Serum leptin concentration is increased in patients with Behçet's syndrome and is correlated with disease activity.

UNLABELLED: Background Behçet's syndrome is a systemic, relapsing immuno-inflammatory disease with a generalized vasculitis of the microvasculature endothelial dysfunction. Leptin, a recently discovered neuroendocrine hormone, is a metabolic peptide that appears to be involved. Serum proinflammatory cytokines upregulate leptin levels and leptin itself directly induces nitric oxide production from endothelial cells with its specific receptors.
OBJECTIVES: To detect changes of serum leptin concentrations in patients with Behçet's syndrome compared with age- and sex-matched healthy volunteers by using enzyme-linked immunosorbent assay. We also investigated whether disease activity or the duration of Behçet's syndrome correlates with leptin concentration.
METHODS: Thirty-five consecutive patients with Behçet's syndrome (41.2 +/- 8.4 years, 16 male, 19 female) and 20 age- and sex-matched healthy control subjects (40.4 +/- 10.91 years, nine male, 11 female) were included in this study. The body mass index (BMI) [weight (kg) height(-1) (m(2))] was calculated for subjects at study enrollment. We measured serum leptin with a leptin enzyme immunoassay kit, and acute-phase reactants, including erythrocyte sedimentation rate, alpha1-antitrypsin, alpha 2-macroglobulin and neutrophil count. The Mann-Whitney U-test was used for statistical analysis and P < 0.05 was considered significant. Values were expressed as mean +/- SD.
RESULTS: The gender ratio, age and BMI were not substantially different among Behçet's patients and controls. The mean serum leptin concentrations in patients with Behçet's syndrome (16.8 +/- 7.49 ng mL(-1)) were significantly (P < 0.001) higher than in healthy control volunteers (7.5 +/- 2.77 ng mL(-1)). Active Behçet's patients had significantly (P = 0.001) higher leptin concentrations (20.5 +/- 7.99 ng mL(-1)) when compared with patients in inactive periods (12.8 +/- 4.43 ng mL(-1)). In addition, patients with longer disease duration (mean, 20.1 +/- 5.15 years) had also significantly (P = 0.013) higher leptin concentrations (20.2 +/- 8.52 ng mL(-1)) than those with shorter disease duration (13.4 +/- 4.52 ng mL(-1)) (mean, 7.4 +/- 3.29 years). All acute-phase reaction parameters were found to be significantly (for each, P < 0.01) increased in active disease.
CONCLUSIONS: Leptin may have a role in modulating endothelial function and may be involved in mechanisms for vessel endothelium repair, during an exacerbation as well as in chronic disease.