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Background: Low-dose glucocorticoid (GC) therapy is widely used in rheumatoid arthritis (RA) but the balance of benefit and harm is still unclear.
Methods: The GLORIA (Glucocorticoid LOw-dose in RheumatoId Arthritis) pragmatic double-blind randomised trial compared 2 years of prednisolone, 5 mg/day, to placebo in patients aged 65+ with active RA. We allowed all cotreatments except long-term open label GC and minimised exclusion criteria, tailored to seniors. Benefit outcomes included disease activity (disease activity score; DAS28, coprimary) and joint damage (Sharp/van der Heijde, secondary). The other coprimary outcome was harm, expressed as the proportion of patients with ≥1 adverse event (AE) of special interest. Such events comprised serious events, GC-specific events and those causing study discontinuation. Longitudinal models analysed the data, with one-sided testing and 95% confidence limits (95% CL).
Results: We randomised 451 patients with established RA and mean 2.1 comorbidities, age 72, disease duration 11 years and DAS28 4.5. 79% were on disease-modifying treatment, including 14% on biologics. 63% prednisolone versus 61% placebo patients completed the trial. Discontinuations were for AE (both, 14%), active disease (3 vs 4%) and for other (including covid pandemic-related disease) reasons (19 vs 21%); mean time in study was 19 months. Disease activity was 0.37 points lower on prednisolone (95% CL 0.23, p<0.0001); joint damage progression was 1.7 points lower (95% CL 0.7, p=0.003). 60% versus 49% of patients experienced the harm outcome, adjusted relative risk 1.24 (95% CL 1.04, p=0.02), with the largest contrast in (mostly non-severe) infections. Other GC-specific events were rare.
Conclusion: Add-on low-dose prednisolone has beneficial long-term effects in senior patients with established RA, with a trade-off of 24% increase in patients with mostly non-severe AE; this suggests a favourable balance of benefit and harm.
Trial Registration Number: NCT02585258.
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Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9209692 | PMC |
http://dx.doi.org/10.1136/annrheumdis-2021-221957 | DOI Listing |
Rheumatology (Oxford)
December 2024
Centre for Rheumatic Diseases, Department of Inflammation Biology, King's College London, London, UK.
Objectives: To update the first-line conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) prescribing pattern, describe change and variation across demographical and geographical factors in the Rheumatoid arthritis (RA) population, and identify individual and hospital factors associated with it.
Methods: This retrospective cohort study included newly diagnosed RA adult patients from 1 May 2018-1 April 2023 in the UK. We used adjusted multinomial logistic regression with random effect to explore associations with different first-line csDMRAD prescription and to account for hospital-level clustering.
Rheumatology (Oxford)
December 2024
Rheumatology, Columbia University Irving Medical Center, New York, NY, U.S.
Lancet Rheumatol
December 2024
Department of Rheumatology, Erasmus Medical Center, Rotterdam, Netherlands; Department of Rheumatology, Leiden University Medical Center, Leiden, Netherlands.
Background: About 20% of patients with rheumatoid arthritis on disease-modifying antirheumatic drugs (DMARDs) can reach sustained DMARD-free remission. Nonetheless, the 2022 EULAR recommendations discourage complete cessation of DMARDs due to flare risk. The evidence behind this recommendation is obtained from trial populations using biological DMARDs, representing only a subgroup of the total population of patients with rheumatoid arthritis.
View Article and Find Full Text PDFLancet Rheumatol
December 2024
Department of Internal Medicine III, Division of Rheumatology, Medical University of Vienna, 1090 Vienna, Austria; Division of Rheumatology, Department of Medicine-Solna, Karolinska Institute, Stockholm, Sweden. Electronic address:
Int Immunopharmacol
December 2024
Department of Medicine, Division of Rheumatology, Queen's University, Kingston, Ontario, Canada; Faculty of Health Sciences, School of Medicine, Queen's University, Kingston, Ontario, Canada; Translational Institute of Medicine, Department of Medicine, Queen's University, Ontario, Canada; Rheumatology Clinic, Kingston Health Science Centre, Kingston, Ontario, Canada. Electronic address:
Introduction: Joint tissues affected by inflammatory arthritis (IA) create hypoxic microenvironments that sustain the inflammatory response. Although targeting molecules in hypoxia-induced pathways has provided valuable insights into potential novel therapies for various types of IA, progress remains preclinical, and no clinical trials have been conducted for IA.
Methods: A literature search was conducted to create a narrative review exploring the role of hypoxia and its signaling pathways in IA pathogenesis, as well as the potential and future directions for IA therapies that target hypoxia-induced molecules before moving forward to clinical applications.
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