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Objectives: To compare two strategies-a hydrocortisone replacement strategy and a prednisone tapering strategy-for their success in glucocorticoid discontinuation in patients with rheumatoid arthritis (RA) with low disease activity (LDA)., Methods: The Strategies for glucocorticoid TApering in Rheumatoid arthritis (STAR) study was a double-blind, double-placebo randomised controlled trial including patients with RA receiving a stable dose of glucocorticoid 5 mg/day for ≥3 months and were in LDA for ≥3 months. Patients were randomly assigned in a 1:1 ratio to either replace prednisone with 20 mg/day of hydrocortisone for 3 months, then reduce to 10 mg/day for 3 months before discontinuation or to taper prednisone by 1 mg/day every month until complete discontinuation, contingent on maintaining LDA. The primary outcome was the percentage of patients achieving glucocorticoid discontinuation at 12 months. Other secondary outcomes were proportion of flares, need for additional glucocorticoid use, disease activity, patient-reported outcomes and the results of adrenocorticotropic hormone (ACTH) stimulation tests., Results: Of the 102 patients randomised in the trial (mean age 62.4 years, 70.6% females), 53 had hydrocortisone replacement and 49 tapered prednisone. At 12 months, 29 patients (55%) in the hydrocortisone replacement group and 23 patients (47%) in the prednisone tapering group achieved glucocorticoid discontinuation (p=0.4). No difference was observed between groups in the secondary outcomes. No cases of acute adrenal insufficiency were observed; however, 17 patients still had an abnormal ACTH stimulation test at 12 months, with no differences between arms., Conclusion: A hydrocortisone replacement strategy was not superior to a prednisone tapering strategy for achieving glucocorticoid discontinuation success in patients with RA in LDA., Trial Registration Number: NCT02997605., Competing Interests: Competing interests: AR-W, CB, MM, VB, MN, ChR, AS, PV-S, RMF, MP, J-EG, MS, PD, SL, LZ, GC, JFB, BJ, YD and AC declare no competing interests. HM declared to have received grants from Celltrion, Healthcare, Lilly, Nordic Pharma, Medac, consulting fees from AbbVie, Accord, CellTrion HealthCare, Johnson & Johnson, UCB, honoraria for presentation from AbbVie, Bristol Myers Squibb, CellTrion HealthCare, Fresenius Kabi, Galapagos, Medac, Nordic Pharma, Novartis, Sanofi, UCB, support for attending meeting from CellTrion HealthCare, Fresenius Kabi, UCB, participated in advisory board for Lilly, Pfizer. CS received grant from Novartis, Roche-Chugai, honoraria for presentations from Novartis, Galapagos, Pfizer, Lilly and support for attending meetings from Lilly, Novartis, Galapagos. JM received grants from Bristol Myers Squib, Fresenius Kabi Novartis, Roche Chugai, Pfizer and Lilly, received honoraria for presentation from AbbVie, Boehringer Ingelheim, Biogen, Lilly, Viatris, Pfizer, Sanofi, from Bristol Myers Squib, Fresenius Kabi, Galapagos, Medac, Novartis, Roche Chugai, support for attending meetings from Bristol Myers Squib, Fresenius Kabi, Lilly, participated in advisory boards for AbbVie, Pfizer, Theramex, Galapagos, Fresenius Kabi and Sanofi. CR received grants from Biogen, Lilly, Nordic Pharma, consulting fees from Novartis, Lilly, AstraZeneca, AbbVie, Pfizer and GSK, received honoraria for presentations from AbbVie, Boehringer Ingelheim, Novartis, Lilly, Galapagos, Pfizer, UCB, support for attending meeting from UCB, Novartis and AstraZeneca. LG received grants from AbbVie, Biogen, Lilly, Novartis, UCB, consulting fees from AbbVie, Amgen, BMS, Celltrion, Janssen, Novartis, Pfizer, UCB, honoraria for presentations from AbbVie, Amgen, BMS, Celltrion, Janssen, Lilly, MSD, Novartis, Pfizer, Sandoz, UCB, support for attending meeting from MSD, Novartis, Pfizer, participated in advisory boards for Janssen, Pfizer, UCB., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ on behalf of EULAR.)

Objective: To determine if a lumbar musculature deficiency (paravertebral - PVM - and psoas - PM - muscles) is associated with a higher prevalence of vertebral fractures in osteoporotic patients., Methods: To constitute the fracture group, data were collected retrospectively from patients with one or more recent osteoporotic vertebral fractures between T10 and L5 such as non-injected computerized tomography (CT), dual-energy X-ray absorptiometry (DXA). A control group was made by matching the patients on age, bone mineral density measured by DXA and gender. We analyzed PM and PVM atrophy based on cross-sectional area (CSA) adjusted to the body area as well as fatty infiltration on a 3-level scale and the average muscle density in Hounsfield units (HU)., Results: One hundred seventeen patients were included in each group. The fracture group had a lower PVM CSA than the control group (2197.92 ± 460.19 versus 2335.20 ± 394.42 mm 2 .m -2 , respectively p = 0.015), but there was no significant difference in the PM (746.92 ± 197.89 versus 731.74 ± 215.53 mm 2 .m -2 , respectively p = 0.575). The fracture group had a higher grade of fatty infiltration than the control group (PM: 1.3 ± 0.46 versus 1.07 ± 0.25, p < 0.001; PVM: 1.93 ± 0.5 versus 1.74 ± 0.5, p = 0.003) and a lower average muscle density (PM: 26.99 ± 12.83 versus 33.91 ± 8.12 HU, p < 0.001; PVM: 3.42 ± 21.06 versus 12.94 ± 18.88 HU, p < 0.001)., Conclusion: This study shows an association between a lack of axial musculature and the occurrence of osteoporotic vertebral fractures. Preventive strengthening exercises could be proposed to osteoporotic patients., Competing Interests: None., (© 2024 The Authors.)

T cells are known to be involved in the pathogenesis of rheumatoid arthritis (RA). Accordingly, and to better understand T cells' contribution to RA, a comprehensive review based on an analysis of the Immune Epitope Database (IEDB) was conducted. An immune CD8+ T cell senescence response is reported in RA and inflammatory diseases, which is driven by active viral antigens from latent viruses and cryptic self-apoptotic peptides. RA-associated pro-inflammatory CD4+ T cells are selected by MHC class II and immunodominant peptides, which are derived from molecular chaperones, host extra-cellular and cellular peptides that could be post-translationally modified (PTM), and bacterial cross-reactive peptides. A large panel of techniques have been used to characterize (auto)reactive T cells and RA-associated peptides with regards to their interaction with the MHC and TCR, capacity to enter the docking site of the shared epitope (DRB1-SE), capacity to induce T cell proliferation, capacity to select T cell subsets (Th1/Th17, Treg), and clinical contribution. Among docking DRB1-SE peptides, those with PTM expand autoreactive and high-affinity CD4+ memory T cells in RA patients with an active disease. Considering original therapeutic options in RA, mutated, or altered peptide ligands (APL) have been developed and are tested in clinical trials.