Adipocytokines have been implicated in the pathogenesis of ankylosing spondylitis (AS), although their exact role remains unclear. Optical coherence tomography (OCT) provides quantitative ocular measurements and may detect subclinical ocular changes in AS. This study evaluated serum adipocytokine levels and OCT findings in patients with radiographic AS and investigated possible correlations between these parameters. This cross-sectional study included 47 patients with radiographic AS diagnosed according to the modified New York criteria and 23 age- and sex-similar healthy controls. Serum visfatin, resistin, adiponectin, and fetuin-A levels were measured using enzyme-linked immunosorbent assay. OCT parameters, including retinal nerve fiber layer (RNFL), ganglion cell complex (GCC), macular thickness, and subfoveal choroidal thickness, were recorded using spectral-domain OCT. Multivariable logistic regression was performed to identify biomarkers independently associated with AS. Visfatin levels were higher (6.7 [3.9-14.0] vs. 4.5 [3.9-8.1] ng/mL, p<0.001), whereas fetuin-A levels were lower (3253 [1652-5565] vs 3724 [2204-5651] ng/mL, p=0.017) in patients with AS compared with controls. Adiponectin and resistin levels did not differ (both p>0.05). Subfoveal choroidal thickness was greater in AS patients (262 [124-387] vs. 197 [101-300] µm, p<0.001), whereas RNFL, GCC, and macular thickness were similar between the groups (all p>0.05). On multivariable analyses adjusted for age, sex, BMI, and CRP, visfatin (OR=3.894, 95% CI 1.378-11.004) and choroidal thickness (OR=1.047, 95% CI 1.007-1.088) remained independently associated with AS (both p<0.05). Conclusion: Elevated visfatin and increased choroidal thickness were independently associated with AS, suggesting subclinical ocular involvement even in the absence of uveitis. Prospective, larger studies are needed to confirm the clinical utility of these parameters.

Behçet's disease (BD) is rare in European populations. Because clinical and immunological characteristics may differ between Caucasians and Middle Eastern patients, we analyzed BD patients from the Polish population. Data from eight patients with BD treated at a rheumatology clinic were analyzed and collected, including demographic data, clinical features, laboratory test results, comorbidities, and treatment options. The study included eight patients (mean age 38.2 ± 13.7 years; 75% female). None of the patients had a family history of the disease. The mean delay in diagnosis was 5.28 ± 4.6 years. The disease began with the development of mucosal ulcerations and a maculopapular rash, and some patients also developed anemia, alopecia, headaches, and arthritis. All patients had mucosal ulcerations and an erythematous or maculopapular rash; joint involvement occurred in 62.5%. Vascular complications (37.5%) included superior sagittal sinus thrombosis, ischemic stroke, and cephalic vein thrombosis. The most common comorbidities were hypertension (50%), dyslipidemia (37.5%), and depression (25%). Inflammatory markers were elevated in half of the patients and normalized after treatment. Antinuclear antibodies were positive in 62.5%, and antineutrophil cytoplasmic antibodies in 25%. Patients were treated with glucocorticosteroids (100%) in combination with azathioprine (62.5%), cyclosporine (25%), methotrexate (12.5%), and hydroxychloroquine (25%). Data from a single center indicate that BD in Caucasians is characterized by heterogeneity in clinical manifestations and develops predominantly in women. The presence of ANA and ANCA antibodiescan be misleading and requires differential diagnosis. The course is generally mild, but severe symptoms (especially thrombosis) require close monitoring by a multidisciplinary team.

EULAR recommends kidney biopsy in systemic lupus erythematosus (SLE) patients with glomerular hematuria, whereas both ACR and KDIGO require the presence of proteinuria and/or impaired kidney function. We explored the value of hematuria for the diagnosis of new-onset lupus nephritis (LN). Cross-sectional study of SLE patients who underwent diagnostic kidney biopsy in two independent centers. Clinically significant LN was defined as ISN/RPS class III, IV, V, or mixed III/IV + V. Presentation patterns were categorized by glomerular hematuria, proteinuria, and impaired kidney function. Among patients with glomerular hematuria, regression models identified factors associated with clinically significant LN, and a nomogram was constructed. Of 227 biopsies, 181 (79.7%) showed clinically significant LN. Isolated glomerular hematuria was evident in 11 patients, of whom 9 revealed non-LN pathology; the two LN cases (class II and III) both demonstrated concurrent SLE serologic activity. Among patients with glomerular hematuria (n = 137), independent factors associated with clinically significant LN included anti-dsDNA positivity (OR 12.00, 95% CI 3.36-51.40), higher non-renal SLEDAI score (OR 1.20 per point, 95% CI 1.02-1.46), higher proteinuria (OR 3.77 per 1 g/d, 95% CI 2.00-9.03), and younger age (OR 0.96 per year, 95% CI 0.91-1.00). The combined presence of these factors yielded a predicted probability of 97% (95% CI 90-99%) of clinically significant LN, whereas their absence was associated with a probability of only 6% (95% CI 1-23%). When considering the need for kidney biopsy in patients with lupus, hematuria should be evaluated in the context of overall disease activity; extra-renal and serologic activity substantially increase the likelihood of clinically significant LN.

Systemic autoimmune diseases can adversely affect the health of childbearing women and pregnancy outcomes. Additionally, some of theadministered medications are teratogenic, prompting international rheumatological societies to recommend effective contraception and preconception counselling. Given the limited structured education in this field, this study aimed to assess reproductive health awareness and perceptions of family planning among women with systemic autoimmune diseases. A survey-based study was conducted at the Division of Clinical Immunology and Rheumatology, University Hospital Centre Zagreb, Zagreb, Croatia. The sample included 165 women aged 18-50 years who completed the ReproKnow questionnaire assessing reproductive health knowledge, while sociodemographic and clinical data were obtained through interviews and medical records. The median ReproKnow score was 5/10 correct answers indicating moderate knowledge of the studied topic. Greater reproductive health awareness was observed among patients with higher education levels and those diagnosed with SLE or vasculitis. Although one-third of participants stated that their diagnosis affected family planning, only one-fifth reported consistent contraception use, even among those receiving teratogenic medications. Knowledge of contraception efficacy was low (25%), but associated with consistent use. Substantial gaps remain in contraception knowledge and use, highlighting the need for targeted educational interventions and further research to improve reproductive health counselling and contraception practice.

Higher risks of cardiovascular mortality and cardiovascular events have been reported in patients with rheumatoid arthritis (RA) compared with the general population. However, data remain scarce in populations of African descent, and the Caribbean region is under-represented in this field. We aimed to assess the burden of hospitalized cardiovascular events (HCE) in Martinique, a French Caribbean overseas territory with a predominantly Afro-Caribbean population. We conducted a retrospective cohort study of patients with RA from Martinique identified through the hospital discharge database. The 10-year cumulative incidence of HCE was estimated using the Fine and Gray competing-risk method, with a sensitivity analysis restricted to the classical 3-point major adverse cardiovascular events (MACE) definition. Among 205 patients with RA, 50.5% had hypertension, 30.0% diabetes mellitus,39.4% had dyslipidemia and 59.5% were overweight or obese. Smoking exposure was uncommon. 10-year cumulative incidence of HCE was 8.3% (95% CI 4.5-12.1) for the overall composite endpoint and 4.0% (95% CI 1.3-6.8) when restricted to 3-point MACE. Acute heart failure (HF) accounted for 47.1% (8/17) of events and was mostly incident, with non-ischemic etiologies. Patients with RA who developed HCE were significantly older at RA diagnosis, more frequently diabetic, and exposed to fewer bDMARDs or tsDMARDs. HCE affected a substantial proportion of patients with RA in Martinique with incidence estimates comparable to other RA cohorts despite a distinct cardiometabolic profile. HF emerged as the leading cardiovascular outcome, supporting the integration of heart failure prevention and early detection into cardiovascular surveillance strategies for RA in this setting.

Fatigue frequently persists after clinically visible inflammation has improved in inflammatory rheumatic diseases (IRDs). This narrative review integrates evidence updated through 21 July 2026 on mechanisms, assessment, and management of fatigue in rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjögren's disease (SjD). Across these conditions, associations between fatigue and conventional inflammatory measures are inconsistent and usually weaker than associations with pain, sleep disturbance, mood symptoms, disability, central pain sensitivity, comorbidity, medication effects, and reduced activity tolerance. Recent quantitative findings reinforce this mismatch. In a 2026 RA cohort of 253 patients, 80% reported fatigue and 10% had severe fatigue; fatigue remained present in some patients in remission. In an international survey of 1,155 people with SjD, physical fatigue was among the most frequent symptoms, while mean work and activity impairment reached 46.6% and 48.4%, respectively. Longitudinal RA data showed that improvement in self-reported central pain sensitivity tracked improvement in fatigue, whereas inflammatory markers and imaging were not consistently associated with fatigue. Recent SLE imaging findings also linked region-specific cerebellar alterations with fatigue and cognitive dysfunction, although no central or metabolic biomarker is ready for routine use. Immune-targeted therapies produce variable, generally small-to-moderate fatigue improvements, whereas personalized exercise, rehabilitation, cognitive-behavioural or self-management interventions, and treatment of sleep disorders have supportive clinical evidence. The mismatch between inflammatory remission and continuing fatigue is framed as a fatigue remission gap. This is a practical signal, not a validated diagnosis, and should prompt direct fatigue measurement and a treatable-traits assessment rather than automatic escalation of immunosuppression. The proposed framework sequentially evaluates disease activity, fatigue severity, pain and fibromyalgia overlap, sleep, mood, comorbidities, medication effects, and deconditioning, then selects a shared, modifiable treatment target for reassessment.

Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a potentially life-threatening extra-articular complication affecting 10-60% of patients with rheumatoid arthritis. Despite its clinical significance, the optimal diagnostic strategy remains uncertain. This systematic review assessed the diagnostic value of currently available methods for detecting RA-ILD. The review followed PRISMA guidelines. Databases were searched for studies evaluating imaging modalities (chest X-ray, high-resolution computed tomography [HRCT], lung ultrasound), pulmonary function tests (forced vital capacity [FVC], total lung capacity [TLC], diffusing capacity for carbon monoxide [DLCO]), clinical features, and serum biomarkers. The risk of bias was assessed using QUADAS-2 tool.Thirty-six studies were included. Risk of bias was low in 20, high in 1, and unclear in 15 studies. Applicability concerns were low in 18, unclear in 17 and high in 1 study. Lung ultrasound was most frequently evaluated, showing sensitivity of 70-100% and specificity of 56-97%. Only one HRCT study was identified; it demonstrated high specificity but moderate sensitivity for detecting a UIP pattern. No studies assessing lung volumes (FVC, TLC) were found. DLCO showed sensitivity for RA-ILD detection but limited specificity and uncertain optimal cut-off values. Among biomarkers, KL-6 was most studied (sensitivity 61-100%, specificity 78-91%), while other biomarkers demonstrated inconsistent results and lacked validation. Lung ultrasound appears diagnostically useful in RA-ILD. Evidence supporting pulmonary function tests is limited. Although KL-6 shows promise, biomarkers cannot currently serve as standalone diagnostic tools. Further well-designed prospective studies are required. https://www.crd.york.ac.uk/PROSPERO/view/CRD420251035610 .

Fibromyalgia Syndrome (FM) is a chronic pain disorder characterized by a complex pathophysiology that lacks definitive biochemical markers. This study aims to evaluate the serum levels of Isthmin-1 (ISM1) and Irisin in patients with FM and to investigate their relationship with clinical parameters such as pain severity and depressive symptoms. This cross-sectional study included 21 female patients diagnosed with FM according to the ACR 2016 criteria and 21 age- and BMI-matched healthy female controls. Pain intensity was assessed using the Visual Analog Scale (VAS), and psychological status was evaluated with the Beck Depression Inventory (BDI). Serum ISM1 and Irisin levels were measured using the Enzyme-Linked Immunosorbent Assay (ELISA) method. Statistical analyses were performed using non-parametric tests, and correlations were evaluated via Spearman's rank correlation coefficient. The FM and control groups were well-matched regarding age [46 (33-59) vs. 47 (35-59) years; p = 0.489] and BMI [27.0 (20.8-34.7) vs. 26.4 (21.3-33.8) kg/m[2]; p = 0.670]. As expected, VAS [7 (6-8) vs. 1 (0-3); p < 0.001] and BDI [34 (26-40) vs. 5 (0-9); p < 0.001] scores were significantly higher in the FM group. Serum ISM1 levels were significantly lower in the FM group compared to the control group [3152.40 (2693.54-3511.76) pg/mL vs. 4083.29 (2659.13-5962.67) pg/mL, respectively; p < 0.001], whereas no significant difference was observed in serum Irisin levels between the groups [423.34 (285.73-554.24) ng/mL vs. 396.95 (274.53-612.71) ng/mL, respectively; p = 0.580]. Correlation analysis within the FM group showed strong negative correlations between serum ISM1 levels and BDI scores (rho = -0.721, p = 0.001), as well as between ISM1 and VAS scores (rho = -0.710, p = 0.001). Additionally, a significant negative correlation was found between serum ISM1 and Irisin levels strictly within the patient cohort (rho = -0.458, p = 0.037). Our findings demonstrate for the first time that serum ISM1 levels are markedly reduced in patients with FM and are strongly associated with both pain and depression. While Irisin levels remained stable, the significant decrease in ISM1 suggests that it may serve as a potential objective biomarker for the diagnosis and clinical monitoring of FM.

Wernicke's encephalopathy (WE) is an acute, reversible but potentially disabling neurological syndrome caused by thiamine deficiency. It is increasingly recognized in non-alcoholic settings, particularly when persistent vomiting, poor intake, malabsorption, or systemic illness rapidly depletes limited thiamine stores. Patients with mixed connective tissue disease (MCTD) may be vulnerable because esophageal/gastrointestinal dysmotility, gastroesophageal reflux, chronic inflammation, and reduced oral intake can overlap and obscure nutritional complications. A 38-year-old woman with a 4-year history of anti-U1 RNP-positive MCTD, interstitial lung disease, Raynaud's phenomenon, sclerodactyly, polyarthritis, GERD, and pre-existing sensory axonal neuropathy presented with two weeks of recurrent postprandial vomiting followed by excessive daytime somnolence, bilateral horizontal nystagmus, lower-limb weakness, and impaired vibration sense. Brain MRI showed symmetrical T2/FLAIR hyperintensities involving the bilateral dorsomedial thalami, mammillary bodies, and periaqueductal gray matter. CSF examination was non-inflammatory, CSF cytology was negative, anti-aquaporin-4 antibody was negative, spinal MRI was normal, and infectious, malignant, metabolic, and neuromyelitis optica spectrum disorder differentials were excluded. Empirical intravenous thiamine 500 mg three times daily was started on day 1; vomiting, alertness, and nystagmus improved within 72 h, and complete neurological recovery was documented at one month. This case highlights non-alcoholic WE as a treatable neurological mimic in autoimmune rheumatic disease. Persistent vomiting with new ocular, cognitive, gait, or motor findings in MCTD should prompt early empiric parenteral thiamine, even when the classical triad is incomplete and serum thiamine is unavailable.

The presence of abnormal nailfold capillaries and antinuclear antibodies (ANA) is associated with increased all-cause mortality in patients presenting with incipient Raynaud's phenomenon (RP). We conducted a retrospective analysis aiming to assess the association between abnormal nailfold capillaries, ANA, and mortality over a 20-year follow-up period. In 2958 patients with incipient RP without previously known connective tissue disease, nailfold capillaroscopies and laboratory tests for ANA and ANA-subsets were obtained. Of these, long-term follow-up data were available for 2922 patients. Over a median follow-up period of 23 (IQR 20.2-25.2) years, 832 patients died, of which 562 were women (25% of female patients) and 270 were men (41% of male patients). Compared to a demographically matched reference population, mortality was increased in female and male patients with RP (log-rank test < 0.001). In female patients with RP, the presence of ANA, anti-Scl-70 antibodies, and a grouping variable consisting of giant capillaries, reduced capillary density, and avascular fields was associated with an increase in all-cause mortality. The highest mortality was observed in patients presenting both abnormal nailfold capillaries and ANA. In the long-term, an excess mortality persists in patients with RP. Our study demonstrates prognostic associations between abnormal nailfold capillaries as well as ANA and mortality.

Patient-reported outcome measures (PROMs) are widely used in musculoskeletal rehabilitation to assess pain, physical function, disability, health-related quality of life, psychological status, and patient-perceived recovery. Although traditionally applied as outcome measures, PROMs may also provide prognostic information and contribute to prediction models of rehabilitation response. However, their dual role as both endpoints and predictors has not yet been sufficiently integrated within a unified methodological framework. This narrative review critically examines the role of PROMs in musculoskeletal rehabilitation, with particular emphasis on their use as endpoints of functional recovery, predictors of rehabilitation outcomes, longitudinal monitoring tools, and instruments supporting shared decision-making. A search of peer-reviewed literature was conducted across global databases, focusing on commonly used PROMs. The available evidence indicates that PROMs capture patient-centred domains that are not fully represented by objective clinical or performance-based measures. As endpoints, they permit evaluation of treatment effectiveness. As predictors, baseline and early-treatment PROMs may contribute to prognostic models, risk stratification, treatment matching, and identification of patients at risk of persistent disability or non-response. Their predictive value is influenced by measurement validity, construct overlap, baseline severity, regression to the mean, ceiling and floor effects, assessment timing, missing data, and validation strategy. The clinical utility of PROM-informed models depends on rigorous instrument selection, transparent modelling, calibration assessment, external validation, and adherence to recognised methodological and reporting standards. PROMs should be considered as potentially valuable components of personalised rehabilitation assessment and prognostic modelling.

To explore patients' experiences and perceptions of physical activity in the context of gout and gout flares. Interpretive description informed the design of this qualitative study. Individual interviews were conducted with 25 people with gout. An interview guide was used to lead discussions, focusing on participants' experiences of gout flares, physical activity engagement, and the perceived impact of flares on activity levels. Key questions were designed to capture culturally specific understandings and experiences related to gout and physical activity. Interviews were audio-recorded and transcribed verbatim. Data were analysed using reflexive thematic analysis. Four themes were generated from the data: (1) The experience of physical activity is shaped by societal misconceptions about gout; (2) A loss of physicality comes with a loss of autonomy; (3) Reclaiming body and identity through physical activity; and (4) Living with uncertainty: wanting to be active but not knowing how. Gout flares disrupted mobility, independence, work, family roles, and identity. Participants described stigma, fear of judgement, activity modification, pacing and uncertainty about whether exercise could trigger flares or damage joints, particularly in the absence of gout-specific advice. This study offers new insights into how societal misconceptions about gout influence the patient experience of physical activity, including loss of autonomy, identity reconstruction through movement, and uncertainty around safe exercise. These findings may inform future intervention development, and patient-centred physical activity guidance that supports people with gout to move safely, confidently, and meaningfully.

This study assesses the relationship between ANCA-associated vasculitis and immune-mediated inflammatory diseases (IMIDs) in first-degree relatives. People with AAV were matched 1-to-1 with control participants with no IMID in a case control study. Participants were asked whether their first-degree relatives had IMID. The likelihood of a positive family history was compared between cases and controls using conditional logistic regression. Additionally, the risk of first-degree relatives of cases having IMID was explored using generalised estimating equations. 145 AAV cases were matched with 145 controls. A family history of IMID was reported by 46.2% of those with AAV and 16.6% of controls. After adjustment for participant age and number of known family members, AAV cases were seven-times more likely to have a positive family history compared to controls (OR 7.25, 95% C.I. 3.27-16.09). 12% of first-degree relatives of AAV participants had an IMID compared to 3.5% of first-degree relatives of control participants. First-degree relatives of AAV participants were four-times more likely to have an IMID compared to a relative of a control (OR 4.03, 95% C.I. 2.46-6.62). Female first-degree relatives had double the risk of having an IMID, compared to male first-degree relatives. A history of IMID in first-degree family members is associated with an increased chance of a person developing AAV. Conversely, the presence of AAV in a first-degree relative is associated with having an increased chance of having an IMID. This implies a shared familial susceptibility between AAV and these diseases.

Rheumatoid arthritis (RA) is a chronic autoimmune disease associated with metabolic dysfunction-associated steatotic liver disease (MASLD), which may contribute to cardiovascular (CV) risk. This study aimed to examine the association between hepatic steatosis, measured by a non-invasive test, and CV risk markers in RA patients. This post-hoc analysis used cross-sectional and longitudinal data from the Franciscus Rheumatoid Arthritis and Cardiovascular Intervention Study (FRANCIS), an open-label randomized controlled trial of intensive CV risk management in patients with rheumatoid arthritis without cardiovascular disease (CVD) or type 2 diabetes. Hepatic steatosis was assessed using the Lipid Accumulation Product (LAP) with sex-specific thresholds for rule-in and rule-out of severe steatosis. Associations between hepatic steatosis and carotid intima-media thickness (cIMT) were assessed using linear regression analysis. Crude associations were first evaluated in unadjusted models, followed by multivariable models adjusting for age, sex, BMI, and systolic blood pressure. Longitudinal changes in cIMT over 3 years were analyzed according to LAP-defined steatosis and treatment strategy. Among 236 RA patients (66% female; mean age 54 ± 10 years), those with LAP-defined steatosis had a more adverse cardiometabolic profile, including higher blood pressure, fasting glucose, and a more atherogenic lipid profile (all p < 0.05). Mean cIMT tended to be higher in the steatosis group (0.61 ± 0.10 vs. 0.57 ± 0.11 mm). In crude regression, LAP-defined steatosis showed a non-significant trend toward higher cIMT (B = 0.036, 95% CI - 0.003-0.076), which was no longer observed after multivariable adjustment (B = - 0.016, 95% CI - 0.050-0.019). Over 3 years, intensive treatment reduced cIMT progression compared with standard treatment in patients without LAP-defined steatosis (ΔcIMT 0.03 ± 0.07 vs. 0.06 ± 0.12 mm; p = 0.013), whereas no treatment effect was observed in patients with LAP-defined steatosis (ΔcIMT 0.05 ± 0.05 vs. 0.04 ± 0.05 mm; p = 0.696). Intensive treatment also produced greater improvements in lipid parameters, including reductions in total cholesterol and apoB in both groups, and increased apoAI mainly in participants with LAP-defined steatosis, while glycemic, hepatic, and inflammatory markers remained largely unchanged. In this exploratory post-hoc analysis, LAP-defined hepatic steatosis identified RA patients with a more adverse cardiometabolic profile. An unadjusted association with subclinical vascular burden was observed but was attenuated after adjustment for established CV risk factors. Intensive CV risk management was associated with lower cIMT progression in patients without LAP-defined steatosis, while no clear vascular effect was observed in those with LAP-defined steatosis. No evidence of differential treatment effects according to LAP-defined steatosis was found.