Background: Behçet’s disease is a multisystem inflammatory disorder with a variable clinical course. This study evaluated the association between inflammatory indices, clinical involvement, and mortality. Methods: This retrospective study included 444 patients with BD. Clinical characteristics and laboratory data were systematically retrieved from electronic medical record system. Inflammatory indices (NLR, PLR, SII) were calculated to reflect systemic inflammation. In addition, CRP-based composite indices (IBI-NLR and IBI-SII) were derived to integrate cellular and acute-phase inflammatory responses. Disease manifestations, major organ involvement, comorbidities, and mortality were recorded to comprehensively assess disease burden and clinical outcomes. Results: In multivariable analysis, vascular involvement was associated with increased ESR level (OR = 1.013, 95% CI: 1.002–1.024, p = 0.018), and male sex (OR = 3.22, 95% CI: 1.83–5.67, p < 0.001;). ROC analysis showed the highest discriminatory performance for vascular involvement, with IBI-NLR (AUC = 0.624, p < 0.001), IBI-SII (AUC = 0.609, p = 0.001) and NLR (AUC = 0.597, p = 0.004). Moreover, NLR (AUC = 0.571, p = 0.017), IBI-NLR (AUC = 0.576, p = 0.010), and IBI-SII (AUC = 0.562, p = 0.036) had modest discrimination for major organ involvement. In contrast, inflammatory indexes were not predictive for mortality (p > 0.05 for all). Mortality was independently associated with higher creatinine (OR = 1.086, p = 0.048), higher ESR (OR = 1.023, p = 0.046), and lower uric acid levels (OR = 0.454, p = 0.002). Conclusions: Inflammatory indices may not predict mortality in BD but can help identify vascular and major organ involvement. Male sex and ESR level are associated more severe disease, while mortality is associated with renal dysfunction and systemic inflammation in BD.

Background: Behçet’s disease is a multisystem inflammatory disorder with a variable clinical course. This study evaluated the association between inflammatory indices, clinical involvement, and mortality. Methods: This retrospective study included 444 patients with BD. Clinical characteristics and laboratory data were systematically retrieved from electronic medical record system. Inflammatory indices (NLR, PLR, SII) were calculated to reflect systemic inflammation. In addition, CRP-based composite indices (IBI-NLR and IBI-SII) were derived to integrate cellular and acute-phase inflammatory responses. Disease manifestations, major organ involvement, comorbidities, and mortality were recorded to comprehensively assess disease burden and clinical outcomes. Results: In multivariable analysis, vascular involvement was associated with increased ESR level (OR=1.013, 95% CI: 1.002–1.024, p=0.018), and male sex (OR=3.22, 95% CI: 1.83–5.67, p<0.001;). ROC analysis showed the highest discriminatory performance for vascular involvement, with IBI-NLR (AUC=0.624, p 0.05 for all). Mortality was independently associated with higher creatinine (OR=1.086, p=0.048), higher ESR (OR=1.023, p=0.046), and lower uric acid levels (OR=0.454, p=0.002). Conclusions: Inflammatory indices may not predict mortality in BD but can help identify vascular and major organ involvement. Male sex and ESR level are associated more severe disease, while mortality is associated with renal dysfunction and systemic inflammation in BD.

Background and Objectives: Vitamin D deficiency is common in systemic lupus erythematosus (SLE) and Behçet’s disease (BD). However, whether it is associated with the same clinical parameters in both conditions remains unknown. Our objective is to compare the clinical correlates of serum 25-hydroxyvitamin D [25(OH)D] levels in patients with SLE and BD. Materials and Methods: This exploratory cross-sectional study included 38 patients with SLE and 32 with BD. Spearman’s correlation analyses, partial correlations controlling for sex, and tertile analyses were performed separately for each disease group. Results: Vitamin D deficiency [25(OH)D < 20 ng/mL] was similarly prevalent in SLE (64.9%) and BD (62.5%). However, distinct disease-specific correlation profiles were noted. In SLE, serum 25(OH)D levels were inversely correlated with body mass index (BMI) (r = −0.47, p = 0.003) and parathyroid hormone (PTH) (r = −0.40, p = 0.01), with no significant associations with inflammatory or haematological parameters. In patients with BD, 25(OH)D levels were positively correlated with haemoglobin (r = 0.63, p < 0.001), haematocrit (r = 0.58, p < 0.001), ferritin (r = 0.47, p = 0.008), uric acid (r = 0.48, p = 0.005), transferrin saturation (r = 0.45, p = 0.02), and triglycerides (r = 0.44, p = 0.01), while they were inversely correlated with total iron-binding capacity (r = −0.50, p = 0.01) and erythrocyte sedimentation rate (ESR) (r = −0.44, p = 0.01). After adjusting for sex, the association between 25(OH)D and haemoglobin remained significant (partial r = 0.43, p = 0.01), as did the associations with haematocrit (partial r = 0.42, p = 0.02) and triglycerides (partial r = 0.43, p = 0.02). In contrast, the correlations with ferritin, ESR, uric acid, and transferrin saturation were attenuated and no longer statistically significant. Tertile analyses demonstrated dose–response relationships between vitamin D levels and BMI (p = 0.01) and PTH (p = 0.008) in SLE, and between vitamin D levels and haemoglobin (p = 0.001) and ferritin (p = 0.02) in BD. Conclusions: Despite the similar prevalence of vitamin D deficiency, patients with SLE and BD exhibit distinct vitamin D-associated clinical profiles. Vitamin D status was primarily associated with metabolic parameters in SLE and haematological parameters in BD. These disease-specific patterns may reflect differences in the underlying inflammatory pathways and pathophysiological mechanisms involved.