Evidence map›Paper›PMID 21153480›Full record

ReviewLangenbeck's archives of surgery2011

Pain mechanisms in chronic pancreatitis: of a master and his fire.

Ihsan Ekin Demir, Elke Tieftrunk, Matthias Maak, Helmut Friess, Güralp Onur Ceyhan

Open access · hybridAbstract readReview
In one paragraph

Review in Langenbeck's archives of surgery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Personalizing treatment of pancreatitis-associated chronic pain: the need for an integrated omics approach.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  5. Review
  6. Opioid dependence in patients with pain in chronic pancreatitis an emerging problem.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2025
    Review
  7. Review
  8. Article
  9. Pain in chronic pancreatitis: What can we do today?World journal of methodology · 2024
    Review
  10. Advances in the Management of Pain in Chronic Pancreatitis.Current gastroenterology reports · 2023
    Review
  11. Arterial Resection for Pancreatic Cancer: Feasibility and Current Standing in a High-Volume Center.Annals of surgery open : perspectives of surgical history, education, and clinical approaches · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Ihsan Ekin DemirDepartment of Surgery, Klinikum Rechts der Isar, Technische Universität München, Ismaninger Str. 22, 81675, Munich, Germany. demir@chir.med.tu-muenchen.de
Elke Tieftrunk
Matthias Maak
Helmut Friess
Güralp Onur Ceyhan
Klinikum rechts der Isar · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnraveling the mechanisms of pain in chronic pancreatitis (CP) remains a true challenge. The rapid development of pancreatic surgery in the twentieth century, usage of advanced molecular biological techniques, and emergence of clinician-scientists have enabled the elucidation of several mechanisms that lead to the chronic, complicated neuropathic pain syndrome in CP. However, the proper analysis of pain in CP should include three main arms of mechanisms: "peripheral nociception," "peripheral/pancreatic neuropathy and neuroplasticity," and "central neuropathy and neuroplasticity." DISCUSSION: According to our current knowledge, pain in CP involves sustained sensitization of pancreatic peripheral nociceptors by neurotransmitters and neurotrophic factors following neural damage. This peripheral pancreatic neuropathy leads to intrapancreatic neuroplastic alterations that involve a profound switch in the autonomic innervation of the human pancreas via "neural remodeling." Furthermore, this neuropathy entails a hyperexcitability of spinal sensory second-order neurons, which are subject to modulation from the brainstem via descending facilitation. Finally, viscerosensory cortical areas react to this central sensitization via spatial reorganization and thus a central neuroplasticity. The present review summarizes the current findings in these arms of mechanisms and introduces a novel concept to consistently describe pain in CP as a "predominantly neuropathic," "mixed-type" pain.

Indexed as

Abdominal PainHumansNeuralgiaNociceptorsPain MeasurementPancreatitis, Chronic

Identifiers

PMID21153480
PMCPMC3026929
OpenAlexW2005222244

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.