Systemic Inflammation in Acute Pancreatitis.Medicina (Kaunas, Lithuania) · 2026Article
- Development of a prediction method for severe pancreatitis using a nomogram.Frontiers in medicine · 2026Article
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- CD36 Induces Inflammation by Promoting Ferroptosis in Pancreas, Epididymal Adipose Tissue, and Adipose Tissue Macrophages in Obesity-Related Severe Acute Pancreatitis.International journal of molecular sciences · 2025Article
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- Involvement of heparanase in the pathogenesis of acute pancreatitis: Implication of novel therapeutic approaches.Journal of cellular and molecular medicine · 2024Article
- L-Arginine-induced acute pancreatitis and its associated lung injury in rats: Down-regulation of TLR-4/MAPK-p38/JNK signaling pathway viaIranian journal of basic medical sciences · 2024Article
- Screening and identification of the hub genes in severe acute pancreatitis and sepsis.Frontiers in molecular biosciences · 2024Article
- Sirtuin4 alleviates severe acute pancreatitis by regulating HIF-1α/HO-1 mediated ferroptosis.Cell death & disease · 2023Article
- Structure-Directed Discovery of Potent Soluble Epoxide Hydrolase Inhibitors for the Treatment of Inflammatory Diseases.Journal of medicinal chemistry · 2023Article
- Lactated Ringer's Solution Reduces Severity, Mortality, Systemic and Local Complications in Acute Pancreatitis: A Systematic Review and Meta-Analysis.Biomedicines · 2023Review
- MicroRNA-28-5p as a potential diagnostic biomarker for chronic periodontitis and its role in cell proliferation and inflammatory response.Journal of dental sciences · 2022Article
- Association of Genetic Variants inGenes · 2022Article
- Necrotizing Pancreatitis from Hypertriglyceridemia: More Severe Disease?Digestive diseases and sciences · 2021Article
- Chemokine receptor 8 expression may be linked to disease severity and elevated interleukin 6 secretion in acute pancreatitis.World journal of gastrointestinal pathophysiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis (AP) is a common emergency condition. In the majority of cases, it presents in a mild and self-limited form. However, about 20% of patients develop severe disease with local pancreatic complications (including necrosis, abscess, or pseudocysts), systemic organ dysfunction, or both. A modern classification of AP severity has recently been proposed based on the factors that are causally associated with severity of AP. These factors are both local (peripancreatic necrosis) and systemic (organ failure). In AP, inflammation is initiated by intracellular activation of pancreatic proenzymes and/or nuclear factor-κB. Activated leukocytes infiltrate into and around the pancreas and play a central role in determining AP severity. Inflammatory reaction is first local, but may amplify leading to systemic overwhelming production of inflammatory mediators and early organ failure. Concomitantly, anti-inflammatory cytokines and specific cytokine inhibitors are produced. This anti-inflammatory reaction may overcompensate and inhibit the immune response, rendering the host at risk for systemic infection. Currently, there is no specific treatment for AP. However, there are several early supportive treatments and interventions which are beneficial. Also, increasing the understanding of the pathogenesis of systemic inflammation and the development of organ dysfunction may provide us with future treatment modalities.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.