Evidence map›Paper›PMID 28569178›Full record

ArticleArthritis research & therapy2017

Prediction of response to remission induction therapy by gene expression profiling of peripheral blood in Japanese patients with microscopic polyangiitis.

Akihiro Ishizu, Utano Tomaru, Sakiko Masuda, Ken-Ei Sada, Koichi Amano, Masayoshi Harigai, Yasushi Kawaguchi, Yoshihiro Arimura, Kunihiro Yamagata, Shoichi Ozaki and 9 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 17 citations in OpenAlex.

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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

19 authors at 13 institutions in 1 country.

Akihiro IshizuFaculty of Health Sciences, Hokkaido University, Kita-12, Nishi-5, Kita-ku, Sapporo, 060-0812, Japan. aishizu@med.hokudai.ac.jp.
Utano TomaruDepartment of Pathology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Sakiko MasudaFaculty of Health Sciences, Hokkaido University, Kita-12, Nishi-5, Kita-ku, Sapporo, 060-0812, Japan.
Ken-Ei SadaDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Koichi AmanoDepartment of Rheumatology and Clinical Immunology, Saitama Medical Center, Saitama Medical University, Saitama, Japan.
Masayoshi HarigaiDepartment of Pharmacovigilance, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Yasushi KawaguchiInstitute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan.
Yoshihiro ArimuraNephrology and Rheumatology, First Department of Internal Medicine, Kyorin University School of Medicine, Tokyo, Japan.
Kunihiro YamagataDepartment of Nephrology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Shoichi OzakiDivision of Rheumatology and Allergology, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Hiroaki DobashiDivision of Hematology, Rheumatology and Respiratory Medicine, Department of Internal Medicine, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Sakae HommaDepartment of Respiratory Medicine, Toho University Omori Medical Center, Tokyo, Japan.
Yasunori OkadaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Hitoshi SugiyamaDepartment of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Joichi UsuiDepartment of Nephrology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Naotake TsuboiDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Seiichi MatsuoDepartment of Nephrology, Internal Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hirofumi MakinoOkayama University Hospital, Okayama, Japan.
Research Committee of the Intractable Vasculitis Syndrome and the Research Committee of the Intractable Renal Disease of the Ministry of Health, Labour, and Welfare of Japan
Hokkaido University · JPNagoya University · JPOkayama University · JPUniversity of Tsukuba · JPKagawa University · JPKeio University · JPKyorin University · JPOkayama University Hospital · JPSaitama Medical University · JPSt. Marianna University School of Medicine · JPToho University Omori Medical Center · JPTokyo Medical and Dental University · JPTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroscopic polyangiitis (MPA), which is classified as an anti-neutrophil cytoplasmic antibody (ANCA)-associated small vessel vasculitis, is one of the most frequent primary vasculitides in Japan. We earlier nominated 16 genes (IRF7, IFIT1, IFIT5, OASL, CLC, GBP-1, PSMB9, HERC5, CCR1, CD36, MS4A4A, BIRC4BP, PLSCR1, DEFA1/DEFA3, DEFA4, and COL9A2) as predictors of response to remission induction therapy against MPA. The aim of this study is to determine the accuracy of prediction using these 16 predictors.

methodsThirty-nine MPA patients were selected randomly and retrospectively from the Japanese nationwide RemIT-JAV-RPGN cohort and enrolled in this study. Remission induction therapy was conducted according to the Guidelines of Treatment for ANCA-Associated Vasculitis published by the Ministry of Health, Labour, and Welfare of Japan. Response to remission induction therapy was predicted by profiling the altered expressions of the 16 predictors between the period before and 1 week after the beginning of treatment. Remission is defined as the absence of clinical manifestations of active vasculitis (Birmingham Vasculitis Activity Score 2003: 0 or 1 point). Persistent remission for 18 months is regarded as a "good response," whereas no remission or relapse after remission is regarded as a "poor response."

results"Poor" and "good" responses were predicted in 7 and 32 patients, respectively. Five out of 7 patients with "poor" prediction and 1 out of 32 patients with "good" prediction experienced relapse after remission. One out of 7 patients with "poor" prediction was not conducted to remission. Accordingly, the sensitivity and specificity to predict poor response was 85.7% (6/7) and 96.9% (31/32), respectively.

conclusionsResponse to remission induction therapy can be predicted by monitoring the altered expressions of the 16 predictors in the peripheral blood at an early point of treatment in MPA patients.

Indexed as

TranscriptomeAdultAgedAsian PeopleCohort StudiesFemaleGene Expression ProfilingHumansImmunosuppressive AgentsMaleMicroscopic PolyangiitisMiddle AgedRemission InductionRetrospective StudiesTreatment OutcomeImmunosuppressive AgentsGene profilingMicroscopic polyangiitisPeripheral bloodPrediction of response to treatment

Identifiers

PMID28569178
PMCPMC5452368
OpenAlexW2618415579

What OpenQuestion holds

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LicenceCC BY
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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.