| pubmed-article:15605661 | pubmed:abstractText | Although the precise pathophysiology of thrombosis is unknown in primary anti-phospholipid syndrome (PAPS), it is assumed that autoantibodies developed against endothelial cells and platelets might be one of the primary mechanisms. However, whether interaction between autoantibodies and endothelium leads to an impaired vasodilator response has not been investigated yet. In this study, we aimed to investigate the endothelial functions in patients with PAPS. Thirty-one patients with PAPS (22 female, nine male, mean age: 34.6+/-8.9 years) and 27 age- and sex-matched, healthy controls were included in the study. Brachial artery responses to reactive hyperaemia (endothelium-dependent dilatation) [EDD] and sublingual nitroglycerine (endothelium-independent dilatation) [EID] were measured by using high-resolution vascular ultrasound both in patients with PAPS and in the controls. The results were expressed as percentage of change in baseline values. Regarding cardiovascular risk factors, there was no significant difference between the two groups. EDD in patients with PAPS was significantly lower than those of controls (6.9+/-4.9 vs. 14.8+/-4.1%; p<0.0001). EID measurements were not significantly different between the groups. In the PAPS group, EDD in patients with arterial involvement (17 patients) was significantly lower than those of patients with venous involvement (12 patients) (4.6+/-3.9 vs. 7.4+/-4.1%; p = 0.02). This study showed that endothelial functions determined by using brachial artery ultrasound were impaired in patients with PAPS, and this was more prominent in the subgroup of patients with arterial involvement compared to patients with venous involvement. | lld:pubmed |
