Evidence map›Paper›PMID 35791391›Full record

ArticleJournal of pain research2022

Testing Topical Products Specifically to Reduce Inflammatory Pain from Gout: Transdermal NSAID Delivery and Monosodium Urate Solubility.

Mark W Hooper, Liang He

Open access · goldAbstract read
In one paragraph

Article in Journal of pain research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
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

2 authors at 2 institutions in 1 country.

Mark W HooperMedCryst Therapeutics Ltd, Centre for Innovation & Enterprise, Oxford University Begbroke Science Park, Oxford, OX5 1PF, UK.
Liang HePharmHe, Chertsey, UK.
United Therapeutics (United Kingdom) · GBUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Gout is caused by crystals of monosodium urate (MSU) in the joints. Topical nonsteroidal anti-inflammatory drug products (NSAIDs) are often the first-choice immediate treatment. This study examined the effect of commercially available and newly developed transdermal NSAID products on the solubility of MSU in a physiologically relevant system, alongside the efficacy of transdermal NSAID delivery. Materials and Methods: Drug permeability of 7 commercially available topical NSAID products, alongside 3 newly developed "Gout Buster" products, was evaluated in vitro using pig's ear skin in Franz diffusion cells. The standard Franz cell experimental protocol was adapted to include assessment of MSU solubility in phosphate buffered saline for each product. Some materials were also tested via direct solubility studies. Results: The amount of drug delivered transdermally varied significantly between different formulations, with the best ibuprofen delivery being ~5 times higher than the lowest, and best diclofenac delivery being ~3.5 times higher than the lowest. Changes in formulations and the drug concentration in the product both affected the amount of drug delivered. Overall ibuprofen permeation was higher than diclofenac. The commercially available products showed little or no effect on the MSU solubility (99-103% vs control). The Gout Buster products showed significant improvement in the MSU solubility after permeation through skin (120-126%). Increased sodium levels reduced the solubility of MSU in direct solubility studies. Conclusion: In these trials, the Gout Buster products showed significantly improved permeation of both ibuprofen and diclofenac over the commercial products at similar drug concentrations, and showed significant improvement for MSU solubility. Increased sodium levels reduced the solubility of MSU and could cause more crystallisation in vivo. Therefore, topical NSAID products with the Gout Buster formulation may have the best likelihood of both reducing inflammation and helping re-dissolve the MSU crystals that cause gout.

Indexed as

Franz-cell experimentsGout Busterin vitro studynonsteroidal anti-inflammatory drug

Identifiers

PMID35791391
PMCPMC9250783
OpenAlexW4283702247

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Registered trials

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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.