WHY most (but perhaps not all) DMARDs work equally well

Robert B. M. Landewé, Alexandre Sepriano, Sytske Anne Bergstra

Research output: Contribution to journalArticleAcademicpeer-review

1 Citation (Scopus)

Abstract

Biological- or targeted-synthetic DMARD-responses reported in randomized clinical trials, placebo-controlled or head-to-head, in patients with rheumatoid arthritis, psoriatic arthritis or spondyloarthritis are unbelievably similar, when looking across trials performed in the same disease and applying the same primary outcome measures. The exception to this rule may be the response to Janus-kinase-inhibitors, which seem to work 10 % better in all trials (JAK-bonus) This article provides a potential explanation for this remarkable phenomenon, including an explanation for the JAK-bonus. It seems as if JAK-inhibitors exert some inflammation-independent effects on pain, fatigue and wellbeing, and that drug treatment of rheumatic diseases is more than the inhibition of inflammation alone.
Original languageEnglish
Article number152316
JournalSeminars in Arthritis and Rheumatism
Volume64
Early online date2024
DOIs
Publication statusPublished - Feb 2024

Keywords

  • Rheumatoid arthritis DMARDs JAK-inhibitors Randomized clinical trials Non-specific treatment effects

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