Rheumatology Digest

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.

Trillions of microorganisms live on your skin, in your mouth and in your gut, and almost none of them cause harm. Episode 1 of the immunology series asks what makes the rare one dangerous: the four kinds of pathogen, why damage rather than species or number defines the line between commensal and pathogen, the three host strategies, and the four layers of defence and how fast each one acts.

Up to 30% of people with psoriasis develop psoriatic arthritis, and nobody can yet say which ones. This review argues the plaque is not just an inflamed patch of skin but a source of immune cells that reach the joint: T cell clones and myeloid precursors shared between skin and synovium. But arrival alone does not cause arthritis. What decides it is the stromal niche, in particular synovial fibroblasts, which act as gatekeepers.

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.

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.

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.

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.

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.