Evidence map›Paper›PMID 39100437›Full record

ReviewHeliyon2024

Clues of HLAs, metabolic SNPs, and epigenetic factors in T cell-mediated drug hypersensitivity reactions.

Rasol Molatefi, Sedighe Talebi, Azam Samei, Neda Roshanravan, Shirin Manshouri, Baran Hashemi, Vahid Ghobadi Dana, Erfan Mosharkesh, Mohammad Ali Bahar, Sholeh Khajoei and 1 more

Abstract readReview
In one paragraph

Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Rasol MolatefiCancer Immunology and Immunotherapy Research Center, Ardabil University of Medical Sciences, Ardabil, Iran.
Sedighe TalebiDepartment of Traditional Medicine, School of Persian Medicine, Shahed University, Tehran, Iran.
Azam SameiDepartment of Laboratory Sciences, School of Allied Medical Sciences, Kashan University of Medical Sciences, Kashan, Iran.
Neda RoshanravanCardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Shirin ManshouriRajaei Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.
Baran HashemiRajaei Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.
Vahid Ghobadi DanaDepartment of Immunology and Allergy, Academic Center for Education, Culture, and Research (ACECR), Tehran, Iran.
Erfan MosharkeshFaculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran.
Mohammad Ali BaharDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Sholeh KhajoeiClinical Research Development Center, Imam Khomeini Hospital, Jiroft University of Medical Sciences, Jiroft, Iran.
Farhad SeifDepartment of Photodynamic Therapy, Medical Laser Research Center, Academic Center for Education, Culture, and Research (ACECR), Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug hypersensitivities are common reactions due to immunologic responses. They are of utmost importance because they may generate severe and fatal outcomes. Some drugs may cause Adverse Drug Reactions (ADRs), such as drug hypersensitivity reactions (DHRs), which can occur due to the interaction of intact drugs or their metabolites with Human Leukocyte Antigens (HLAs) and T cell receptors (TCRs). This type develops over a period of 24-72 h after exposure and is classified as type IV of DHRs. Acute generalized exanthematic pustulosis (AGEP), Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) and drug reaction with eosinophilia and systemic symptoms (DRESS) are types of Severe Cutaneous Adverse Reactions (SCARs). In this review, we aim to discuss the types of ADRs, the mechanisms involved in their development, and the role of immunogenetic factors, such as HLAs in type IV DHRs, single-nucleotide polymorphisms (SNPs), and some epigenetic modifications, e.g., DNA/histone methylation in a variety of genes and their promoters which may predispose subjects to DHRs. In conclusion, development of promising novel in vitro or

Indexed as

Adverse drug reactionDrug hypersensitivity reactionEpigeneticsHuman leukocyte antigenSingle-nucleotide polymorphismT cell

Identifiers

PMID39100437
PMCPMC11296025

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.