Thrombosis and Haemostasis, Table of Contents Thromb Haemost 2006; 96(04): 391-392DOI: 10.1160/TH06-08-0502 Theme Issue Editorial Focus Schattauer GmbH COX-2 inhibitors and the thrombotic risk Karsten Schrör Institut für Pharmakologie und Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany , Artur-Aron Weber Institut für Pharmakologie und Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany › Author Affiliations Recommend Article Abstract Buy Article Full Text References References 1 Morham SG. et al. Prostaglandin synthase 2 gene disruption causes severe renal pathology in the mouse. Cell 1995; 83: 463-82. 2 Langenbach R. et al. Prostaglandin synthase1 gene disruption in mice reduces arachidonic acid-induced inflammation and indomethacin-öinduced gastric ulceration. Cell 1995; 83: 483-92. 3 McAdam BF. et al. Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2 - the human pharmacology of a selective inhibitor of COX-2. Proc Natl Acad Sci USA 1999; 96: 272-7. 4 FitzGerald GA. et al. Prostacyclin biosynthesis is increased in patients with severe atherosclerosis and platelet activation. N Engl J Med 1984; 310: 1065-8. 5 Belton O. et al. Cyclooxygenase-1 and -2-dependent prostacyclin formation in patients with atherosclerosis. Circulation 2000; 102: 840-5. 6 Cheng Y. et al. Role of prostacyclin in the cardiovascular response to thromboxane A2. Science 2002; 296: 539-41. 7 Grosser T. et al. Biological basis for the cardiovascular consequences of COX-2 inhibition: therapeutic challenges and opportunities. J Clin Invest 2006; 116: 4-15. 8 Grosser T. The pharmacology of selective inhibition of COX-2. Thromb Haemost 2006; 96: 393-400. 9 Marwali MR, Mehta JL. COX-2 inhibitors and cardiovascular risk. Inferences based on biology and clinical studies. Thromb Haemost 2006; 96: 401-6. 10 Mukherjee D. Does a coxib-associated thrombotic risk limit the clinical use of the compounds as analgesic anti-inflammatory drugs? Arguments in favor. Thromb Haemost 2006; 96: 407-12. 11 Weber A-A. et al. Does a coxib-associated thrombotic risk limit the clinical use of the compounds as analgesic anti-inflammatory drugs? Arguments against. Thromb Haemost 2006; 96: 413-6. 12 Helin-Salmivaara A. et al. NSAID use and the risk of hospitalization for first myocardial infarction in the general population: a nationwide case-control study in Finnland. Eur Heart J 2006; 27: 1657-63. 13 Kearney PM. et al. Do selective cyclo-oxygenase-2 inhibitors and traditional nonsteroidal anti-inflammatory drugs increase the risk of atherothrombosis? Metaanalysis of randomised trials. Br Med J 2006; 332: 1302-8. 14 Trebino CE. et al. Impaired inflammatory and pain responses in mice lacking an inducible prostaglandin E synthase. Proc Natl Acad Sci USA 2003; 100: 9044-9. 15 Wu KK. Transcription-based COX-2 inhibition: a therapeutic strategy. Thromb Haemost 2006; 96: 417-22. 16 Saunders MA. et al. Selective expression of C/EBPß binding and COX-2 promoter activity by sodium salicylate in quiescent human fibroblasts. J Biol Chem 2001; 276: 18897-904. 17 Cieslik K. et al. Salicylate suppresses macrophage nitric oxide synthase-2 and cyclooxygenase-2 expression by inhibiting CCAAT/enhancer-binding protein-beta binding via a common signaling pathway. J Biol Chem 2002; 277: 49304-10. 18 Curfman GD. et al. Expression of concern: Bombardier et al., “Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis”. N Engl J Med 2000; 343: 1520-8. N Engl J Med 2005; 3563: 2813–4. 19 Bombardier C. et al. Response to expression of concern regarding VIGOR study. N Engl J Med 2006; 354: 1196-9. 20 Heim H-K, Broich K. Selective COX-2 inhibitors and risk of thromboembolic events - regulatory aspects. Thromb Haemost 2006; 96: 423-32. 21 Schrör K. et al. Cardiovascular risk of selective cyclooxygenase-2 inhibitors. J Cardiovasc Pharmacol Ther 2005; 10: 95-101.
