Evidence map›Paper›PMID 30235330›Full record

ArticlePloS one2018

Independent association of HLA-DPB1*02:01 with rheumatoid arthritis in Japanese populations.

Hiroshi Furukawa, Shomi Oka, Kota Shimada, Atsushi Hashimoto, Akiko Komiya, Shinichiro Tsunoda, Akiko Suda, Satoshi Ito, Koichiro Saisho, Masao Katayama and 11 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  4. Review
  5. Observational
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

21 authors at 9 institutions in 1 country.

Hiroshi FurukawaClinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital, Sagamihara, Japan.ORCID 0000-0003-1353-8056
Shomi OkaClinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital, Sagamihara, Japan.
Kota ShimadaDepartment of Rheumatology, National Hospital Organization Sagamihara National Hospital, Sagamihara, Japan.
Atsushi HashimotoDepartment of Rheumatology, National Hospital Organization Sagamihara National Hospital, Sagamihara, Japan.
Akiko KomiyaClinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital, Sagamihara, Japan.
Shinichiro TsunodaDivision of Rheumatology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Akiko SudaDepartment of Rheumatology, Yokohama Minami Kyosai Hospital, Yokohama, Japan.
Satoshi ItoDepartment of Rheumatology, Niigata Rheumatic Center, Shibata, Japan.
Koichiro SaishoDepartment of Orthopedics/Rheumatology, Miyakonojo Medical Center, National Hospital Organization, Miyakonojo, Japan.
Masao KatayamaDepartment of Internal Medicine, Nagoya Medical Center, National Hospital Organization, Nagoya, Japan.
Satoshi ShinoharaTochigi Rheumatology Clinic, Utsunomiya, Japan.ORCID 0000-0001-8850-0859
Takeo SatoDivision of Rheumatology and Clinical Immunology, Jichi Medical University, Shimotsuke, Japan.
Katsuya NagataniDivision of Rheumatology and Clinical Immunology, Jichi Medical University, Shimotsuke, Japan.
Seiji MinotaDivision of Rheumatology and Clinical Immunology, Jichi Medical University, Shimotsuke, Japan.
Toshihiro MatsuiClinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital, Sagamihara, Japan.
Naoshi FukuiClinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital, Sagamihara, Japan.
Shoji SugiiDepartment of Rheumatic Diseases, Tokyo Metropolitan Tama Medical Center, Fuchu, Japan.
Hajime SanoDivision of Rheumatology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Kiyoshi MigitaClinical Research Center, Nagasaki Medical Center, National Hospital Organization, Omura, Japan.
Shouhei NagaokaDepartment of Rheumatology, Yokohama Minami Kyosai Hospital, Yokohama, Japan.
Shigeto TohmaClinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital, Sagamihara, Japan.
National Sagamihara Hospital · JPJichi Medical University · JPHyogo Medical University · JPNational Hospital Organization · JPUniversity of Tsukuba · JPYokohama Minami Kyosai Hospital · JPFukushima Medical University · JPTochigi Medical Center · JPTokyo Metropolitan Tama Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRheumatoid arthritis (RA) is a chronic autoimmune disease characterized with joint destructions; environmental and genetic factors were thought to be involved in the etiology of RA. The production of anti-citrullinated peptide antibodies (ACPA) is specifically associated with RA. DRB1 is associated with the susceptibility of RA, especially ACPA-positive RA [ACPA(+)RA]. However, a few studies reported on the independent associations of DPB1 alleles with RA susceptibility. Thus, we investigated the independent association of DPB1 alleles with RA in Japanese populations.

methodsAssociation analyses of DPB1 were conducted by logistic regression analysis in 1667 RA patients and 413 controls.

resultsIn unconditioned analysis, DPB1*04:02 was nominally associated with the susceptibility of ACPA(+)RA (P = 0.0021, corrected P (Pc) = 0.0275, odds ratio [OR] 1.52, 95% confidence interval [CI] 1.16-1.99). A significant association of DPB1*02:01 with the susceptibility of ACPA(+)RA was observed, when conditioned on DRB1 (Padjusted = 0.0003, Pcadjusted = 0.0040, ORadjusted 1.47, 95%CI 1.19-1.81). DPB1*05:01 was tended to be associated with the protection against ACPA(+)RA, when conditioned on DRB1 (Padjusted = 0.0091, Pcadjusted = 0.1184, ORadjusted 0.78, 95%CI 0.65-0.94). When conditioned on DRB1, the association of DPB1*04:02 with ACPA(+)RA was disappeared. No association of DPB1 alleles with ACPA-negative RA was detected.

conclusionThe independent association of DPB1*02:01 with Japanese ACPA(+)RA was identified.

Indexed as

AdultArthritis, RheumatoidCase-Control StudiesFemaleGenotypeHLA-DP beta-ChainsHumansJapanMaleMiddle AgedHLA-DPB1 antigenHLA-DP beta-Chains

Identifiers

PMID30235330
PMCPMC6157818
OpenAlexW2890671582

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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.