The identification of responders to methotrexate (MTX) would optimize the therapy of patients with early rheumatoid arthritis (eRA). Our aim was to identify protein biomarkers for the prediction of the response to MTX.

Understanding the impact of intensive treatment on pain in patients with rheumatoid arthritis (RA) and psoriatic arthritis (PsA) is crucial to informing the application of evidence-based arthritis pain care. The impact of intensive treatment on inflammatory arthritis pain has received relatively limited attention. We addressed this through a detailed secondary analysis of three trials evaluating varying intensities of disease-modifying anti-rheumatic drug treatment. We considered a range of pain outcomes of clinical relevance to patients, including the achievement of mild endpoint pain scores and clinically-meaningful pain reductions.

ANCA-associated vasculitis (AAV) is a group of systemic autoimmune diseases affecting small blood-vessels. Class-II HLA genes often reported as major genetic determinants. We conducted a systematic review and meta-analysis to evaluate the susceptibility conferred by HLA genes in AAV and five sub-types i.e. PR3+AAV, MPO+AAV, Granulomatosis with polyangiitis (GPA), Microscopic polyangiitis (MPA) and Eosinophilic granulomatosis with polyangiitis (EGPA).

The role of neutrophil extracellular traps (NETs) in immunoglobulin A vasculitis (IgAV) pathogenesis is emerging, with NETosis-associated markers potentially linked to disease activity. This study aimed to explore the relationship between NETosis biomarkers and IgAV disease phases.

The Fibrosis-4 index (FIB-4), a non-invasive tool for assessing liver fibrosis, has also been linked to cardiovascular (CV) risk in the general population. This connection is due to the association of chronic liver diseases, particularly fibrosis or non-alcoholic fatty liver disease, with systemic inflammation, metabolic syndrome, and atherosclerosis. In this study, we aimed to calculate the FIB-4 index in patients with rheumatoid arthritis (RA), a condition associated with increased CV disease risk. We then examined its association with disease characteristics and CV comorbidities, including lipid profile, subclinical carotid atherosclerosis, and insulin resistance indices.

Cognitive dysfunction is a common neuropsychiatric manifestation in systemic lupus erythematosus (SLE), particularly affecting processing speed and memory. This study aims to identify behaviorally relevant topological networks of functional connectivity underlying neuropsychological test performances, using connectome-based predictive modeling (CPM).

We systematically reviewed the literature to identify the incidence of psoriatic arthritis (PsA) flare, criteria used to define it, and associated risk factors.

Imaging holds a pivotal yet contentious role in the early diagnosis of axial spondyloarthritis. Although MRI has enhanced our ability to detect early inflammatory changes, particularly bone marrow oedema in the sacroiliac joints, the poor specificity of this finding introduces a substantial risk of overdiagnosis. The well intentioned push by rheumatologists towards earlier intervention could inadvertently lead to the misclassification of mechanical or degenerative conditions (eg, osteitis condensans ilii) as inflammatory disease, especially in the absence of structural lesions. Diagnostic uncertainty is further fuelled by anatomical variability, sex differences, and suboptimal imaging protocols. Current strategies-such as quantifying bone marrow oedema and analysing its distribution patterns, and integrating clinical and laboratory data-offer partial guidance for avoiding overdiagnosis but fall short of resolving the core diagnostic dilemma. Emerging imaging technologies, including high-resolution sequences, quantitative MRI, radiomics, and artificial intelligence, could improve diagnostic precision, but these tools remain exploratory. This Viewpoint underscores the need for a shift in imaging approaches, recognising that although timely diagnosis and treatment is essential to prevent long-term structural damage, robust and reliable imaging criteria are also needed. Without such advances, the imaging field risks repeating past missteps seen in other rheumatological conditions.

Application of the ASAS classification criteria for axSpA in classifying axPsA is a topic of debate. In this study, we aimed to determine the prevalence of axPsA in patients with psoriasis and back pain who do not meet the entry pain features of the ASAS classification criteria.

To evaluate the discordance between patients' global assessments (PGA) and evaluators' global assessments (EGA) in psoriatic arthritis (PsA), and to explore the association of clinical variables, patient-reported outcomes (PROs), and ultrasound (US) factors with this discordance.

In patients with systemic sclerosis, it is common practice to treat interstitial lung disease (ILD) in patients in whom progression has already occurred. We sought to clarify whether observed progression of systemic sclerosis-associated ILD confers risk for subsequent progression.

Artificial intelligence (AI) tools, particularly Large Language Models (LLMs), are revolutionizing medical practice, including rheumatology. However, their diagnostic capabilities remain underexplored in the African context. To assess the diagnostic accuracy of ChatGPT-4, Gemini, Copilot, and Claude AI in rheumatology within an African population.

This study aims to analyze the expression profiles, phenotypes, functions, and cell-cell communication of various cell subpopulations in the affected aortic tissues of patients with Behçet's syndrome (BS) at the transcriptomic level.

B cell depletion therapy has been used for over two decades to treat systemic lupus erythematosus (SLE), but there is a lack of studies reporting its impact on damage progression. This study aims to assess the effectiveness of rituximab in slowing damage acquisition.

For IFN-driven diseases, such as juvenile dermatomyositis (JDM), there is a critical need for targeted therapies. We aimed to develop an in vitro model, using Siglec-1 as read-out, to evaluate inhibition of IFN-mediated responses with different JAK inhibitors (JAKi).

Giant cell arteritis (GCA) is a large vessel vasculitis characterized by granulomatous inflammation classically affecting the carotid artery branches. GCA most often presents with one or more classic clinical features which include headache, jaw claudication, temporal scalp tenderness, and polymyalgia rheumatica. In a minority of cases, GCA can adopt an "occult" presentation (i.e., failure to thrive in the setting of unexplained inflammation) where vascular manifestations affect vascular beds, such as lingual ulceration, not amenable to biopsy. While the diagnosis of GCA is often supported by temporal artery biopsy or imaging studies, such as temporal artery ultrasound or magnetic resonance angiography, these techniques are known to have limited sensitivity. As a result, there is the potential for GCA to be misdiagnosed where it presents both in the absence of classic clinical manifestations and without clear diagnostic evidence by imaging or histopathology.

Data regarding the relationship between socioeconomic status (SES) and incidence of Giant Cell Arteritis (GCA) is conflicting. No previous studies have explored whether SES influences the likelihood of undergoing temporal artery biopsy (TAB). The aim of this study was to determine whether SES influences access to TAB and rate of biopsy positivity in those with suspected GCA.

Once regarded as passive bystander cells of the tissue stroma, fibroblasts have emerged as active orchestrators of tissue homeostasis and disease. From regulating immunity and controlling tissue remodelling to governing cell growth and differentiation, fibroblasts assume myriad roles in guiding normal tissue development, maintenance and repair. By comparison, in chronic inflammatory diseases such as rheumatoid arthritis, fibroblasts recruit and sustain inflammatory leukocytes, become dominant producers of pro-inflammatory factors and catalyse tissue destruction. In other disease contexts, fibroblasts promote fibrosis and impair host control of cancer. Single-cell studies have uncovered striking transcriptional and functional heterogeneity exhibited by fibroblasts in both normal tissues and diseased tissues. In particular, advances in the understanding of fibroblast pathology in rheumatoid arthritis have shed light on pathogenic fibroblast states in other chronic diseases. The differentiation and activation of these fibroblast states is driven by diverse physical and chemical cues within the tissue microenvironment and by cell-intrinsic signalling and epigenetic mechanisms. These insights into fibroblast behaviour and regulation have illuminated therapeutic opportunities for the targeted deletion or modulation of pathogenic fibroblasts across many diseases.

Many monogenic autoinflammatory diseases, including DADA2 (deficiency of adenosine deaminase 2), HA20 (haploinsufficiency of A20), SAVI (STING-associated vasculopathy with onset in infancy), COPA syndrome, LAVLI (LYN kinase-associated vasculopathy and liver fibrosis) and VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome, present predominantly with vasculitis and constitute a substantial subgroup of vasculitic conditions associated with a 'probable aetiology'. The spectrum of monogenic vasculitis encompasses all sizes and types of blood vessel, ranging from large vessels to medium-size and small vessels, and from the arterial side to the venous side of the vasculature. Monogenic vasculitis typically starts early in life during infancy or childhood; VEXAS syndrome, which presents in late adulthood, is an exception. The activation of myeloid cells via inflammasome and nuclear factor-κB pathways, type I interferon-enhanced autoimmune mechanisms and/or dysregulated adaptive immune responses have an important role in the development of immune-mediated endothelial dysfunction and vascular damage. Genetic testing is essential for the diagnosis of underlying monogenic autoinflammatory diseases; however, the penetrance of genetic variants can vary. Increased awareness and recognition of distinctive clinical findings could facilitate earlier diagnosis and allow for more-targeted treatments.

To evaluate the effectiveness and safety of secukinumab in patients with giant cell arteritis (GCA) who experienced an inadequate response to tocilizumab.