Rheumatology news.

A longitudinal study of 13 patients with VEXAS syndrome, combined with human monocytic cell-line experiments, identified genotype-dependent inflammatory programs. RNASE1 expression correlated with disease activity, while RIPK3 inhibition attenuated pathological features in cell models.

An observational proteomics study used two independent 88-participant cohorts to identify and validate a plasma protein signature associated with high structural damage in ankylosing spondylitis. The five-protein model achieved a validation AUC of 0.917, although its ability to predict future damage was not established.

An observational study of 40 patients with VEXAS syndrome found endothelial activation, altered von Willebrand factor profiles, and increased thrombin generation compared with age-matched controls. Twenty-one patients (52.5%) had experienced thrombosis; whether targeting these pathways improves outcomes remains unknown.

An observational study of 34 patients with chronic recurrent multifocal osteomyelitis and 20 controls found neutrophil activation and reduced PSTPIP2 protein levels. Activation correlated with MRI lesion burden; patients receiving anti-TNF therapy had normalized activation and PSTPIP2 levels, although treatment causality cannot be established.

A French observational cohort study emulating a target trial included 1,997 patients with incident giant cell arteritis. Two-year incidence of a composite of coronary events, ischemic stroke, or all-cause death was 6.4% with tocilizumab versus 10.7% with methotrexate; the association does not establish causality.

An American Heart Association scientific statement reviews primary and secondary Raynaud phenomenon, including quality of life and treatment options. It highlights the risk of digital ischemia and tissue loss in secondary disease, while noting limited clinical trial evidence for treatment.

A prospective US registry study of 585 patients with systemic autoimmune rheumatic disease–associated progressive pulmonary fibrosis found substantial baseline impairment and frequent progression over 24 months. Adjusted analyses found no significant outcome differences by rheumatic disease subtype.

A preclinical mouse study found that deleting Cd248 shifted synovial fibroblast progenitors toward a destructive lining-layer phenotype and accelerated bone damage in experimental arthritis. Bone erosion also occurred in aged knockout mice without an inflammatory stimulus, raising caution about therapeutic targeting of CD248.

A claims-based target trial emulation involving 6,168 patients with nonrenal systemic lupus erythematosus compared infection-related hospitalization across four immunosuppressant therapies. Initial differences were no longer statistically significant after accounting for time-varying glucocorticoid exposure.

A mechanistic mouse study examined how colon-derived CD4+ intraepithelial lymphocytes change after leaving the intestinal epithelium. The findings suggest that extraintestinal environments shape their activation state, offering a potential cellular mechanism for the gut–joint axis in spondyloarthritis.