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• W2118084768 abstract "Both endothelial dysfunction and a proinflammatory state are present during the early stages of atherosclerosis. In this context, increased expression of cyclooxygenase-2 (COX-2) results in higher levels of vasoconstrictive and proinflammatory substances. The aim of this study was to investigate the influence of COX-2 activity on endothelial dysfunction associated with peripheral arterial disease (PAD).Brachial artery flow-mediated dilatation (BAFMD), endothelin and high-sensitivity C-reactive protein (hsCRP) levels, and the lipid profile were assessed in 40 patients with intermittent claudication. Of these, 20 were randomly assigned to a group in which they received the selective COX-2 inhibitor celecoxib for 1 week (Group 1), while the other 20 served as controls (Group 2).In Group 1, BAFMD increased significantly both 3 hours after the first dose of celecoxib (3.33+/-4.11 vs. 6.97+/-3.27%; P=.008) and 1 week after (3.33+/-4.11 vs. 7.09+/-4.40%; P=.001). The endothelin level decreased significantly in Group 1 (2.92+/-1.87 vs. 1.93+/-1.07 pg/ ml; P=.018), as did the levels of hsCRP (4.78+/-2.73 vs. 2.95+/-2.11 mg/l; P=.023) and low-density lipoprotein cholesterol (106.38+/-18.89 vs. 90.8+/-28.58 mg/dl; P=.019). In Group 2, none of these parameters changed significantly.COX-2 products contribute to endothelial dysfunction and an inflammatory state in PAD. This study's findings provide evidence that these phenomena are implicated in the initiation of atherosclerosis and could prove a new means of investigating alternative approaches to the treatment of early-stage disease." @default.
• W2118084768 created "2016-06-24" @default.
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• W2118084768 date "2009-08-01" @default.
• W2118084768 modified "2023-10-16" @default.
• W2118084768 title "Selective Cyclooxygenase-2 Inhibition Reduces Endothelial Dysfunction and Improves Inflammatory Status in Patients With Intermittent Claudication" @default.
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• W2118084768 doi "https://doi.org/10.1016/s1885-5857(09)72649-0" @default.
• W2118084768 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19706240" @default.
• W2118084768 hasPublicationYear "2009" @default.
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