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.
Sex differences in rheumatic disease are usually pinned on oestrogen, but this review argues the picture is far more tangled. Oestradiol drives disease in SLE while appearing protective in Sjögren’s and RA; X chromosome dosage raises risk independently of hormones — triple X carries a 2.9-fold higher Sjögren’s prevalence; and gut bacteria reactivate oestrogen through β-glucuronidase, closing a loop between all three mechanisms.
In a UCL cohort of prolonged SACQ lupus patients — elevated anti-dsDNA and/or low C3 for 6+ months with no clinical activity — 63% flared over a mean 3.3 years. Rising IgG anti-dsDNA and falling C3 at one visit independently predicted flare and sustained activity at the next, including moderate-to-severe disease, in a visit-by-visit longitudinal model. The risk from low C3 rose sharply below 0.9 g/L and flattened above it.
A 2026 review of cutaneous lupus therapeutics, now organised almost entirely around the type I interferon axis — from TLR7/8 and pDCs through IFNAR to TYK2 — alongside the practical foundation of photoprotection, early hydroxychloroquine and smoking cessation. No therapy is yet FDA-approved specifically for CLE, and almost all evidence is borrowed from SLE trials where skin was a secondary endpoint.
ALLEGORY is a phase 3 RCT of the type II anti-CD20 antibody obinutuzumab added to standard therapy in active non-renal SLE. It met its primary endpoint (SRI-4 76.7% vs 53.5% at week 52) and all five key secondary endpoints, achieving both steroid-sparing and a ~40% reduction in flare hazard — reinforcing that depth of B-cell depletion matters and that type II succeeds where rituximab failed.
WILLOW Cohort A is the first placebo-controlled RCT of a TLR7/8 inhibitor in lupus: the oral agent enpatoran met its primary endpoint with a dose-dependent reduction in cutaneous disease activity (CLASI-A) at 16 weeks, and — the headline — rapidly and reversibly switched off the skin type I interferon signature, pinning TLR7/8 as an upstream driver of cutaneous IFN activation. Steroid-sparing was not demonstrated.
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.