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.
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.
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.
A 60-year-old woman on checkpoint-inhibitor therapy for breast cancer develops a week of fevers, a new pancytopenia and a markedly raised CRP — and every infectious test comes back negative. Work through the case one finding at a time, with thirteen multiple-choice checkpoints covering the exposure history, the trap of the post-surgical seroma, and the timing detail that finally separates two immunotherapy complications.
Skin disease in PsA is not a side note to joint management — specific phenotypes (nail, scalp, palmoplantar, inverse) carry their own diagnostic and prognostic weight, and discordant skin/joint responses are a leading driver of complex-to-manage PsA. This review maps the phenotypes, the shared IL-23/IL-17/TNF pathogenesis, and how drug-class selection should follow the cutaneous pattern in front of you, not just the joint count.
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.
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.
Relapsing polychondritis is not one disease with variable severity. A French cohort splits it into three clusters whose mortality runs 4%, 13% and 58% — and the worst cluster is almost certainly VEXAS, which this review argues should be treated as a disease mimic rather than a subtype. Chondritis is absent at presentation in 40%, there is no confirmatory test, and no randomised trial has ever been conducted.
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.