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Similar graphs were generated for ICAM, fibrinogen and homocysteine. Given the relatively low incidence of VTE in this study, investigation of a correlation between VTE and markers of endothelial stress and coagulation was not possible. Treatment and laboratory data were available for 32 patients. Overall, 23 patients (72%) received the pulsed schedule of dexamethasone and http://www.selleckchem.com/products/loxo-101.html 9 (28%) received the weekly schedule; 1 patient with baseline data only was not included (Fig?3). Compared with the weekly schedule, the pulsed schedule was associated with significantly greater variation in mean adjusted relative marker values for the following markers: fibrinogen (SD 0��42 vs. 0��26); P�Cselectin (SD 0��45 vs. 0��23); and VEGF (SD 0��69 vs. 0��35; P? http://www.selleckchem.com/products/abc294640.html dexamethasone required dose reductions for expected toxicity associated with this agent and this may have confounded the results. This study is one of the most comprehensive assessments to-date of markers of coagulation and endothelial stress in patients with MM treated with lenalidomide and dexamethasone and provides novel insights into the mechanism of VTE in this setting. Our main findings suggest that the schedule of dexamethasone influences the level of endothelial stress and that the conventional, pulsed schedule of dexamethasone induces a greater degree http://www.selleck.cn/products/ON-01910.html of endothelial injury than the weekly schedule. This effect may contribute to the increase in risk of VTE seen with pulsed administration of dexamethasone when given in combination with lenalidomide. Fig?5 illustrates possible mechanisms by which the combination of lenalidomide and dexamethasone may contribute to endothelial injury in MM patients and so activate other putative downstream effects that could lead to thrombosis. Lenalidomide and dexamethasone are likely to have direct and indirect effects on endothelial cells that could stimulate production of endothelial stress markers (e.g. ICAM and PAI-1) and pro-angiogenic factors, such as VEGF. Treatment may also induce the coagulation cascade, leading to increases in fibrinogen, P-selectin and homocysteine, which may in turn contribute to a hypercoagulable state beyond the pro-thrombotic effects of the disease itself.