Evidence map›Paper›PMID 38424191›Full record

ArticleExperimental & molecular medicine2024

Synergistic toxicity with copper contributes to NAT2-associated isoniazid toxicity.

Jihoon G Yoon, Dong Geon Jang, Sung-Gyu Cho, Chaeyoung Lee, Shin Hye Noh, Soo Kyung Seo, Jung Woo Yu, Hyeon Woo Chung, KyeoRe Han, Soon Sung Kwon and 13 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
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  4. 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

23 authors at 5 institutions in 1 country.

Jihoon G Yoon *Department of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-4401-7803
Dong Geon Jang *Department of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea.
Sung-Gyu Cho *Department of Microbiology and Immunology, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0009-0008-1567-2754
Chaeyoung LeeDepartment of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea.
Shin Hye NohDepartment of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea.
Soo Kyung SeoDepartment of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jung Woo YuDepartment of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hyeon Woo ChungDepartment of Microbiology and Immunology, Yonsei University College of Medicine, Seoul, Republic of Korea.
KyeoRe HanDepartment of Microbiology and Immunology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Soon Sung KwonDepartment of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea.
Dai Hoon HanDivision of Hepatobiliary and Pancreatic Surgery, Department of Surgery, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0003-2787-7876
Jaeseong OhDepartment of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine and Hospital, Seoul, Republic of Korea.ORCID 0000-0001-6275-8587
In-Jin JangDepartment of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine and Hospital, Seoul, Republic of Korea.
Sang-Hoon KimDepartment of Internal Medicine, Eulji University School of Medicine, Seoul, Republic of Korea.
Young-Koo JeeDepartment of Internal Medicine, Dankook University College of Medicine, Cheonan, Republic of Korea.
Hyun LeeDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of Korea.
Dong Won ParkDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of Korea.
Jang Won SohnDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-7132-2988
Ho Joo YoonDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of Korea.
Chul Hoon KimDepartment of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jae Myun LeeDepartment of Microbiology and Immunology, Yonsei University College of Medicine, Seoul, Republic of Korea. jaemyun@yuhs.ac.
Sang-Heon KimDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of Korea. sangheonkim@hanyang.ac.kr.ORCID 0000-0001-8398-4444
Min Goo LeeDepartment of Pharmacology, BK21 Project of Yonsei Advanced Medical Science, Woo Choo Lee Institute for Precision Drug Development, Yonsei University College of Medicine, Seoul, Republic of Korea. mlee@yuhs.ac.ORCID 0000-0001-7436-012X
Yonsei University · KRHanyang University · KREulji University · KRSeoul National University Hospital · KRDankook University · KR

Funding

Korea Health Industry Development Institute (KHIDI) HI15C1543National Research Foundation of Korea (NRF) 2022R1A2C3002917National Research Foundation of Korea (NRF) 2022R1A4A1031336
6 · The paper itself

Abstract

Anti-tuberculosis (AT) medications, including isoniazid (INH), can cause drug-induced liver injury (DILI), but the underlying mechanism remains unclear. In this study, we aimed to identify genetic factors that may increase the susceptibility of individuals to AT-DILI and to examine genetic interactions that may lead to isoniazid (INH)-induced hepatotoxicity. We performed a targeted sequencing analysis of 380 pharmacogenes in a discovery cohort of 112 patients (35 AT-DILI patients and 77 controls) receiving AT treatment for active tuberculosis. Pharmacogenome-wide association analysis was also conducted using 1048 population controls (Korea1K). NAT2 and ATP7B genotypes were analyzed in a replication cohort of 165 patients (37 AT-DILI patients and 128 controls) to validate the effects of both risk genotypes. NAT2 ultraslow acetylators (UAs) were found to have a greater risk of AT-DILI than other genotypes (odds ratio [OR] 5.6 [95% confidence interval; 2.5-13.2], P = 7.2 × 10

Indexed as

Arylamine N-AcetyltransferaseChemical and Drug Induced Liver InjuryMitochondrial DiseasesTuberculosisAntitubercular AgentsCopperGenotypeHumansIsoniazidAntitubercular AgentsArylamine N-AcetyltransferaseCopperIsoniazidNAT2 protein, human

Identifiers

PMID38424191
PMCPMC10984958
OpenAlexW4392767002

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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.