In the 194-patient phase 3 INDIGO trial, weekly subcutaneous obexelimab, a bifunctional antibody that dampens B cells through CD19 and FcγRIIb without depleting them, cut the risk of IgG4-related disease flare by more than half (HR 0.44) and reduced rescue glucocorticoid exposure by about two-thirds over 52 weeks. The comparator was a steroid taper alone, and fewer than 4 in 10 patients on obexelimab reached complete remission.
In 670 biologic-naïve patients with active psoriatic arthritis, the oral TYK2 inhibitor deucravacitinib achieved ACR20 in 54.2% versus 34.1% on placebo at week 16, with gains in skin, function and quality of life sustained to week 52. But the pre-specified radiographic endpoint was negative, the testing hierarchy broke at enthesitis, and the claim of structural protection rests on a post hoc reanalysis.
Anti-MDA5 antibody testing takes two to eight weeks and fails to detect 17% of cases — so in rapidly progressive ILD, the skin exam is the faster test. This review covers the pathognomonic and characteristic DM rashes, the specific findings that flag anti-MDA5, TIF1γ and NXP2, why DM-specific rashes appear in antisynthetase and overlap myositis, presentations in skin of colour, and the treatments for refractory cutaneous disease.
Glucocorticoids remain the leading cause of secondary osteoporosis, and oral steroid use in rheumatic disease has risen over the last twenty years despite steroid-sparing agents. This review covers how quickly bone is lost, why DXA systematically underestimates fracture risk on steroids, how much the underlying rheumatic disease contributes, the steroid-sparing evidence in SLE, GCA, PMR and ANCA vasculitis, and what the trial data actually support.
Fatigue affects 35–82% of patients with musculoskeletal disease and roughly one in two reports it as severe — yet it correlates poorly with CRP, DAS28 and even MRI-detected synovitis. This review covers what fatigue is, how to measure it, the biology proposed to explain it, why remission so often fails to resolve it, and what actually works: biologics, exercise, CBT and the EULAR non-pharmacological recommendations.
A full map of EGPA therapy — why reduced-dose steroid regimens validated in GPA and MPA may not transfer, what REOVAS and MAINRITSEG actually showed about rituximab (no superiority in either), and how anti-IL-5 therapy has made complete glucocorticoid withdrawal a realistic trial endpoint. Also carries a development many will have missed: avacopan’s marketing approval is being withdrawn after ADVOCATE’s primary endpoint data were found to have been manipulated.
Fifteen patients with multidrug-resistant RA received blinatumomab at roughly a tenth of the haematology dose. All 15 achieved at least ACR20 and synovial B cells were depleted, but 14 of 15 flared within a median five months. The more provocative observation is what happened next: seven patients responded for over three months to b/tsDMARDs that had already failed them — raising the possibility that partial depletion resensitises rather than resets.
Up to 40% of children with JIA don’t respond to methotrexate, and we currently have no way to know in advance. This three-centre study of 195 patients found that erythrocyte ITPA enzyme activity measured before the first dose separates responders from non-responders, and outperforms genotyping the ITPA variant. But the cutoffs run at 60% sensitivity and 63% specificity — enough to shift a prior, not enough to decide on its own.
An individual patient data meta-analysis of 16 phase 3 trials and 11,883 patients shows JAK inhibitor response falls in a graded way as BMI rises — roughly 18 fewer ACR20 responders per 100 treated at class 3 obesity. Crucially, no such gradient appears in the placebo arms, and within-trial interaction analyses confirm obesity modifies the treatment effect rather than simply marking worse disease.
RA-ILD gets the attention, but COPD, bronchiectasis and bronchiolitis are common, under-recognised and carry their own mortality — and screening guidance now exists for only one of them. This review maps all eight pulmonary manifestations, the mucosal-origins case for the lung as where RA autoimmunity begins, and why 25 years of RA trials have produced almost no evidence for treating the lung.