Objective To comprehensively assess evidence on the measurement properties of the minimal disease activity (MDA) criteria, a composite measure of the state of disease activity in psoriatic arthritis (PsA).
Methods A targeted literature review was conducted to identify studies that informed the validity and/or ability of the MDA to detect change among patients known to have experienced a change in clinical status. The search was conducted using MEDLINE and Embase databases (published as of October 2017). Pertinent articles provided by investigators and identified from select conference proceedings were also evaluated.
Results A total of 20 publications met the inclusion criteria. The MDA criteria were consistently associated with other indicators of disease activity/severity. The ability of the MDA criteria to detect change was supported in randomised controlled trials (n=10), with a greater percentage of patients randomised to active treatments achieving MDA relative to patients in comparator arms. Long-term observational studies (n=2) provided additional support for the ability of the MDA to detect within-subject change in the real-world settings.
Conclusion Evidence supports the MDA as a valid measure of disease activity in PsA that can detect between-group and within-subject change. The MDA is a comprehensive measure and clinically meaningful endpoint to assess the impact of interventions on PsA disease activity.
- psoriatic arthritis
- minimal disease activity
- ability to detect change
- clinical trials
- literature review
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Contributors All authors listed meet the requirements for authorship and have read and approved this final version of the modified manuscript.
Funding This targeted literature review was funded by Amgen.
Disclaimer The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, or the Department of Health.
Competing interests LCC has received research funding and/or honoraria from AbbVie, Amgen, BMS, Celgene, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Prothena, Sun Pharma, and UCB. LCC is funded by a National Institute for Health Research Clinician Scientist award. The research was supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre (BRC). VS consults for Amgen, AbbVie, AstraZeneca, BMS, Boehringer Ingelheim, Celltrion, GSK, Janssen, Kezar, Lilly, Merck, Novartis, Pfizer, Samsung, Sandoz, Sanofi, and UCB. HW was an Evidera employee during study conduct and Evidera received research funding for the project from Amgen. HW is currently an employee of Boehringer Ingelheim. DR is employed by Evidera which received research support from Amgen for this project and received research support from Pfizer. DR owns stock in AbbVie, Pfizer, and Amgen. BS, AS and JBC are employees of Amgen and are Amgen stock owners. DG received grant support and/or consulting fees from AbbVie, Amgen, BMS, Celgene, Eli Lilly, Gilead, Galapagos, Janssen, Novartis, Pfizer and UCB. PJM has received research funding, consulting or speaker honoraria from AbbVie, Amgen, BMS, Celgene, Galapagos, Genentech, Janssen, Lilly, Merck, Novartis, Pfizer, Prothena, Sun Pharma and UCB.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement All data relevant to the study are included in the article or uploaded as online supplementary information.
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