ArticleBritish journal of pain2026
Pathophysiology of pain in acute pancreatitis: A narrative review.
Article in British journal of pain, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and objective: Pain affects between 80 and 95% of patients with acute pancreatitis (AP). However, despite its importance and severity, the pathophysiological mechanisms are not well understood. This narrative review aims to review current knowledge about the pathophysiological mechanisms of pain in AP. Methods databases and data treatment: A search of electronic databases (PubMed/MEDLINE, Embase, and Cochrane) was conducted from January 31 2024 to July 25 2025. Inclusion criteria included any study on acute pancreatitis and pain (management). Exclusion criteria included the absence of relevant content or specific information about pain in AP. Results: We identified 11 studies. Two potential pain pathways were identified, categorised as nociceptive and neuropathic. Nociceptive signals are enhanced through the release of inflammatory mediators, such as nuclear factor-kappa B, nitric oxide and interleukin-6, in response to tissue damage. Furthermore, the characteristic visceral and referred pain is likely attributed to high levels of overlap of primary sensory afferent fibre activation and neuronal convergence. Damage of the central and peripheral nervous system through the upregulation of voltage-gated ion channels, vanilloid receptors and transmembrane proteins may cause neuropathic-like pain. This triggers neurogenic inflammation and further release of neuropeptides, inducing an auto-amplification loop between neurogenic inflammation and neuropathic pain, with one positively reinforcing the other. Conclusions: Diagnostic approaches in AP should consider nociceptive and neuropathic mechanisms, which should guide specific pain management. However, the knowledge gap remains significant, for example, for specific biomarkers and mechanisms enabling the development of target-specific personalised treatments for pain in AP in the future. Significance statement: In 2023, the James Lind Alliance priority-setting partnership in pancreatitis indicated that the number one priority for AP is establishing more effective ways to manage pain.
Indexed as
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.