Evidence map›Paper›PMID 23774753›Full record

ArticleScientific reports2013

Common dysfunctional variants in ABCG2 are a major cause of early-onset gout.

Hirotaka Matsuo, Kimiyoshi Ichida, Tappei Takada, Akiyoshi Nakayama, Hiroshi Nakashima, Takahiro Nakamura, Yusuke Kawamura, Yuzo Takada, Ken Yamamoto, Hiroki Inoue and 19 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 5 pooled it
5.5field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 5 syntheses or guidelines pooled it, 131 citations in OpenAlex.

  1. Pooled it
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  5. A meta-analysis of the associations between the Q141K and Q126X ABCG2 gene variants and gout risk.International journal of clinical and experimental pathology · 2015
    Pooled it
  6. Article
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  15. Dysuricemia.Biomedicines · 2023
    Review
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  20. Article

11 more citing papers are in PubMed but not listed here.

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

29 authors at 10 institutions in 2 countries.

Hirotaka MatsuoDepartment of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan. hmatsuo@ndmc.ac.jp
Kimiyoshi Ichida
Tappei Takada
Akiyoshi Nakayama
Hiroshi Nakashima
Takahiro Nakamura
Yusuke Kawamura
Yuzo Takada
Ken Yamamoto
Hiroki Inoue
Yuji Oikawa
Mariko Naito
Asahi Hishida
Kenji Wakai
Chisa Okada
Seiko Shimizu
Masayuki Sakiyama
Toshinori Chiba
Hiraku Ogata
Kazuki Niwa
Makoto Hosoyamada
Atsuyoshi Mori
Nobuyuki Hamajima
Hiroshi Suzuki
Yoshikatsu Kanai
Yutaka Sakurai
Tatsuo Hosoya
Toru Shimizu
Nariyoshi Shinomiya
National Defense Medical College · JPNagoya University · JPJikei University School of Medicine · JPToho University · JPUniversity of Tokyo Hospital · JPKyushu University · JPMidorigaoka Hospital · JPOsaka University · JPSeirei Social Welfare Community · JPTeikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gout is a common disease which mostly occurs after middle age, but more people nowadays develop it before the age of thirty. We investigated whether common dysfunction of ABCG2, a high-capacity urate transporter which regulates serum uric acid levels, causes early-onset gout. 705 Japanese male gout cases with onset age data and 1,887 male controls were genotyped, and the ABCG2 functions which are estimated by its genotype combination were determined. The onset age was 6.5 years earlier with severe ABCG2 dysfunction than with normal ABCG2 function (P = 6.14 × 10(-3)). Patients with mild to severe ABCG2 dysfunction accounted for 88.2% of early-onset cases (twenties or younger). Severe ABCG2 dysfunction particularly increased the risk of early-onset gout (odds ratio 22.2, P = 4.66 × 10(-6)). Our finding that common dysfunction of ABCG2 is a major cause of early-onset gout will serve to improve earlier prevention and therapy for high-risk individuals.

Indexed as

AdolescentAdultAge of OnsetATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Case-Control StudiesGoutHumansMaleNeoplasm ProteinsYoung AdultABCG2 protein, humanATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Neoplasm Proteins

Identifiers

PMID23774753
PMCPMC3684804
OpenAlexW2090058293

What OpenQuestion holds

Textmetadata
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.