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1 an intravenous infusion of either placebo or drotrecogin alfa activated (24 microg per kilogram of bo
2 idence of serious bleeding was higher in the drotrecogin alfa activated group than in the placebo gro
6 We report for the first time on the use of drotrecogin alfa activated in six lung transplant recipi
9 3 trial, we assessed whether treatment with drotrecogin alfa activated reduced the rate of death fro
11 ely defined primary analysis, treatment with drotrecogin alfa activated was associated with a reducti
13 Food and Drug Administration (FDA) approved drotrecogin alfa (activated) (DrotAA) for adults who had
14 istics and outcomes of patients treated with drotrecogin alfa (activated) (DrotAA) in clinical practi
16 of recombinant human activated protein C, or drotrecogin alfa (activated) (DrotAA), for the treatment
20 the magnitude of the treatment benefit with drotrecogin alfa (activated) across the underlying predi
22 e report observed 28-day mortality rates for drotrecogin alfa (activated) and placebo patients for su
23 ent Food and Drug Administration approval of drotrecogin alfa (activated) and the potential of severa
24 Hospital mortality was reduced by 18% with drotrecogin alfa (activated) compared with controls (rel
33 s for experimental and analytical studies of drotrecogin alfa (activated) in adults with severe sepsi
34 , and actual mortality rates were lower with drotrecogin alfa (activated) in all subgroups defined by
35 ts, provides evidence to support the role of drotrecogin alfa (activated) in modulating nuclear facto
36 ger absolute risk reductions were found with drotrecogin alfa (activated) in patients with a higher b
37 er the first 28 days (short-term Base Case), drotrecogin alfa (activated) increased the costs of care
38 ected to lifetime (lifetime Reference Case), drotrecogin alfa (activated) increased the costs of care
39 articipated in placebo-controlled studies of drotrecogin alfa (activated) infusion before an intraven
40 ed as an example of the protective effect of drotrecogin alfa (activated) on endothelial and mononucl
43 ious bleeding or thrombotic event rates with drotrecogin alfa (activated) treatment between heterozyg
44 zygous carriers and non-Leiden carriers with drotrecogin alfa (activated) treatment were 20.3% and 24
46 spital mortality for single-group studies of drotrecogin alfa (activated) was 41% (95% CI 35-48), and
50 Metaregression showed greater benefits of drotrecogin alfa (activated) with increasing control mor
51 propose a broad anti-inflammatory effect of drotrecogin alfa (activated), acting on both endothelium
52 stasis, and activated recombinant protein C, drotrecogin alfa (activated), has been shown to reduce m
58 from recombinant human activated protein C (drotrecogin alfa [activated]) as non-factor V Leiden car
61 d ENHANCE (a single-arm, open-label study of drotrecogin alfa [activated]) studies are reported here.
66 rial, recombinant human activated protein C (drotrecogin alfa) reduced mortality in patients with sev
67 al antibiotics, early goal-directed therapy, drotrecogin alfa, steroids, intensive insulin therapy, a
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