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.
IgA vasculitis and IgA nephropathy share HLA susceptibility, 21 GWAS risk loci, elevated Gd-IgA1 and renal biopsies that cannot be told apart — yet IgAN now has five approved therapies and IgAV has none, because IgAV patients were excluded from every trial that delivered them. What changes today: KDIGO 2025 lowers the treatment threshold to 0.5 g/day of proteinuria, and it explicitly covers IgA vasculitis.
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.
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.
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.
A 2026 overview of drug- and vaccine-induced ANCA-associated vasculitis — clinically near-indistinguishable from idiopathic AAV, but with a recognisable serological fingerprint (dual MPO/PR3 positivity, elastase-ANCA, high IgM MPO-ANCA, low C4, neutropenia), a milder course, and one intervention no immunosuppressant can substitute for: stopping the drug. Antithyroid drugs, hydralazine and levamisole-adulterated cocaine dominate practice.
A 2026 NEJM Clinical Practice review reframing fibromyalgia as nociplastic pain — CNS sensitisation to painful and non-painful stimuli — so therapy aims to calm the CNS rather than repair peripheral tissue. Covers the positive (non-exclusion) diagnosis, the chronic overlapping pain conditions, and management where non-pharmacologic treatment outperforms drugs, amitriptyline at night leads the drugs, and opioids are harmful.
A 2026 narrative review of T-cell engagers (TCEs) in autoimmune rheumatic disease — off-the-shelf bispecific antibodies that redirect a patient’s own T cells against autoreactive B/plasma cells, pitched as a repeatable, dose-adjustable alternative to CAR-T. Early efficacy across SLE, SSc, RA, myositis and Sjögren’s is real but preliminary, and the review’s headline problem is under-dosing relative to oncology, which likely drives frequent relapse.
A 2026 narrative review arguing that B cells are the single through-line of Sjögren disease — connecting autoantibodies, glandular pathology, the highest lymphoma risk of any autoimmune disease, and the emerging drug pipeline. Endotyping by B-cell activity may identify who develops lymphoma and who responds to B-cell-targeted therapy, as newer BAFF/APRIL, CD40L, BTK and FcRn agents succeed where rituximab failed.
A 2026 review of steroid-sparing therapy across the GCA–PMR spectrum: glucocorticoids still induce remission but drive substantial cumulative toxicity, so the field has pivoted to IL-6 receptor inhibition (tocilizumab in GCA, sarilumab in PMR) and JAK inhibition (upadacitinib now approved for GCA) — none of which reliably restores treatment-free remission, against a backdrop of weak monitoring tools and GCA-specific vascular-damage risk.