Evidence map›Paper›PMID 36672685›Full record

ReviewBiomedicines2023

Delayed Drug Hypersensitivity Reactions: Molecular Recognition, Genetic Susceptibility, and Immune Mediators.

Mu-Tzu Chu, Wan-Chun Chang, Shih-Cheng Pao, Shuen-Iu Hung

Abstract readReview
In one paragraph

Review in Biomedicines, 2023. 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
–field-weighted citation impact
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.

  1. Article
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  7. Review
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  11. Review
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  14. Review
  15. Severe cutaneous adverse reactions.Nature reviews. Disease primers · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. 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

4 authors.

Mu-Tzu ChuCancer Vaccine & Immune Cell Therapy Core Lab, Department of Medical Research, Chang Gung Memorial Hospital, Linkou Branch, Taoyuan 333, Taiwan.ORCID 0000-0002-0279-7581
Wan-Chun ChangDivision of Translational Therapeutics, Department of Paediatrics, Faculty of Medicine, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.
Shih-Cheng PaoCancer Vaccine & Immune Cell Therapy Core Lab, Department of Medical Research, Chang Gung Memorial Hospital, Linkou Branch, Taoyuan 333, Taiwan.ORCID 0000-0001-7407-1053
Shuen-Iu HungCancer Vaccine & Immune Cell Therapy Core Lab, Department of Medical Research, Chang Gung Memorial Hospital, Linkou Branch, Taoyuan 333, Taiwan.

Funding

Linkou Chang Gung Memorial Hospital CIRPG3I0041~43, CIRPG3I0021~23, CIRPG3I0031~33, CIRPG2I0011~13Ministry of Science and Technology, Taiwan MOST 108-2320-B-182A-023 -MY3, MOST 109-2320-B-182A-008-MY3
6 · The paper itself

Abstract

Drug hypersensitivity reactions are classified into immediate and delayed types, according to the onset time. In contrast to the immediate type, delayed drug hypersensitivity mainly involves T lymphocyte recognition of the drug antigens and cell activation. The clinical presentations of such hypersensitivity are various and range from mild reactions (e.g., maculopapular exanthema (MPE) and fixed drug eruption (FDE)), to drug-induced liver injury (DILI) and severe cutaneous adverse reactions (SCARs) (e.g., Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), drug reaction with eosinophilia and systemic symptoms (DRESS), and acute generalized exanthematous pustulosis (AGEP)). The common culprits of delayed drug hypersensitivity include anti-epileptics, antibiotics, anti-gout agents, anti-viral drugs, etc. Delayed drug hypersensitivity is proposed to be initiated by different models of molecular recognition, composed of drug/metabolite antigen and endogenous peptide, HLA presentation, and T cell receptor (TCR) interaction. Increasing the genetic variants of HLA loci and drug metabolic enzymes has been identified to be responsible for delayed drug hypersensitivity. Furthermore, preferential TCR clonotypes, and the activation of cytotoxic proteins/cytokines/chemokines, are also involved in the pathogenesis of delayed drug hypersensitivity. This review provides a summary of the current understanding of the molecular recognition, genetic susceptibility, and immune mediators of delayed drug hypersensitivity.

Indexed as

drug hypersensitivitydrug reaction with eosinophilia and systemic symptomsHLAsevere cutaneous adverse reactionsStevens–Johnson syndromeT lymphocytes

Identifiers

PMID36672685
PMCPMC9855900

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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.