Rheumatology Digest

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 Also carries a development many will have missed: avacopan’s marketing approval is being withdrawn after ADVOCATE’s primary endpoint data were found to have been manipulated.

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.

Up to 40% of children with JIA don’t respond to methotrexate, and we currently have no way to know in advance. This three-centre study of 195 patients found that erythrocyte ITPA enzyme activity measured before the first dose separates responders from non-responders, and outperforms genotyping the ITPA variant. But the cutoffs run at 60% sensitivity and 63% specificity — enough to shift a prior, not enough to decide on its own.

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.

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.

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.