Despite reports of clinical benefits, concerns persist about the stress associated with high-intensity interval training (HIIT) in patients with inflammatory arthritis (IA). This review aimed to assess the effects of HIIT on disease activity, immune function, symptoms, cardiorespiratory fitness (CRF), and overall health-related quality of life (HRQoL) in patients with IA.

Platelets are central players in inflammatory and thrombotic responses that drive the onset and progression of rheumatic diseases. In particular, they regulate immunothrombosis, a defence mechanism in which the immune and blood-clotting systems cooperate to contain infections or vascular damage. Although immunothrombosis can help to preserve blood-vessel integrity and promote healing, it becomes harmful when exaggerated or chronic. In rheumatic diseases, such as systemic lupus erythematosus, systemic sclerosis and antiphospholipid syndrome, immunothrombosis contributes to persistent inflammation, abnormal blood-clot formation and long-term damage to the small blood vessels. It has also been implicated in maintaining autoimmune responses to autoantigens released by neutrophils. Platelets are among the first responders to vascular injury and influence the activity of immune cells, particularly neutrophils, by promoting the formation of neutrophil extracellular traps. Platelets express proteins such as P-selectin and the damage-associated molecule high-mobility group box 1 (HMGB1), which have distinct and non-redundant roles, both via direct interactions locally at sites of vascular damage and systemically via the release of extracellular vesicles. Understanding how platelets contribute to vascular inflammation and clotting in autoimmune settings elucidates disease mechanisms and might lead to the identification of new therapeutic targets.

The main homeostatic function of the synovial fluid is joint lubrication. However, during knee osteoarthritis (KOA), synovial fluid becomes modified with drivers of disease that contribute to symptoms (pain) and joint-related pathology. Acting as a sink of factors from both systemic circulation and local tissues, including articular cartilage, subchondral bone, synovium, and the infrapatellar fat pad, the synovial fluid enables bidirectional communication promoting KOA pathogenesis. Synovial fluid constituents might also be detected in circulation, functioning not only as accessible biomarkers but also as potential mediators of KOA-driven systemic effects. Factors deposited in synovial fluid have the ability to affect nervous system activity, acting at the neuronal projections that are integrated into joint tissues from dorsal root ganglia. Non-coding RNAs (microRNAs, long non-coding RNAs, circular RNAs), metabolites, cytokines and other secreted proteins of the synovial fluid in KOA have emerged as biomarkers of disease progression, therapeutic efficacy, and pain. These molecules might also function as molecular mediators of KOA, supporting them as candidates for therapeutic intervention. This review consolidates literature published primarily within the past 4 years, focussing on factors identified within synovial fluid as biomarkers and molecular mediators of KOA symptoms and pathology. Emerging therapeutic modalities to target synovial fluid molecular mediators are also discussed.

Epidemiological data on polymyalgia rheumatica (PMR) in Germany is limited. Current national prevalence estimates are low by international standards. This study aimed to gain up-to-date data representative of Germany.

To investigate how the M694I variant of MEFV contributes to familial Mediterranean fever (FMF) pathophysiology using knock-in mice, focusing on T helper 17 (Th17) cell responses and the underlying molecular mechanisms.

To evaluate the measurement properties of SLE-DAS, using the Brazilian-Portuguese version (SLE-DAS Pt-BR).

Patients with autoimmune rheumatic diseases have high rates of surgical procedures including joint replacements despite the use of disease-modifying anti-rheumatic drugs (DMARDs). This scoping review compares clinical practice guideline recommendations for the perioperative management of DMARDs in such patients.

Conflicting data exist on TNF inhibitors' (TNFi) role in preventing PsA in psoriasis. Using propensity score matching, we compared PsA incidence in severe psoriasis patients treated with TNFi vs narrow-band ultraviolet B (nbUVB) phototherapy over a decade of follow-up.

RA is a chronic inflammatory disease characterized by synovial membrane hyperplasia and joint degeneration. Aberrant protein expression has shed light on their association with disease pathogenesis. This study emphasized the mechanistic role of one of the major altered proteins, Inter-alpha-trypsin-inhibitor heavy chain 4 (ITIH4), in RA pathogenesis.

Initial success with B cell-targeted chimeric antigen receptor (CAR) T cells for the treatment of systemic lupus erythematosus and other rheumatic diseases has generated enthusiasm for the broad application of this technology outside of the field of oncology. Paediatric patients with severe rheumatic diseases require lifelong therapy with a substantial toxicity burden and a high cost of care. Paradigm-shifting treatments, including CAR T cells, are desperately needed. Although CAR T cell therapy shows promise for paediatric rheumatic diseases, there are unique aspects of care compared with adults, which require careful consideration and expertise. In response, we established the Integrated Multidisciplinary Paediatric Autoimmunity and Cell Therapy (IMPACT) working group, comprising international experts in the fields of paediatric rheumatology, oncology and cellular therapy, immunology and nephrology, to address the challenges of introducing cell therapies to patients with paediatric-onset autoimmune diseases. Given the possible benefits, we advocate for the study of CAR T cells in paediatric patients with rheumatic diseases who carry a lifelong risk of morbidity and mortality from chronic illness and medication toxicity. As this patient population is relatively small, consensus around definitions of success, robust study of predictors of response and uniform assessment and reporting of toxicities are critical to advancing the field.

SSc is a complex connective tissue disease frequently complicated by interstitial lung disease (ILD), which remains the leading cause of mortality. Nailfold videocapillaroscopy (NVC) is a widely used non-invasive technique for assessing microvascular damage in SSc, but its role in predicting ILD progression remains underexplored. Additionally, Krebs von den Lungen-6 (KL-6) has emerged as a potential biomarker for ILD severity, yet its relationship with NVC patterns and pulmonary function decline requires further investigation. We aim to determine whether baseline NVC abnormalities predict pulmonary function decline, ILD progression and longitudinal changes in serum biomarkers (KL-6, IL-18, IL-18BP), inflammatory markers and disease activity indices (EUSTAR 2017, SCTC-DI) over a 2-year follow-up in patients with SSc.

Primary Sjögren's disease (SjD) is a chronic autoimmune disease (AD) that primarily affects the exocrine glands, particularly lacrimal and salivary glands, presenting extra glandular manifestations in a significant number of patients. Although it is a prevalent and globally widespread disease, its pathogenesis has not been fully elucidated. Recently, high-throughput omics technologies are providing unprecedented insights into the molecular landscape of various ADs, including SjD. These technical advances are prepared to decipher new aspects of its pathogenesis and to eventually enable the development of more effective treatment strategies. This review explores recent developments in genetics, transcriptomics, epigenomics, proteomics and metagenomics in SjD, highlighting the potential of integrating multiple omics datasets to identify better drug targets and useful biomarkers for precision medicine.

Rheumatoid Arthritis (RA) is a chronic autoimmune disease that mostly breaks out at the joints. It further causes bone erosion and decreased life quality due to severe pain. Current drugs are mainly focused on reducing pain, but unable to terminate the disease progression. This study aims to determine the effect of diet types (Western, Vegan and Mediterranean) on RA progression. Some dietary supplements and drug administration (Huayu-Qiangshen-Tongbi formula or Leflunomide plus Methotrexate) in a six-month-period were also simulated to elucidate their effects on gut microbiota growth and exchange metabolite fluxes. The computational analyses showed that Haemophilus parainfluenzae had the highest growth rate in the RA community with the Western diet. Enterococcus faecalis was the most notable bacterial species considering butyrate exchange rates without any dependency on the diet; however diet type became important for Clostridium celatum for acetate and formate exchanges. Focal interactions for RA communities signify Mediterranean diet had the most homogeneous exchange flux distribution. With iron and ornithine supplementation, Clostridium celatum outshined the rest of the bacteria in the RA community with the potential being an RA biomarker. The Mediterranean diet could be studied further for drug administration studies since the bacterial species under this diet exhibited different outputs. In the near future, by utilizing the potential of the gut microbiota to be altered with diet, it might be possible to manipulate the progression of RA.

Treatment of rheumatoid arthritis (RA) with biologic drugs in patients with cancer could potentially result in poor cancer outcomes. This study aimed to identify the beliefs, preferences, and informational needs of patients with RA and cancer regarding the harms, benefits, and uncertainties surrounding the use of RA therapy with respect to cancer.

To investigate a patient-level single imputation approach for patient reported outcomes (PROs) that express similar contents or associated PROs, where a PRO whose value is missing at a particular timepoint is substituted by another PRO whose value is available at the same timepoint.

Systemic capillary leak syndrome (SCLS) is a rare disorder characterized by increased vascular permeability leading to third-spacing of fluids and protein. Drug-induced hypersensitivity reactions can mimic SCLS clinically and radiologically.