Behçet's disease (BD) is a complex, relapsing multisystem disorder characterized by autoinflammatory features. Because disease-specific diagnostic biomarkers are lacking and clinical presentation varies according to geographic background and organ involvement, diagnosis may be delayed, particularly in non-endemic regions and in patients with atypical manifestations. Therapeutic management is highly individualized and guided by disease severity and dominant organ involvement. Severe, refractory, or organ-threatening disease often requires aggressive immunosuppressive treatment, including targeted biologic therapy with monoclonal anti-tumor necrosis factor (anti TNF) alpha agents such as infliximab and adalimumab. Therapeutic drug monitoring (TDM), based on serum trough drug concentrations and anti-drug antibodies, is routinely used to optimize anti-TNF therapy in inflammatory bowel disease and is increasingly discussed in other immune-mediated inflammatory diseases treated with monoclonal antibodies. In Behçet's disease, however, TDM is not yet standard practice, and Behçet-specific therapeutic trough targets for infliximab and adalimumab have not been validated. Nevertheless, integrating TDM with clinical assessment may support more individualized decision-making by helping distinguish insufficient drug exposure, immunogenicity, and pharmacodynamic failure. In this article, we discuss the rationale for TDM in anti-TNF-treated BD, summarize the current direct and indirect evidence, and propose a cautious, clinically guided approach. Behçet's disease; infliximab; adalimumab; anti-TNF therapy; therapeutic drug monitoring; trough levels; anti-drug antibodies; treatment optimization.

Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare antineutrophil cytoplasmic antibody-associated vasculitis that typically presents with asthma, eosinophilia and small-to-medium vessel inflammation. Central nervous system infarction is an uncommon complication and typically occurs during active disease. Recurrent stroke despite apparent disease remission is rare and presents a diagnostic challenge.We report a man in his 60s with EGPA who developed recurrent multifocal cerebral infarcts. His initial presentation occurred in the context of marked eosinophilia and systemic inflammation, consistent with active vasculitis. However, subsequent cerebrovascular events occurred despite well-suppressed eosinophil counts and inflammatory markers. His later course was complicated by pulmonary embolism, iliac vein thrombosis, nephrotic-range proteinuria and autoimmune serological abnormalities, raising suspicion of a superimposed prothrombotic state. Renal biopsy, performed in view of nephrotic syndrome and initial autoimmune serology, demonstrated neural epidermal growth factor-like 1 protein membranous glomerulonephritis-to our knowledge a previously unreported association with EGPA.This case highlights the complexity of stroke mechanisms in EGPA and emphasises the importance of reconsidering alternative or additional contributors when cerebrovascular events recur despite apparent disease control.

Behçet's disease (BD) is a chronic, multisystem vasculitis characterized by dysregulated immune responses and prominent Th1/Th17 polarization; however, the upstream epigenetic regulatory mechanisms driving this inflammatory imbalance remain incompletely understood. Here, we investigated the coordinated expression and diagnostic relevance of key long non-coding RNAs (lncRNAs; NEAT1 and MEG3) and microRNAs (miR-124 and miR-146a), and their association with IL-17/IL-6-mediated inflammation in BD. In a case-control study, serum levels of the selected non-coding RNAs were quantified by quantitative real-time PCR, while cytokine concentrations were measured using ELISA, complemented by bioinformatic interaction analysis and integrated statistical and machine learning approaches. Patients with BD exhibited marked downregulation of NEAT1, MEG3, miR-124, and miR-146a (p < 0.0001), accompanied by significantly elevated IL-17 and IL-6 levels. Individually, biomarkers demonstrated strong discriminatory capacity (AUC 0.83-0.92), while combined panels further improved classification performance. Multivariate modeling identified these non-coding RNAs as independent predictors of BD, and machine learning analysis identified miR-146a and IL-17 as the most influential contributors to disease classification. Notably, selected biomarkers showed associations with specific clinical manifestations, supporting their potential clinical relevance. Bioinformatic analyses identified putative interactions between NEAT1 and miR-124/miR-146a, while MEG3 demonstrated independent diagnostic value without evidence of direct interaction with the investigated miRNAs. Collectively, these findings provide a hypothesis-generating framework for future mechanistic investigations and support the potential diagnostic value of the investigated biomarker panel, although validation in larger multicenter cohorts and disease-control populations is warranted.

Patients with autoimmune rheumatic diseases, particularly rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), experience excess cardiovascular risk that is not fully captured by conventional lipid measurements. In active RA, lower cholesterol may coexist with higher vascular risk, a pattern known as the lipid paradox. We propose that systemic inflammation can uncouple lipid concentration from lipoprotein function and organize the evidence along five mechanistic axes. Inflammatory cytokines, mainly interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), IL-1β, IL-17/IL-23 and type I interferons, remodel lipoprotein metabolism. High-density lipoproteins (HDL) lose protective functions and may become pro-inflammatory. Apolipoprotein-B particles are oxidized or otherwise modified, linking lipid metabolism to autoimmunity. Macrophage cholesterol imbalance and cholesterol crystals activate inflammasome pathways in experimental atherosclerosis, while immune-cell metabolic rewiring may amplify cytokine output; these mechanisms are treated as extrapolated when direct rheumatic-disease evidence is limited. The pathways converge on endothelial dysfunction and thrombo-inflammation. RA and SLE are the mechanistic anchors, whereas psoriatic disease, axial spondyloarthritis, systemic sclerosis, vasculitides and antiphospholipid syndrome are weighted by evidence category. Standard lipid panels may therefore underestimate risk in selected contexts, especially during active inflammatory disease.

The article describes a clinical case of Behcet's disease, manifested by recurrent aphthae in the oral cavity and genital ulcers. The disease occurred in childhood in the form of chronic recurrent aphthous stomatitis.