Increased levels of inflammatory mediators in lung cancer and their modulation by oral anticoagulant treatment
Bildiriler > Özet Bildiri
Yazarlar: D. A. Hoppensteadt, A. Ciftci, M. Demir, G. Altiay, M. Tobu, O. Iqbal, D. Fareed, R. Bick, J. Fareed
Journal of Clinical Oncology, , , Uluslararası, Özet Bildiri, Wos, cilt 24, ss 17050-17050
DOI: 10.1200/jco.2006.24.18_suppl.17050
Özet
17050 Background: Venous thromboembolic events (VTE) are associated with lung cancer and significantly contributes to the increased mortality in these patients. While the increased prevalence of VTE is fully recognized in lung cancer, its pathogenesis is not fully understood. Even the patients undergoing therapeutic interventions are at high risk to develop VTE. These patients provide a unique clinical setting to investigate the pathogenesis of lung cancer associated thrombosis. Methods: In a prospective, randomized, controlled study patients with inoperable lung cancer (n = 100) were randomized to receive chemotherapy, radiation and warfarin (INR 1.5–2.5) or chemotherapy, radiation without warfarin (n = 50). Blood samples were drawn prior to and after the second treatment cycle with warfarin. All samples were analyzed for tumor necrosis factor alpha (TNF α), CD 40 ligand (CD 40L), C-reactive protein (CRP), interleukin 1 beta (IL-1β), asymmetric dimethylarginine (ADMA) and nitric oxide (NO). Results: Summarized in the table given below. All of the surrogate markers of inflammation showed a decreased trend (13–50%) in the warfarin treated group, whereas the non-warfarin treated group exhibited an increase (18–46%) in all markers except CRP and ADMA. Conclusions: The levels of various inflammatory markers are upregulated in lung cancer suggesting a pathogenic role of this process in lung cancer. Warfarin down regulated the inflammatory process in contrast to the non-warfarin treated group. The clinical relevance of these observations require additional analysis. [Table: see text] No significant financial relationships to disclose.