Objective: Behçet's disease (BD) is a chronic multisystem vasculitis characterized by endothelial dysfunction and vascular inflammation. Asprosin is a recently identified adipokine implicated in endothelial injury and proinflammatory signaling. This study aimed to investigate serum asprosin concentrations in patients with BD and their relationship with disease activity and major clinical manifestations. Methods: This cross‐sectional case–control study enrolled 49 patients who fulfilled the International Criteria for Behçet's Disease and 48 healthy controls. Disease activity was stratified as mild, moderate, or severe based on organ involvement using Yosipovitch's Behçet's Disease Classification. Serum asprosin levels were quantified using an enzyme‐linked immunosorbent assay. Associations among asprosin levels, disease activity, clinical manifestations, and inflammatory markers were analyzed. Results: Serum asprosin concentrations were markedly elevated in individuals with Behçet's disease relative to healthy controls [12.18 (8.27–16.76) vs. 6.12 (4.76–8.61) ng/mL, p < 0.001] and increased incrementally as disease activity intensified ( p < 0.001). Patients with vascular involvement and uveitis demonstrated markedly elevated asprosin levels compared to patients without these manifestations ( p < 0.01). Correlation analysis revealed a strong positive association between serum asprosin levels and disease activity ( r = 0.821, p < 0.001), and a moderate correlation with C‐reactive protein (CRP) levels ( r = 0.431, p = 0.002). In multivariate analysis, both disease activity and CRP levels were independently associated with serum asprosin concentrations. Conclusion: Serum asprosin levels are elevated in BD and closely associated with disease activity, systemic inflammation, and major organ involvement, particularly vascular manifestations and uveitis. Asprosin may represent a potential biomarker of the inflammatory and vascular burden in BD.

This study aimed to investigate the roles of cytokines and other laboratory parameters in determining the need for intensive care in COVID-19 patients. This is a retrospective observational study. Demographic, clinical, and laboratory parameters of the patients were evaluated. Thirteen cytokines were measured along with baseline laboratory tests at admission and at 48-hour intervals: IL-1β, IFN-α, IFN-β, TNF-α, MCP-1, IL-6, IL -8, IL-10, IL-2p70, IL-17A, IL-18, IL-23, and IL-33. COVID-19 was confirmed by PCR in 116 hospitalized patients. The mean age was 55.3 ± 16.4 years. Seventy-four (63.8%) of the patients were male and 42 (36.2%) were female. Twenty-two (18.9%) patients (16 male, 6 female) were transferred to the intensive care unit. A significant increase in white blood cell (WBC), neutrophil (Neu) and lymphocyte (Lym) counts, Neu/Lym ratio (NLR), lactate dehydrogenase (LDH), INR (international normalized ratio), activated prothrombin time (aPTT), D-dimer (D-D), troponin (Trop), Pro-BNP (BNP), procalcitonin (PCT), ferritin (Fer), and alanine aminotransferase (ALT) values were observed in those requiring intensive care. A significant decrease was found in albumin (Alb) levels and Lym counts. Alb levels appeared to be protective against admission to intensive care. Except for IFN- α, IL-23, and IL-33, the baseline values of other cytokines were above the threshold values. MCP-1 and IL-6 were higher in patients requiring intensive care. High NLR and LDH and low Alb levels, especially with an increase in MCP-1 and IL-6, were found to be the best predictors of a serious COVID-19 infection.

Aim:Psoriatic arthritis (PsA) is expected to cause an increased risk of scoliosis because it affects the axial skeleton asymmetrically. In this study, we compared the frequency of scoliosis in PsA patients with that in healthy controls (HC) and axial spondyloarthritis (axSpA) patients. Thus, we aimed to explore whether scoliosis might be a clinical feature of PsA and to assess its potential role in differentiating PsA from axSpA. Material and Methods:The study included 60 PsA patients, 60 axSpA patients and 40 HC. All individuals in the study were assessed for the presence of scoliosis by physical examination. Scoliosis radiography was performed in those with a positive scoliosis test on physical examination. The Cobb angle was measured using the appropriate method. A two-tailed significance level of 0.05 was considered in all analyses. Results:Within this research, the frequency of scoliosis in PsA patients was compared with the axSpA and HC groups. The Cobb angle value was notably higher in the PsA group compared to axSpA and HC (p=0.006 and p=0.007, respectively). On physical examination, scoliosis findings and coronal spinal curvature, were observed at elevated rates in the PsA group relative to the other two groups (p>0.05 for all, indicating no statistical significance). Scoliosis was more frequent in the PsA group than in the axSpA group (p=0.046). All scoliosis cases in PsA were mild or moderate in severity. Conclusion:Both the frequency of scoliosis and Cobb angle values were greater in PsA than those in axSpA. This outcome may be associated with the asymmetric involvement of lateral spinal structures typical of PsA. Overall, these results indicate that scoliosis could serve as a supportive marker for PsA and may aid in differentiating PsA from axSpA.

Objective: The aggregate index of systemic inflammation (AISI) is a recently introduced composite inflammatory marker derived from neutrophil, monocyte, lymphocyte, and platelet counts. This study aimed to evaluate AISI values in patients with Behçet’s disease (BD), compare them with healthy controls, and investigate their association with disease activity assessed by the BD Current Activity Form (BDCAF). Methods: This observational cross-sectional study enrolled 104 patients with BD and 82 age- and sex-matched healthy individuals. Demographic, clinical, and laboratory data were recorded. The AISI was determined according to the following formula: neutrophil Å~monocyte Å~ platelet / lymphocyte count. Disease activity was assessed using BDCAF. To assess the relationships between variables and determine whether AISI was independently associated with disease activity, correlation analysis, receiver operating characteristic (ROC) analysis, and multivariable linear regression analysis were performed. Results: The AISI was significantly positively correlated with BDCAF scores (ρ = 0.630, P < .001). ROC analysis demonstrated that AISI showed discriminative ability between patients with BD and healthy controls within this cohort (area under the curve = 0.871, 95% CI: 0.818-0.918), with a sensitivity of 74.0% and specificity of 86.6%. Moreover, in multivariable linear regression analysis, higher AISI values remained independently associated with higher BDCAF scores after adjustment for age and sex (β = 0.0044, 95% CI: 0.003-0.006, P < .001). Conclusion: The AISI is significantly associated with inflammatory burden and disease activity in BD. As a readily available hematological index, it may serve as a complementary marker for the assessment of systemic inflammation. Prospective longitudinal studies are needed to determine its clinical applicability.

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease associated with increased cardiometabolic risk. Adipokines are implicated in inflammation and metabolic dysregulation in RA; however, clinical data on serum asprosin, a novel glucogenic adipokine, remain limited. This study aimed to evaluate serum asprosin levels in patients with RA and to assess their relationship with disease activity. In this single-center, cross-sectional observational study conducted between June and August 2025, 42 patients with RA and 40 control participants were included. Serum asprosin levels were measured using enzyme-linked immunosorbent assay (ELISA). Disease activity was assessed using the Disease Activity Score in 28 joints, based on the erythrocyte sedimentation rate (DAS28-ESR). Associations between asprosin levels and clinical, laboratory, and serological parameters were analyzed. Serum asprosin levels differed significantly between patients with RA and control participants, with median (interquartile range) values of 12.43 (9.98) and 9.96 (3.47) ng/mL, respectively ( P = .025); however, this association was no longer statistically significant after adjustment for age, sex, BMI, smoking status, and comorbidity in a multivariable regression model (adjusted P = .986). No significant correlations were observed between asprosin and DAS28-ESR, CRP, ESR, RF, or anti-CCP. ROC analysis demonstrated limited discriminatory performance (AUC = 0.643; 95% CI: 0.52–0.767; P = .02). Serum asprosin levels differed between patients with RA and control participants in unadjusted analysis; however, this difference was not retained after adjustment for potential confounders, and no significant association with disease activity or inflammatory markers was identified. These findings suggest that serum asprosin may have limited clinical utility as a standalone biomarker in RA. Further prospective studies with larger sample sizes are needed to clarify the potential role of asprosin in RA pathophysiology.