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.
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.
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.
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.
Population-based data from Olmsted County finally give a usable number for how often a seronegative RA diagnosis turns out to be something else: about 13% over ten years, front-loaded into the first five, and most often spondyloarthritis. A quarter achieve sustained drug-free remission lasting a median of 6.3 years, one in five needs a biologic — and nothing measured at baseline predicts which.
ACPA-positive and ACPA-negative RA take the same total time from first symptom to arthritis — but split it in mirror image. Seropositive patients reach the rheumatologist later and convert faster; seronegative patients arrive sooner and linger, leaving roughly twice as long an actionable window once they are in front of you. Each entity carries its own signature before arthritis exists.
A 2026 Personal View arguing that ‘seronegative’ usually describes the assay rather than the patient — and that separating genuinely seronegative disease (myeloid/CD8-driven, MHC class I-associated, rituximab-unresponsive) from merely undetected seropositivity is the field’s necessary next step. Includes a disease-by-disease audit of seronegativity rates and why classification criteria naming the antibody but not the method matters.