Vascular endothelial function and oxidative stress mechanisms in patients with Behcet's syndrome

Citation
Jc. Chambers et al., Vascular endothelial function and oxidative stress mechanisms in patients with Behcet's syndrome, J AM COL C, 37(2), 2001, pp. 517-520
Citations number
15
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
37
Issue
2
Year of publication
2001
Pages
517 - 520
Database
ISI
SICI code
0735-1097(200102)37:2<517:VEFAOS>2.0.ZU;2-F
Abstract
OBJECTIVES We sought to test the hypothesis that vascular endothelial funct ion is impaired in Behcet's syndrome and reflects increased levels of oxida tive stress. BACKGROUND Behcet's syndrome is a multisystem inflammatory disorder commonl y complicated by vascular thrombosis and arterial aneurysm formation. The p recise mechanisms underlying vascular disease in Behcet's syndrome are not known. METHODS We studied 19 patients with Behcet's syndrome (18 to 50 years old, 9 men) and 21 healthy volunteers (18 to 50 years old, 10 men). Brachial art ery flow-mediated dilation (endothelium-dependent), and nitroglycerin (NTG) -induced dilation (endothelium-independent) were measured. To investigate o xidative stress mechanisms, vascular studies were repeated 1 h alter admini stration of vitamin C (1 g, intravenous) in 12 patients and 12 control subj ects. RESULTS Flow-mediated dilation was reduced in patients with Behcet's syndro me as compared with control subjects (0.7 +/- 0.9% vs. 5.7 +/- 0.9%, p = 0. 001). In contrast, there were no significant differences in the brachial ar tery diameter (4.2 +/- 0.2 vs. 4.0 +/- 0.2 mm, p = 0.47) or NTG-induced dil ation (19.7 +/- 1.9% vs. 19.7 +/- 1.2%, p = 0.98). In regression analysis, Behcet's syndrome was associated with impaired flow-mediated dilation indep endent of age, gender, brachial artery diameter, blood pressure, cholestero l and glucose. Vitamin C increased flow-mediated dilation in Behcet's syndr ome (0.2 +/- 0.7% to 3.5 +/- 1.0%, p = 0.002), but not in control subjects (4.3 +/- 0.6% to 4.7 +/- 0.4%, p = 0.51). In both groups, NTG-induced dilat ion and brachial artery diameter were unchanged after vitamin C treatment. CONCLUSION Vascular endothelial function is impaired in Behcet's syndrome a nd can be rapidly improved by vitamin C treatment. Our results support a ro le for oxidative stress in the pathophysiology of Behcet's syndrome and pro vide a rationale for therapeutic studies aimed at reducing vascular complic ations in this disorder.