Evidence map›Paper›PMID 36835420›Full record

ArticleInternational journal of molecular sciences2023

DUOX1 Gene Missense Mutation Confers Susceptibility on Type 2 Amiodarone-Induced Thyrotoxicosis.

Olga Biakina, Yulia Mitina, Daria Gognieva, Marina Axenova, Alexandra Ermolaeva, Afina Bestavashvili, Valentin Fadeev, Abram Syrkin, Philipp Kopylov

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

3 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
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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

9 authors at 3 institutions in 2 countries.

Olga BiakinaDepartment of Cardiology, Functional and Ultrasound Diagnostics of N.V. Sklifosovsky Institute for Clinical Medicine, I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.
Yulia MitinaDepartment of Anatomy and Physiology, School of Biomedical Sciences, University of Melbourne, Melbourne 3010, Australia.ORCID 0000-0003-3742-7959
Daria GognievaDepartment of Cardiology, Functional and Ultrasound Diagnostics of N.V. Sklifosovsky Institute for Clinical Medicine, I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.
Marina AxenovaFederal State Organization "Centre for Strategic Planning and Management of Biomedical Health Risks", Ministry of Health of the Russian Federation, 119121 Moscow, Russia.
Alexandra ErmolaevaDepartment of Endocrinology No. 1 of N.V. Sklifosovsky Institute for Clinical Medicine, I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.ORCID 0000-0002-6471-8252
Afina BestavashviliWorld-Class Research Center «Digital Biodesign and Personalized Healthcare», I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.
Valentin FadeevDepartment of Endocrinology No. 1 of N.V. Sklifosovsky Institute for Clinical Medicine, I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.ORCID 0000-0002-3026-6315
Abram SyrkinDepartment of Cardiology, Functional and Ultrasound Diagnostics of N.V. Sklifosovsky Institute for Clinical Medicine, I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.
Philipp KopylovDepartment of Cardiology, Functional and Ultrasound Diagnostics of N.V. Sklifosovsky Institute for Clinical Medicine, I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.
Sechenov University · RUMinistry of Health of the Russian Federation · RUThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Possible triggers and genetic markers involved in pathogenesis of amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH) are currently unknown. This study aimed to analyze the association between polymorphisms in the genes involved in thyroid hormones biosynthesis and metabolism. Thirty-nine consecutive patients with confirmed type 2 amiodarone-induced thyrotoxicosis were enrolled; 39 patients on the same therapy for at least 6 months without thyroid pathology were included as a control group. A comparative study was carried out to determine the distribution and genotypes of polymorphic markers of the (Na)-iodide symporter (NIS) genes (rs7250346, C/G substitution), thyroid stimulating hormone receptor (TSHR) (rs1991517, C/G substitution), thyroid peroxidase (TPO) (rs 732609, A/C substitution), DUOX 1-1 (C/T substitution), DUOX 1-2 (G/T substitution), DUOX 1-3 (C/T substitution), glutathione peroxidase 3 (GPX3) (C/T substitution), glutathione peroxidase 4 (GPX4) (C/T substitution). Statistical analysis was performed using Prism (Version 9.0.0 (86)). This study showed that the risk of AIT2 is 3.18 times higher in the G/T of the DUOX1 gene carriers. This study is the first report of genetic markers associated with amiodarone-related adverse events conducted in humans. The obtained results indicate the necessity for a personalized approach to amiodarone administration.

Indexed as

AmiodaroneAnti-Arrhythmia AgentsDual OxidasesThyrotoxicosisGenetic MarkersHumansMutation, MissenseAmiodaroneAnti-Arrhythmia AgentsDual OxidasesDUOX1 protein, humanGenetic Markersamiodarone-induced thyrotoxicosis 2 typeDUOX1 genegenetic markers

Identifiers

PMID36835420
PMCPMC9964217
OpenAlexW4321242693

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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.