To seek risk factors of gangrene secondary to systemic lupus erythematosus (SLE).

Glucocorticoid-induced osteoporosis (GIO) is the most common drug-induced osteoporosis. Early detection and treatment may decrease the fragility fractures. Several GIO guidelines exist, although they vary in recommended intervention thresholds for initiating pharmacologic treatment. This study aimed to evaluate the performance of intervention thresholds in treating GIO under various guidelines.

Proteinuria, amyloidosis, and kidney failure are the main long-term renal complications of familial Mediterranean fever (FMF). This study assesses their risk factors, independent of ethnicity or residence.

Dual-energy CT (DECT) is a novel and more effective approach for identifying bone marrow oedema lesions than MRI. We aimed to investigate the performance of DECT in diagnosing bone marrow oedema (BME) in rheumatoid arthritis (RA) patients and its potential for assessing RA disease activity.

To compare the performance of QRESEARCH risk estimator (QRISK)3, Systematic Coronary Risk Evaluation (SCORE)2, Predicting Risk of cardiovascular disease EVENTs (PREVENT)-cardiovascular disease (CVD), and PREVENT-atherosclerotic cardiovascular disease (ASCVD) equations in predicting cardiovascular (CV) risk among individuals with chronic inflammatory rheumatic diseases (CIRD) enrolled in the Spanish CARMA project.

Vamorolone, a dissociated steroidal compound with reduced side effects, offers a promising alternative to traditional glucocorticoids for inflammatory diseases. Unlike conventional glucocorticoids, vamorolone lacks the hydroxyl or ketone groups required for metabolism by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), a key enzyme that modulates glucocorticoid activity. This study investigates vamorolone's resistance to 11β-HSD1 metabolism and assesses its therapeutic efficacy in the murine tumour necros factor-alpha-overexpressing (TNFtg) model of polyarthritis.

Although axial spondyloarthritis typically begins before age 45, late-onset axial spondyloarthritis has been widely recognized. While existing literature describes this subgroup, data on therapeutic approaches remain limited. Therefore, we aimed to evaluate the efficacy and safety of biologic disease-modifying antirheumatic drugs in patients with late-onset axial spondyloarthritis.

Osteoarthritis (OA) is a leading cause of chronic pain worldwide, resulting in substantial disability and placing a substantial burden on patients and society. The hallmark symptom of OA is joint pain. Despite extensive research, new treatments for OA pain remain limited, partly owing to a lack of understanding of underlying pain mechanisms. For a long time, OA pain was seen as a reflection of nociceptive activity at the joint level, and the brain has been viewed as a passive recipient of such information. In this Review, we challenge these concepts and discuss how, over time, the activation of peripheral nociceptors leads to adaptations in the brain that dictate the properties and experience of OA pain. These adaptations are further influenced by the inherent properties of the brain. We review general concepts that distinguish pain from nociception, present evidence on the incongruity between joint injury and experience of OA pain, and review brain circuits that are crucial in the perception of OA pain. Finally, we propose a model that integrates nociception, spinal-cord mechanisms, and central nervous system dynamics, each contributing uniquely to pain perception. This framework has the potential to inform the development of personalized treatment strategies.

Data on the efficacy of biological disease-modifying antirheumatic drug (DMARD) therapies such as anakinra, canakinumab, and tocilizumab as a primary therapeutic option in adult-onset Still's disease (AOSD) are scarce, and treatment recommendations rely mainly on data extrapolated from paediatric studies. The aim of this study was to compare the effectiveness of first-line biological DMARD therapy versus conventional synthetic DMARD therapy in AOSD.

Chimeric antigen receptor (CAR)-based therapies developed for the treatment of haematological malignancies have recently been repurposed to treat refractory systemic autoimmune diseases. In this Review we critically discuss the current data available on the use of CAR-based therapy in systemic autoimmune diseases, the current challenges, and the potential next steps toward their implementation into clinical practice. Beyond the targeting of B cells via CD19, we discuss the advantages and potential pitfalls of targeting plasma cells (B-cell Maturation Antigen or CD138) and other non-immune targets, such as fibroblast activated protein, and of aiming to restore immune homeostasis using CAR T regulatory cells. Crucial points need to be addressed for CAR-based therapy to become a viable treatment option for patients with systemic autoimmune diseases.

To analyze positive 3 patient distress MDHAQ (multidimensional health assessment questionnaire) screening indices, MAS2 (MDHAQ anxiety screen), MDS2 (MDHAQ depression screen), and FAST3F (fibromyalgia assessment screening tool), for possible elevations of rheumatoid arthritis (RA) activity/severity indices in routine care patients.

Articular cartilage can withstand substantial compressive and shear forces within the joint and also reduces friction during motion. The exceptional mechanical properties of articular cartilage stem from its highly organized extracellular matrix (ECM). The ECM is composed mainly of collagen type II and is pivotal in conferring mechanical durability to the tissue within its proteoglycan-rich matrix. Articular cartilage is prone to injury and degeneration, and current treatments often fail to restore the mechanical function of this tissue. A key challenge is replicating the intricate collagen-proteoglycan network, which is essential for the long-lasting restoration and mechanical durability of the tissue. Understanding articular cartilage development, which arises between late embryonic and early juvenile development, is vital for the creation of durable therapeutic strategies. The development of the articular ECM involves the biosynthesis, fibrillogenesis and self-assembly of the collagen type II network, which, along with proteoglycans and minor ECM components, shapes the architecture of adult articular cartilage. A deeper understanding of these processes could inform biomaterial-based therapies aimed at improving therapeutic outcomes. Emerging biofabrication technologies offer new opportunities to integrate developmental principles into the creation of durable articular cartilage implants. Bridging fundamental biology with innovative engineering offers novel approaches to generating more-durable 3D implants for articular cartilage restoration.