Evidence map›Paper›PMID 8922554›Full record

ReviewDrugs1996

The mechanisms of action of NSAIDs in analgesia.

J N Cashman

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Drugs, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05074056 (Evaluation of Perioperative Usage of Ketorolac on Postoperative Pain Reduction in Pediatric Patients with Adenotonsillectom), which is not on this map. Cited by 161 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 11 pooled it
9.0field-weighted citation impact, top 2% 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.

NCT05074056 phase4completednot on this mapstarted 2022, after this paper: background citation

Evaluation of Perioperative Usage of Ketorolac on Postoperative Pain Reduction in Pediatric Patients with Adenotonsillectom

TypeinterventionalSponsorSt. Louis UniversityRan2022 to 2024Enrolled142ConditionsAdenotonsillar Hypertrophy, Obstructive Sleep Apnea, Sleep-Disordered Breathing, Acute Post Operative PainArmsKetorolac
3 · Its place in the literature

Who cites it

161 citing papers in PubMed, 11 syntheses or guidelines pooled it, 491 citations in OpenAlex.

  1. Pooled it
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  6. Non-opioid Analgesics and Emerging Therapies.Cancer treatment and research · 2021
    Pooled it
  7. Guideline
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  15. Comparison of Local and Systemic Ibuprofen for Relief of Postoperative Pain in Symptomatic Teeth with Apical Periodontitis.Medical science monitor : international medical journal of experimental and clinical research · 2022
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  20. Effect of Celecoxib on Surgical Site Inflammation after Total Knee Arthroplasty: A Randomized Controlled Study.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2018
    Trial

101 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

J N CashmanDepartment of Anaesthetics, St George's Hospital, London, England.
St George's Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traditionally, the analgesic action of nonsteroidal anti-inflammatory drugs (NSAIDs) has been explained on the basis of their inhibition of the enzymes that synthesise prostaglandins. However, it is clear that NSAIDs exert their analgesic effect not only through peripheral inhibition of prostaglandin synthesis but also through a variety of other peripheral and central mechanisms. It is now known that there are 2 structurally distinct forms of the cyclo-oxygenase enzyme (COX-1 and COX-2). COX-1 is a constitutive member of normal cells and COX-2 is induced in inflammatory cells. Inhibition of COX-2 activity represent the most likely mechanism of action for NSAID-mediated analgesia, while the ratio of inhibition of COX-1 to COX-2 by NSAIDs should determine the likelihood of adverse effects. In addition, some NSAIDs inhibit the lipoxygenase pathway, which may itself result in the production of algogenic metabolites. Interference with G-protein-mediated signal transduction by NSAIDs may form the basis of an analgesic mechanism unrelated to inhibition of prostaglandin synthesis. These is increasing evidence that NSAIDs have a central mechanism of action that augments the peripheral mechanism. This effect may be the result of interference with the formation of prostaglandins within the CNS. Alternatively, the central action may be mediated by endogenous opioid peptides or blockade of the release of serotonin (5-hydroxytryptamine; 5-HT). A mechanism involving inhibition of excitatory amino acids of N-methyl-D-aspartate receptor activation has also been proposed.

Indexed as

AnalgesiaAnimalsAnti-Inflammatory Agents, Non-SteroidalArachidonic AcidCyclooxygenase InhibitorsHumansInflammationLipoxygenaseLipoxygenase InhibitorsN-MethylaspartatePainProstaglandin-Endoperoxide SynthasesRatsAnti-Inflammatory Agents, Non-SteroidalArachidonic AcidCyclooxygenase InhibitorsLipoxygenaseLipoxygenase InhibitorsN-MethylaspartateProstaglandin-Endoperoxide Synthases

Identifiers

PMID8922554
OpenAlexW2057812714

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.