Evidence map›Paper›PMID 38457949›Full record

ArticleSeminars in arthritis and rheumatism2024

Reasons for multiple biologic and targeted synthetic DMARD switching and characteristics of treatment refractory rheumatoid arthritis.

Gregory C McDermott, Michael DiIorio, Yumeko Kawano, Mary Jeffway, Megan MacVicar, Kumar Dahal, Su-Jin Moon, Thany Seyok, Jonathan Coblyn, Elena Massarotti and 3 more

Abstract read
In one paragraph

Article in Seminars in arthritis and rheumatism, 2024. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Observational
  4. Article
  5. Observational
  6. Review
  7. Article
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

13 authors.

Gregory C McDermottDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA. Electronic address: gmcdermott@bwh.harvard.edu.
Michael DiIorioDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Yumeko KawanoDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Mary JeffwayDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA.
Megan MacVicarDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA.
Kumar DahalDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA.
Su-Jin MoonDivision of Rheumatology, Department of Internal Medicine, Yeouido St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Thany SeyokDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA.
Jonathan CoblynDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Elena MassarottiDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Michael E WeinblattDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Dana WeisenfeldDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA.
Katherine P LiaoDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.

Funding

MECHANISMS OF ARTHRITIC &DERMATOLOGY DISORDERST32AR007530 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Michael B. Brenner, Ellen M Gravallese · 1986 to 2026
$10.4M
Training in Orthopaedic and Musculoskeletal Clinical ResearchT32AR055885 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI KATZ, JEFFREY NEIL, LOSINA, ELENA · 2008 to 2023
$4.0M
Mechanisms of Intrinsic Resistance to HIV Infection in Primary Human T CellsR21AI078839 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI UNUTMAZ, DERYA · 2008 to 2009
$466k
Studying exceptional treatment non-responders and genetics to predict treatment response in rheumatoid arthritisR21AR078339 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI CAI, TIANXI, LIAO, KATHERINE PHOENIX · 2021 to 2022
$444k
NIAID NIH HHS R21 AI078839NIAMS NIH HHS R21 AR078339NIAMS NIH HHS T32 AR007530NIAMS NIH HHS T32 AR055885
6 · The paper itself

Abstract

objectiveSwitching biologic and targeted synthetic DMARD (b/tsDMARD) medications occurs commonly in RA patients, however data are limited on the reasons for these changes. The objective of the study was to identify and categorize reasons for b/tsDMARD switching and investigate characteristics associated with treatment refractory RA.

methodsIn a multi-hospital RA electronic health record (EHR) cohort, we identified RA patients prescribed ≥1 b/tsDMARD between 2001 and 2017. Consistent with the EULAR "difficult to treat" (D2T) RA definition, we further identified patients who discontinued ≥2 b/tsDMARDs with different mechanisms of action. We performed manual chart review to determine reasons for medication discontinuation. We defined "treatment refractory" RA as not achieving low disease activity (<3 tender or swollen joints on <7.5 mg of daily prednisone equivalent) despite treatment with two different b/tsDMARD mechanisms of action. We compared demographic, lifestyle, and clinical factors between treatment refractory RA and b/tsDMARD initiators not meeting D2T criteria.

resultsWe identified 6040 RA patients prescribed ≥1 b/tsDMARD including 404 meeting D2T criteria. The most common reasons for medication discontinuation were inadequate response (43.3 %), loss of efficacy (25.8 %), and non-allergic adverse events (13.7 %). Of patients with D2T RA, 15 % had treatment refractory RA. Treatment refractory RA patients were younger at b/tsDMARD initiation (mean 47.2 vs. 55.2 years, p < 0.001), more commonly female (91.8% vs. 76.1 %, p = 0.006), and ever smokers (68.9% vs. 49.9 %, p = 0.005). No RA clinical factors differentiated treatment refractory RA patients from b/tsDMARD initiators.

conclusionsIn a large EHR-based RA cohort, the most common reasons for b/tsDMARD switching were inadequate response, loss of efficacy, and nonallergic adverse events (e.g. infections, leukopenia, psoriasis). Clinical RA factors were insufficient for differentiating b/tsDMARD responders from nonresponders.

Indexed as

Antirheumatic AgentsArthritis, RheumatoidBiological ProductsDrug SubstitutionAdultAgedFemaleHumansMaleMiddle AgedAntirheumatic AgentsBiological ProductsBiological therapyDisease modifying antirheumatic drugsRheumatoid arthritis

Identifiers

PMID38457949
PMCPMC11088978

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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.