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.
Growth is the question paediatric rheumatologists ask of any JAK inhibitor, because growth hormone signals through JAK2. In 225 children with JIA followed for a median of 3.6 years on tofacitinib, height stayed close to age-appropriate norms, younger children grew faster than the WHO reference, and IGF-1, IGFBP3 and osteocalcin did not fall. It is a post hoc analysis with no untreated comparator, so it reassures rather than proves.
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.
There are no PJP prophylaxis guidelines for rheumatic disease, so practice varies widely between clinicians. This review assembles what the evidence supports: prophylaxis clearly works, the harms are real enough to matter, and the number needed to treat swings from about 4 in VEXAS to over 900 in rheumatoid arthritis — which is why the underlying disease, not the steroid dose alone, should drive the decision.
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.
Hair loss in rheumatic disease is rarely just cosmetic — it can mark active inflammation, a drug effect, or an irreversible scarring process. This review walks through the mechanisms behind alopecia in lupus, RA, sarcoidosis, scleroderma and dermatomyositis, the DMARDs that cause shedding, the scarring alopecias that mimic systemic disease, and a stepwise bedside approach for the non-dermatologist.
Secukinumab doubled sustained remission at 52 weeks in relapsed polymyalgia rheumatica — 41% versus 20% on a prednisone taper alone — and halved the need for escape steroid. But 150 mg worked as well as 300 mg, the component data show the drug maintains remission rather than inducing it, and roughly six in ten treated patients still did not reach the endpoint.
A 2026 overview of drug- and vaccine-induced ANCA-associated vasculitis — clinically near-indistinguishable from idiopathic AAV, but with a recognisable serological fingerprint (dual MPO/PR3 positivity, elastase-ANCA, high IgM MPO-ANCA, low C4, neutropenia), a milder course, and one intervention no immunosuppressant can substitute for: stopping the drug. Antithyroid drugs, hydralazine and levamisole-adulterated cocaine dominate practice.
A propensity-score analysis of the Lupus–Cruces–Bordeaux inception cohort: early (first-year) methylprednisolone pulses were associated with a ~40% reduction in long-term irreversible damage or death in active SLE, with benefit concentrated in moderate–severe disease — likely reflecting an MP-anchored low-steroid strategy rather than the molecule alone.
A 2026 practical distillation of the 2023 ACR/CHEST guidelines on SSc-ILD — the single leading cause of death in systemic sclerosis. Covers proper screening (full PFTs + non-contrast HRCT), monitoring schedules, the first-line drug evidence (mycophenolate, tocilizumab, rituximab, nintedanib), and the strong recommendation against glucocorticoids.