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1                                              rFVIIa (80 microg/kg) significantly reversed warfarin ef
2 ic events occurring in patients administered rFVIIa.
3              However, these parameters after rFVIIa treatment were not significantly different from p
4           However, in the 24-hr period after rFVIIa administration, blood loss (p = .140) and transfu
5 ing episodes treated with a bypassing agent (rFVIIa or aPCC), FVIII, or DDAVP among 501 registered pa
6   The effects of warfarin (experiment 1) and rFVIIa (5-80 microg/kg; experiment 2) were evaluated.
7 Analysis of the relationship between AEs and rFVIIa is hindered by concomitant medications, preexisti
8 ed patients with a similar incidence between rFVIIa (2.9%) and aPCC (4.8%).
9         Bleeding control was similar between rFVIIa and aPCC (93.0%; P = 1).
10 philia therapy and that FVII displacement by rFVIIa is a negligible mechanistic component.
11  FFP :PRBC transfusion, and in severe cases, rFVIIa.
12 , 0.03 [95% CI, 0.01 to 0.06]) and high-dose rFVIIa use (RD, 0.06 [CI, 0.01 to 0.11]).
13 romboembolism was increased with medium-dose rFVIIa use (risk difference [RD], 0.03 [95% CI, 0.01 to
14   On the basis of this preliminary evidence, rFVIIa may be beneficial for treating bleeding after car
15     We established a dose-response curve for rFVIIa that is useful to explain dosing strategies.
16 o 14%]) were the most common indications for rFVIIa use.
17                A total of 431 AE reports for rFVIIa were found, of which 168 reports described 185 th
18                    Recombinant factor FVIIa (rFVIIa) is used as a hemostatic agent to treat bleeding
19 pharmacological effect of recombinant FVIIa (rFVIIa) in hemophilia patients.
20 hy and its treatment with recombinant FVIIa (rFVIIa).
21 onths posthepatocyte transplantation, higher rFVIIa doses were required, suggesting loss of transplan
22 e sepsis were associated with an increase in rFVIIa requirement.
23 ized to receive placebo (n=68), 40 microg/kg rFVIIa (n=35), or 80 microg/kg rFVIIa (n=69).
24  40 microg/kg rFVIIa (n=35), or 80 microg/kg rFVIIa (n=69).
25 ture dose optimization and evaluation of new rFVIIa analogs currently under development.
26 ief discussion of the mechanism of action of rFVIIa and its role in facilitating hemostasis and a rev
27  experiments, we conclude that the action of rFVIIa at pharmacologic doses is dominated by the TF-dep
28                  The mechanisms of action of rFVIIa have also been interesting and have provided insi
29 ive care unit (ICU) to the administration of rFVIIa and for the following 24 hrs.
30 Safe, rapid, and effective administration of rFVIIa corrects critically prolonged INRs and can avert
31 ed in the period after the administration of rFVIIa.
32 rtually absent at pharmacological amounts of rFVIIa.
33 terns raise concern about the application of rFVIIa to conditions for which strong supporting evidenc
34 estigate the safety and possible benefits of rFVIIa in patients who bleed after cardiac surgery.
35 ramatically up-regulated by a combination of rFVIIa and factor F(X) in malignant melanoma.
36 value were given three successive dosages of rFVIIa (5, 20, and 80 micrograms/kg) during a 3-week per
37                             A single dose of rFVIIa was sufficient to fully prevent the development o
38 r from that of FVIII-/- mice, and 3 doses of rFVIIa partly protected against hemophilic synovitis in
39 control requires supraphysiological doses of rFVIIa, posing both high expense and uncertain thromboti
40 and after administration of varying doses of rFVIIa.
41 s study was to evaluate the effectiveness of rFVIIa in nonbleeding volunteer patients with the coagul
42 phase 1 trial assessed safety and effects of rFVIIa in reversing warfarin-induced changes in bleeding
43 eded to establish the safety and efficacy of rFVIIa in patients without hemophilia.
44 l were used to provide national estimates of rFVIIa use.
45 thway to reconcile the 2 major mechanisms of rFVIIa action, a necessary step to understanding future
46  body weight (276 patients), or 80 microg of rFVIIa per kilogram (297 patients) within 4 hours after
47 with 18% in the group receiving 20 microg of rFVIIa per kilogram (P=0.09) and 11% in the group receiv
48  P=0.08) in the group receiving 20 microg of rFVIIa per kilogram and by 3.8 ml (95% CI, 0.9 to 6.7; P
49 eceive placebo (96 patients) or 40 microg of rFVIIa per kilogram of body weight (108 patients), 80 mi
50 receive placebo (268 patients), 20 microg of rFVIIa per kilogram of body weight (276 patients), or 80
51                  Treatment with 80 microg of rFVIIa per kilogram resulted in a significant reduction
52 oup, 26% in the group receiving 20 microg of rFVIIa per kilogram, and 29% in the group receiving 80 m
53 iven 40 microg, 80 microg, and 160 microg of rFVIIa per kilogram, respectively (P=0.01 for the compar
54 frequent in the group receiving 80 microg of rFVIIa than in the placebo group (9% vs. 4%, P=0.04).
55 nts who were given 40, 80, and 160 microg of rFVIIa, respectively (P=0.004 for the comparison of the
56 erebral infarction, occurred in 7 percent of rFVIIa-treated patients, as compared with 2 percent of t
57 y and rapidly in all patients, regardless of rFVIIa dose (range, 15 to 90 microg/kg of body weight).
58 021 showed an effect comparable with that of rFVIIa.
59 es and abstracts to identify clinical use of rFVIIa for the selected indications and identified all r
60 orted thromboembolic AEs followed the use of rFVIIa for unlabeled indications and occurred in arteria
61          From 2000 to 2008, off-label use of rFVIIa in hospitals increased more than 140-fold, such t
62  other publications have examined the use of rFVIIa in related conditions such as traumatic brain inj
63                             Off-label use of rFVIIa in the hospital setting far exceeds use for appro
64  the recent medical literature on the use of rFVIIa in trauma patients, including current guidelines
65                       Indications for use of rFVIIa included an INR greater than 10 in high-risk pers
66 oke, in those patients randomized to receive rFVIIa.
67 -line hemostatic agent, 174 (56.7%) received rFVIIa, 63 (20.5%) aPCC, 56 (18.2%) FVIII, and 14 (4.6%)
68 n postlicensure clinical trials who received rFVIIa.
69 e propagation phase in hemophilia A required rFVIIa concentrations above the range where a physiologi
70                  When used as a last resort, rFVIIa was safe but not incrementally efficacious over c
71                 This preliminary trial shows rFVIIa to be effective in transiently reversing the prol
72 rent explanations for the supraphysiological rFVIIa dosing requirement: (1) the need to overcome comp
73             These data strongly suggest that rFVIIa acts independently of TF in hemophilia therapy an
74 ma (p = .063) were not different between the rFVIIa and control groups.
75 ization, significantly fewer patients in the rFVIIa group underwent a reoperation as a result of blee
76                                       In the rFVIIa group, which also received conventional hemostati
77 boembolic complications were observed in the rFVIIa group.
78  more critical serious adverse events in the rFVIIa groups.
79 reased more in the placebo group than in the rFVIIa groups.
80 bo, as compared with 18 percent in the three rFVIIa groups combined (P=0.02).
81 ely (P=0.004 for the comparison of the three rFVIIa groups with the placebo group).
82 vely (P=0.01 for the comparison of the three rFVIIa groups with the placebo group).
83 ntribute simultaneously and independently to rFVIIa-driven thrombin generation in FVII-deficient huma
84 the use of recombinant-activated factor VII (rFVIIa) as an adjunct for reversal of coagulopathy in tr
85 gests that recombinant activated factor VII (rFVIIa) can decrease intractable bleeding in patients af
86 ne whether recombinant activated factor VII (rFVIIa) can reduce hematoma growth after intracerebral h
87            Recombinant activated factor VII (rFVIIa) is a non-plasma-derived, rapid-acting, and rapid
88 y in which recombinant activated factor VII (rFVIIa) reduced growth of the hematoma and improved surv
89 rement for exogenous recombinant factor VII (rFVIIa) to approximately 20% of that before cell transpl
90 fficacy of recombinant activated factor VII (rFVIIa) used as the last resort for refractory bleeding
91 ilic agent recombinant activated factor VII (rFVIIa).
92 ent introduction of recombinant factor VIIa (rFVIIa) has been a welcome addition to the pharmacologic
93                     Recombinant factor VIIa (rFVIIa) is approved for treatment of bleeding in patient
94                     Recombinant factor VIIa (rFVIIa) is used for treatment of hemophilia patients wit
95 blem are not ideal, recombinant factor VIIa (rFVIIa) may be useful in correcting the prolonged PT obs
96 d recombinant human coagulation factor VIIa (rFVIIa) on March 25, 1999, for bleeding in patients with
97                     Recombinant factor VIIa (rFVIIa), a hemostatic agent approved for hemophilia, is
98  component therapy, recombinant factor VIIa (rFVIIa, NovoSeven), assists in turning on the extrinsic
99 oembolism (RD, 0.05 [CI, 0.01 to 0.10]) with rFVIIa.
100 following stimulation of melanoma cells with rFVIIa and FX.
101  hemorrhage, mortality was not improved with rFVIIa use across a range of doses.
102 cations suggests no mortality reduction with rFVIIa use.
103 31, 2004, for thromboembolic AE reports with rFVIIa.
104                      Hemostatic therapy with rFVIIa reduced growth of the hematoma but did not improv
105                               Treatment with rFVIIa within four hours after the onset of intracerebra

 
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