Evidence map›Paper›PMID 21060839›Full record

ArticlePloS one2010

Diclofenac hypersensitivity: antibody responses to the parent drug and relevant metabolites.

Andrea Harrer, Roland Lang, Robert Grims, Michaela Braitsch, Thomas Hawranek, Werner Aberer, Lothar Vogel, Walther Schmid, Fatima Ferreira, Martin Himly

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 56 citations in OpenAlex.

  1. Ex vivo Drug Metabolism Using Primary Human Hepatocytes for the Detection of Metabolite-Dependent Antibodies to Red Blood Cells.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2025
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  16. Immediate-type hypersensitivity drug reactions.British journal of clinical pharmacology · 2014
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  18. Mediators released during human anaphylaxis.Current allergy and asthma reports · 2012
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  19. 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

10 authors at 5 institutions in 2 countries.

Andrea HarrerDivision of Allergy and Immunology, Department of Molecular Biology, University of Salzburg, Salzburg, Austria.
Roland Lang
Robert Grims
Michaela Braitsch
Thomas Hawranek
Werner Aberer
Lothar Vogel
Walther Schmid
Fatima Ferreira
Martin Himly
University of Salzburg · ATMedical University of Graz · ATParacelsus Medical University · ATUniversity of Vienna · ATPaul Ehrlich Institut · DE

Funding

Austrian Science Fund FWF P 18820
6 · The paper itself

Abstract

backgroundHypersensitivity reactions against nonsteroidal antiinflammatory drugs (NSAIDs) like diclofenac (DF) can manifest as Type I-like allergic reactions including systemic anaphylaxis. However, except for isolated case studies experimental evidence for an IgE-mediated pathomechanism of DF hypersensitivity is lacking. In this study we aimed to investigate the possible involvement of drug- and/or metabolite-specific antibodies in selective DF hypersensitivity. METHODOLOGY/PRINCIPAL

findingsDF, an organochemically synthesized linkage variant, and five major Phase I metabolites were covalently coupled to carrier proteins. Drug conjugates were analyzed for coupling degree and capacity to crosslink receptor-bound IgE antibodies from drug-sensitized mice. With these conjugates, the presence of hapten-specific IgE antibodies was investigated in patients' samples by ELISA, mediator release assay, and basophil activation test. Production of sulfidoleukotrienes by drug conjugates was determined in PBMCs from DF-hypersensitive patients. All conjugates were shown to carry more than two haptens per carrier molecule. Immunization of mice with drug conjugates induced drug-specific IgE antibodies capable of triggering mediator release. Therefore, the conjugates are suitable tools for detection of drug-specific antibodies and for determination of their anaphylactic activity. Fifty-nine patients were enrolled and categorized as hypersensitive either selectively to DF or to multiple NSAIDs. In none of the patients' samples evidence for drug/metabolite-specific IgE in serum or bound to allergic effector cells was found. In contrast, a small group of patients (8/59, 14%) displayed drug/metabolite-specific IgG. CONCLUSIONS/SIGNIFICANCE: We found no evidence for an IgE-mediated effector mechanism based on haptenation of protein carriers in DF-hypersensitive patients. Furthermore, a potential involvement of the most relevant metabolites in DF hypersensitivity reactions could be excluded.

Indexed as

AnimalsAntibodiesAnti-Inflammatory Agents, Non-SteroidalBasophilsDiclofenacDrug HypersensitivityEnzyme-Linked Immunosorbent AssayFemaleHumansImmunoglobulin EMiceMice, Inbred BALB CAntibodiesAnti-Inflammatory Agents, Non-SteroidalDiclofenacImmunoglobulin E

Identifiers

PMID21060839
PMCPMC2965666
OpenAlexW2094582553

What OpenQuestion holds

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LicenceCC BY
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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.