Serum advanced glycation end products and glyoxalase-1 levels in Behçet's disease: a cross-sectional study.

Objectives

Behçet's disease (BD) is a chronic, systemic inflammatory disorder. Despite the presence of chronic inflammation in BD, a clear increase in atherosclerotic cardiovascular mortality has not been documented. However, chronic inflammation may contribute to atherogenesis through various pathways, including accelerated generation of advanced glycation end products (AGEs). The objective of this study was to assess serum AGEs, Nε-carboxymethyllysine (CML), and glyoxalase-1 (GLO1) levels in a cohort of individuals with BD.

Methods

This cross-sectional study comprised 81 patients with BD (mean age: 43±11 years; 51 men/30 women) and 56 control subjects (mean age: 52±11 years; 45 women/11 men). Serum concentrations of AGEs, CML, and GLO1 were assessed using enzyme-linked immunosorbent assay (ELISA).

Results

AGE levels in patients with BD were significantly higher than those in the control group (BD: median 555 [453-864] ng/L vs. controls: median 512 [430-557] ng/L; p=0.008). CML levels in patients with BD were also higher than those in controls (median 532 [443-694] ng/mL vs. median 360 [308-442] ng/mL; p<0.001). Moreover, GLO1 levels in patients with BD were significantly lower than those in controls (median 15 [13-22] ng/mL vs. median 21 [18-27] ng/mL; p<0.001). No significant differences were observed in AGEs, CML, or GLO1 levels in individuals with BD according to smoking status, BMI, colchicine, glucocorticoids, immunosuppressive therapies, or major organ involvement.

Conclusions

Elevated levels of advanced glycation end products and decreased glyoxalase-1 levels were observed in BD. This pattern suggests that the inflammatory process in BD may be associated with AGE accumulation and attenuation of protective antioxidant/dicarbonyl-detoxification pathways. Elevated AGEs may contribute to the pathogenesis of atherosclerosis in individuals with BD.