Elevated Serum Levels of Visfatin in Patients with Henoch-Schönlein Purpura
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Background: Henoch-Schönlein purpura (HSP) is an immunecomplex-mediated disease predominantly characterizedby the deposition of circulating immune complexes containingimmunoglobulin A (IgA) on the walls of small vessels. Although the pathogenesis of HSP is not yet fully understood,some researchers proposed that B-cell activation might playa critical role in the development of this disease. Objective:To investigate the serum levels of visfatin (pre-B-cell colony-enhancing factor), B-cell-activating factor (BAFF), andCXCL13, and to analyze their association with diseaseseverity. Methods: The serum levels of visfatin, BAFF, andCXCL13 were measured by using a double-antibody sandwichenzyme-linked immunosorbent assay (ELISA) in 43patients with HSP and 45 controls. The serum levels of IgAanticardiolipin antibodies (ACA) were detected by using adouble-antigen sandwich ELISA. Results: Levels of visfatinbut not BAFF and CXCL13 were significantly elevated in thesera of patients with HSP in the acute stage, and restored tonormal levels in the convalescent stage. Furthermore, serumlevels of visfatin were significantly higher in patients withHSP having renal involvement than in those without renalinvolvement. Serum levels of visfatin were correlated withthe severity of HSP and serum concentration of ACA-IgA. Conclusion: We show for the first time that the serum levelsof visfatin are abnormally elevated in patients with HSP. Visfatin may be associated with the pathogenesis of HSP.
Abstract
Background: Henoch-Schönlein purpura (HSP) is an immunecomplex-mediated disease predominantly characterizedby the deposition of circulating immune complexes containingimmunoglobulin A (IgA) on the walls of small vessels. Although the pathogenesis of HSP is not yet fully understood,some researchers proposed that B-cell activation might playa critical role in the development of this disease. Objective:To investigate the serum levels of visfatin (pre-B-cell colony-enhancing factor), B-cell-activating factor (BAFF), andCXCL13, and to analyze their association with diseaseseverity. Methods: The serum levels of visfatin, BAFF, andCXCL13 were measured by using a double-antibody sandwichenzyme-linked immunosorbent assay (ELISA) in 43patients with HSP and 45 controls. The serum levels of IgAanticardiolipin antibodies (ACA) were detected by using adouble-antigen sandwich ELISA. Results: Levels of visfatinbut not BAFF and CXCL13 were significantly elevated in thesera of patients with HSP in the acute stage, and restored tonormal levels in the convalescent stage. Furthermore, serumlevels of visfatin were significantly higher in patients withHSP having renal involvement than in those without renalinvolvement. Serum levels of visfatin were correlated withthe severity of HSP and serum concentration of ACA-IgA. Conclusion: We show for the first time that the serum levelsof visfatin are abnormally elevated in patients with HSP. Visfatin may be associated with the pathogenesis of HSP.
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