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Relapsing polychondritis, a rare inflammatory disorder that affects cartilaginous structures, presents challenges in diagnosis owing to overlapping symptoms with other conditions. This Review provides a clinical update on relapsing polychondritis, emphasizing the importance of distinguishing this disease from similar conditions.
Granzyme serine proteases are known for their perforin-dependent cytotoxic activities, but evidence also indicates that they have a range of non-cytotoxic, pro-inflammatory intracellular and extracellular functions. In this Review, the authors discuss granzyme biology with an emphasis on its involvement in rheumatic disease pathology.
Medication adherence in gout is low, and discontinuation of urate-lowering therapy puts patients at risk of flares and cardiovascular events. A strategy to regularly monitor serum urate levels and the dissolution of urate deposits (particularly if visualized by patients) might encourage adherence in the long term.
Multidimensional and single-cell profiling of peripheral blood and inflamed tissues is a powerful and high-resolution tool for the stratification of patients with autoimmune rheumatic diseases into distinct cellular and/or molecular endotypes. The road towards precision rheumatology is long, but the time has come to enter the territory of clinical validation.
Early identification of osteoarthritis (OA) prior to the development of symptoms is challenging. Post-traumatic OA provides a model for the development of OA following a defined event. In this Review, the authors describe the existing knowledge relating to the biomarkers of post-traumatic OA, which might also be applicable to the identification of early non-traumatic OA.
This Review discusses joint-specific memory (the tendency of arthritis to recur in previously inflamed joints), explores the involvement of resident memory T cells and other contributors, and evaluates how arthritis might spread to new joints, emphasizing the important of sustained treatment.
In a head-to-head phase III trial of two drugs that target IL-5 or its receptor, benralizumab was noninferior to mepolizumab for the induction of remission in patients with eosinophilic granulomatosis with polyangiitis.
Despite the transformative potential of treatments for systemic autoinflammatory diseases, these conditions remain underfunded and understudied. Urgent, coordinated action among stakeholders is needed to overcome regulatory and research barriers, as is innovation and advocacy for the development of effective therapies for these rare diseases.
Rheumatoid arthritis has a substantial genetic component, some of which is associated with the presence of low-frequency or rare variants. Next-generation sequencing in large and well-defined cohorts can continue to identify these variants and thereby contribute to the future prediction, diagnosis and treatment of rheumatoid arthritis.
A nanoparticle-based formulation of the anticancer drug pazopanib, which inhibits VEGFR1 and VEGFR2, shows promise as a disease-modifying drug for osteoarthritis.
EULAR’s 2023 updated recommendations for the non-pharmacological treatment of hip and knee osteoarthritis reiterates and confirms, in an abbreviated form, what we have known for more than a decade. Unfortunately, the abbreviated format of the updated recommendations lacks specificity and clinical usefulness. More detailed guidance could have facilitated wider uptake and improved care.
In this Evidence-Based Guideline article, an international multidisciplinary working group of the European Society for Clinical and Economic Aspects of Osteoporosis, Osteoarthritis and Musculoskeletal Diseases presents recommendations for the diagnosis, monitoring and treatment of osteoporosis in men.
Gout is associated with various cardiometabolic–renal comorbidities that increase the risk of mortality. Sodium–glucose cotransporter type 2 (SGLT2) inhibitors show promise in both addressing the symptoms of gout and managing relevant comorbidities to help prevent premature mortality.
Characteristic patterns of joint involvement exist in different forms of arthritis. Research now indicates that epigenetic programming of synovial fibroblasts diversifies their response to inflammatory cascades, leading to this anatomical variation in arthritis and its response to treatment.
In 2006, a linear immunological continuum of autoinflammatory and autoimmune disorders ranging from monogenic diseases of innate immunity at one end to monogenic diseases of adaptive immunity at the other end was proposed to classify these conditions. Deep immunophenotyping has now revealed a cell-based nosology of these disorders.