Glucocorticoids (GCs) are the gold standard for treatment of giant cell arteritis (GCA); however, there is a need for studies on GC-sparing agents, given that up to 85% of patients receiving GC only develop adverse events. Previous randomised controlled trials (RCTs) have applied different primary endpoints, limiting the comparison of treatment effects in meta-analyses and creating an undesired heterogeneity of outcomes. The harmonisation of response assessment is therefore an important unmet need in GCA research. In this viewpoint article, we discuss the challenges and opportunities with the development of new, internationally accepted response criteria. A change of disease activity is a fundamental component of response; however, it is debatable whether the ability to taper GC and/or the maintenance of a disease state for a specific time period, as applied in recent RCTs, should be part of response assessment. The role of imaging and novel laboratory biomarkers as possible objective markers of disease activity needs further investigation but might be a possibility when drugs directly or indirectly influence the levels of traditional acute-phase reactants such as erythrocyte sedimentation rate and C reactive protein. Futures response criteria might be constructed as a multidomain set, but the questions about which domains will be included and what their relative weights will be still need to be answered.
- Giant Cell Arteritis
- Outcome Assessment, Health Care
- Patient Reported Outcome Measures
- Biological Therapy
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Handling editor Josef S Smolen
Contributors CD wrote the first version of the manuscript. All authors reviewed the manuscript, made extensive comments and appropriate changes to it, and approved the final version of the manuscript.
Funding This work was supported by a grant from the ACR and EULAR (grant number QoC 004).
Competing interests CD received grant support by AbbVie and consulting/speaker’s fees from Abbvie, Eli Lilly, Janssen, Galapagos, Novartis, Pfizer, Sparrow, Roche and Sanofi, all unrelated to this manuscript. SR received research grants from AbbVie, Galapagos, MSD, Novartis, Pfizer and UCB and consultancy fees from AbbVie, Eli Lilly, MSD, Novartis, Pfizer, Sanofi and USB. ZT, MB, MS, CS-A: none. CL received grant support from Bristol-Myers Squibb, GlaxoSmithKline, ChemoCentryx, AstraZeneca and National Institutes of Health and served as a non-paid consultant to Bristol-Myers Squibb, AbbVie and AstraZeneca.
Patient and public involvement Patients and/or the public were involved in the design, conduct, reporting or dissemination plans of this research.
Provenance and peer review Not commissioned; externally peer reviewed.