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.
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.
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.
Antimicrobial peptides are innate defence molecules — but in RA they become autoantigens, immune adjuvants and drivers of bone erosion. This review tracks LL-37, the defensins and the S100 proteins across five stages, from mucosal predisposition through to chronic synovitis, and makes the case that they amplify rather than initiate disease. Calprotectin already outperforms CRP and ESR for reflecting joint inflammation, yet no AMP-based agent has entered an RA trial since a phase II failure in 2019.
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.
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.