To evaluate plasma lipid peroxidation and enzymatic and non-enzymatic antioxidant systems in patients with Behçet's disease, plasma malondialdehyde levels and total antioxidant status, erythrocyte superoxide dismutase and whole blood glutathione peroxidase activities were studied in 15 patients with active disease and in 30 with inactive disease, and compared with 20 age-matched healthy control subjects. Plasma malondialdehyde levels were significantly higher in patients with active Behçet's disease than in patients with inactive disease, who had significantly higher levels than control subjects. The plasma total antioxidant status of both groups of patients was significantly lower than that of controls. Furthermore, whole blood glutathione peroxidase activity was significantly lower in patients with active versus inactive Behçet's disease. There were no significant differences in erythrocyte superoxide dismutase levels between the groups. In conclusion, there is an increase in oxidative stress in Behçet's disease. Despite this stress, the antioxidant system is deficient and inadequate, especially in patients who are in an active phase of the disease.

No abstract

We conclude that changes in parameters associated with oxidative stress such as NO-related processes, activities of antioxidant enzymes in the bloodstream and erythrocytes and total plasma antioxidant capacity are involved in the aetiopathogenesis of the vasculitis seen in BD.

SUMMARYVasoactive intestinal polypeptide (VIP) contributes to the regulation of coronary vasomotor tone and circulating levels of VIP have been reported to increase during acute myocardial infarction. However, the changes in VIP concentration during exercise-induced ischemia have not been studied yet. Therefore, we sought to determine whether circulating levels of VIP change during treadmill exercise testing and whether they could be used as a marker of exercise-induced myocardial ischemia. Twenty-nine subjects with definitive positive (group-I) and 20 subjects (group-II) with negative results on treadmill exercise testing were included in this study. In order to assess circulating levels of VIP, blood samples were collected in both groups before exercise, at 5 minutes of exercise, at peak exercise, and at 10 minutes in the recovery period. There were no differences between the two groups with respect to the baseline demographics of age, sex, heart rate, or blood pressure. The metabolic equivalents (METs) values, peak heart rate achieved, peak systolic-diastolic blood pressure, and exercise duration did not differ between the two groups. No significant differences were found in the circulating levels of VIP at any stage of the exercise between the two groups (10.5 ± 2.5 versus 11.0 ± 3.5 pmol/L, P = 0.5, 10.6 ± 2.3 versus 10.6 ± 3.3 pmol/L, P = 0.9, 10.9 ± 3.1 versus 11.5 ± 3.4 pmol/L, P = 0.5, and 10.7 ± 1.8 versus 11.7 ± 4.1 pmol/L, P = 0.3, respectively).There was no relationship between the circulating level of VIP and exercise-induced myocardial ischemia, and therefore it could not be used as a marker of exercise-induced myocardial ischemia. (Int Heart J 2005; 46: 363-371)