Evidence map›Paper›PMID 31179526›Full record

Observational studyClinical rheumatology2019

Association between seropositivity and discontinuation of tumor necrosis factor inhibitors due to ineffectiveness in rheumatoid arthritis.

Yoshikazu Ogawa, Nobunori Takahashi, Atsushi Kaneko, Yuji Hirano, Yasuhide Kanayama, Yuichiro Yabe, Takeshi Oguchi, Takayoshi Fujibayashi, Hideki Takagi, Masahiro Hanabayashi and 9 more

Abstract readMulticenter StudyObservational Study
PubMed Publisher
In one paragraph

Observational study in Clinical rheumatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 19 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 12 institutions in 1 country.

Yoshikazu OgawaDepartment of Orthopaedic Surgery, Nakatsugawa Municipal General Hospital, 1522-1 Komaba, Nakatsugawa, 508-8502, Japan. yoshoga@yahoo.co.jp.
Nobunori TakahashiDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, 466-8550, Japan.
Atsushi KanekoDepartment of Orthopedic Surgery and Rheumatology, Nagoya Medical Center, Nagoya, Japan.
Yuji HiranoDepartment of Rheumatology, Toyohashi Municipal Hospital, Toyohashi, Japan.
Yasuhide KanayamaDepartment of Orthopedic Surgery, Toyota Kosei Hospital, Toyota, Japan.
Yuichiro YabeDepartment of Rheumatology, Tokyo Shinjuku Medical Center, Tokyo, Japan.
Takeshi OguchiDepartment of Orthopedic Surgery, Anjo Kosei Hospital, Anjo, Japan.
Takayoshi FujibayashiDepartment of Orthopedic Surgery, Konan Kosei Hospital, Konan, Japan.
Hideki TakagiDepartment of Orthopedic Surgery, Nagoya Central Hospital, Nagoya, Japan.
Masahiro HanabayashiDepartment of Orthopedic Surgery, Ichinomiya Municipal Hospital, Ichinomiya, Japan.
Koji FunahashiDepartment of Orthopedic Surgery, Kariya-Toyota General Hospital, Kariya, Japan.
Masatoshi HayashiDepartment of Rheumatology, Nagano Red Cross Hospital, Nagano, Japan.
Seiji TsuboiDepartment of Orthopedic Surgery, Shizuoka Kosei Hospital, Shizuoka, Japan.
Shuji AsaiDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, 466-8550, Japan.
Nobuyuki AsaiDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, 466-8550, Japan.
Takuya MatsumotoDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, 466-8550, Japan.
Yasumori SobueDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, 466-8550, Japan.
Naoki IshiguroDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, 466-8550, Japan.
Toshihisa KojimaDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, 466-8550, Japan.
Nagoya University · JPAnjo Kosei Hospital · JPIchinomiya Municipal City Hospital · JPKariya Toyota General Hospital · JPKashiwa Municipal Hospital · JPKensei Hospital · JPKonan Kosei Hospital · JPNagano Red Cross Hospital · JPNagoya Central Hospital · JPNagoya Medical Center · JPToyohashi Municipal Hospital · JPToyota Kosei Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

INTRODUCTION/

objectivesDiscontinuation of biologic therapy in rheumatoid arthritis is attributable to various reasons, with the most important cause being insufficient response. In this study, we investigated the association between rheumatoid factor (RF) and anti-citrullinated protein autoantibody (ACPA) status and the discontinuation of tumor necrosis factor inhibitors (TNFi) therapy due to insufficient response in bio-naïve rheumatoid arthritis (RA) patients.

methodThis study included patients enrolled in the Tsurumai Biologic Communication Registry in Japan. The crude comparison of TNFi discontinuation due to ineffectiveness between seropositive and seronegative patients was analyzed using the cumulative incidence function of competing events and Gray test. We assessed the associations between baseline patient characteristics and discontinuation of TNFi therapy due to insufficient response using Fine-Gray proportional hazard regression. Fine-Gray proportional hazard analysis considered competing events of interest, including insufficient response, adverse event, palliation, and personal reasons.

resultsOf 1237 patients evaluated, 79.3% were positive for RF and 85.4% for ACPA; 72.6% were double positive and 11.1% were double negative. TNFi therapy had been discontinued because of insufficient response at 200 weeks in 19.8% RF-positive, 16.7% RF-negative, 23.0% ACPA-positive, and 13.8% ACPA-negative patients. There was a significantly higher discontinuation rate due to insufficient response in ACPA-positive patients than in ACPA-negative patients using Gray test, with a similar trend as that for RF status. RF positivity was significantly predictive of the discontinuation of TNFi therapy due to ineffectiveness using Fine-Gray proportional hazard regression analysis after adjusting for baseline characteristics, including age, sex, stage, class, disease activity at baseline, methotrexate use, and prednisolone use [hazard ratio 1.73 (95% confidence interval 1.07-2.80)].

conclusionsUsing Fine-Gray proportional hazard regression, we demonstrated that RF positivity was related to a higher discontinuation rate of TNFi therapy due to ineffectiveness in bio-naïve RA patients. Key Points • RF positivity is related to a higher discontinuation rate of TNFi therapy due to ineffectiveness. • ACPA is not predictive of a discontinuation of TNFi therapy due to ineffectiveness.

Indexed as

AdultAgedAnti-Citrullinated Protein AntibodiesAntirheumatic AgentsArthritis, RheumatoidBiological TherapyFemaleHumansIncidenceJapanMaleMethotrexateMiddle AgedPrednisolonePrognosisProportional Hazards ModelsAnti-Citrullinated Protein AntibodiesAntirheumatic AgentsMethotrexatePrednisoloneRheumatoid FactorTumor Necrosis Factor InhibitorsBiological therapyRheumatoid factorSurvival analysisTumor necrosis factor

Identifiers

PMID31179526
OpenAlexW2949759864

What OpenQuestion holds

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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.