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1 crucial to reduce the risk of postoperative hepatic insufficiency.
2 try with the mTLV underestimates the risk of hepatic insufficiency.
3 ccurs in proportion to the degree of induced hepatic insufficiency.
4 blood through portosystemic collaterals) and hepatic insufficiency.
5 sult from cirrhosis: portal hypertension and hepatic insufficiency.
6 ted gene therapy to correct various types of hepatic insufficiency.
7 changes to hemostasis occur in patients with hepatic insufficiency.
8 gement of bleeding episodes in patients with hepatic insufficiency.
9 nt of thromboembolic events in patients with hepatic insufficiency.
10 dosing adjustments are required for renal or hepatic insufficiency.
11 urn induce regeneration in selected cases of hepatic insufficiency.
12 eed for PVO, and thus PVO was not performed, hepatic insufficiency (22.2%; P = 0.001) and mortality (
15 developed high fever, progressed rapidly to hepatic insufficiency and coma, and died 8 days later.
16 not evidence the need for PVO, postoperative hepatic insufficiency and mortality were 4.9% and 0.6%,
19 neration implicate the metabolic response to hepatic insufficiency as an important source of signals
22 data suggest that the metabolic response to hepatic insufficiency might be the proximal signal that
24 ratio 1.5, 95% confidence interval 1.1-1.9), hepatic insufficiency (odds ratio 1.5, 95% confidence in
26 ions in metabolism that occur in response to hepatic insufficiency promote liver regeneration, and th
28 blood through portosystemic collaterals) and hepatic insufficiency resulting in the accumulation of n
29 blood through portosystemic collaterals) and hepatic insufficiency that result in the accumulation of