Evidence map›Paper›PMID 29215084›Full record

Trial reportJournal of human genetics2018

Variants of ALPK1 with ABCG2, SLC2A9, and SLC22A12 increased the positive predictive value for gout.

Hung-Pin Tu, Albert Min-Shan Ko, Su-Shin Lee, Chi-Pin Lee, Tzer-Min Kuo, Chung-Ming Huang, Ying-Chin Ko

Abstract readClinical TrialMulticenter Study
PubMed Publisher
In one paragraph

Trial report in Journal of human genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Polymorphism rs3733591 of theFrontiers in genetics · 2024
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Evaluation of the Influence of Genetic Variants ofJournal of clinical medicine · 2020
    Article
  10. 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

7 authors at 4 institutions in 2 countries.

Hung-Pin TuDepartment of Public Health and Environmental Medicine, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Albert Min-Shan KoKey Laboratory of Vertebrate Evolution and Human Origins of Chinese Academy of Sciences, IVPP, CAS, Beijing, 100044, China.
Su-Shin LeeDivision of Plastic Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Chi-Pin LeeEnvironment-Omics-Disease Research Center, China Medical University Hospital, China Medical University, Taichung, 40402, Taiwan.
Tzer-Min KuoEnvironment-Omics-Disease Research Center, China Medical University Hospital, China Medical University, Taichung, 40402, Taiwan.
Chung-Ming HuangDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, 404, Taiwan.
Ying-Chin KoEnvironment-Omics-Disease Research Center, China Medical University Hospital, China Medical University, Taichung, 40402, Taiwan. ycko0406@gmail.com.
China Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWChina Medical University Hospital · TWChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the interactions of ALPK1 variants and the loci of ABCG2, SLC2A9, and SLC22A12 on gout risk. We conducted two case-control studies. Participants were recruited from hospitals (n = 410; 104 gout cases and 306 controls) and communities (n = 678; 373 gout cases and 305 controls) in Taiwan. The genotypes of ALPK1 (rs11726117 M861T, rs231247 R1084R, and rs231253 3' UTR), ABCG2 (rs2231142 Q141K and rs2231137 V12M), SLC2A9 (rs3733591 R265H and rs1014290), and SLC22A12 (rs3825016 H86H, rs11231825 H142H, and rs475688) were genotyped. Under a recessive model, the joint effects of ALPK1 variants and the SNPs rs2231142 of ABCG2, rs1014290 of SLC2A9, or rs475688 and rs3825016 of SLC22A12 were associated with gout. The rs11726117 [CC] of ALPK1 and rs2231142 [TT] of ABCG2 with the sequential addition of the rs1014290 [AA] of SLC2A9 and rs3825016 [CC] of SLC22A12 were associated with gout risk (odds ratio (OR): 13.01, 15.11, and 55.00 and positive predictive value (PPV): 56%, 69%, and 99% in the Han group, respectively; OR: 3.76, 5.78, and 12.30 and PPV: 74%, 80%, and 81% in the aboriginal group, respectively). Combined exposure to the four high-risk genotypes of ALPK1 and the uric-acid-related loci of ABCG2, SLC2A9, and SLC22A12 was associated with an increased gout risk and a high PPV for gout.

Indexed as

Genetic LociPolymorphism, GeneticAdultAgedATP Binding Cassette Transporter, Subfamily G, Member 2Glucose Transport Proteins, FacilitativeGoutHumansMaleMiddle AgedNeoplasm ProteinsOrganic Anion TransportersOrganic Cation Transport ProteinsPredictive Value of TestsProtein KinasesABCG2 protein, humanALPK1 protein, humanATP Binding Cassette Transporter, Subfamily G, Member 2Glucose Transport Proteins, FacilitativeNeoplasm ProteinsOrganic Anion TransportersOrganic Cation Transport ProteinsProtein KinasesSLC22A12 protein, humanSLC2A9 protein, human

Identifiers

PMID29215084
OpenAlexW2767912471

What OpenQuestion holds

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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.