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1 rimary nonfunction of hepatic allografts and fulminant hepatic failure.
2 symptomatic laboratory derangements to fatal fulminant hepatic failure.
3 t is associated with increased mortality and fulminant hepatic failure.
4 ection is associated with high mortality and fulminant hepatic failure.
5 traumatic brain injury, ischemic stroke, and fulminant hepatic failure.
6 pper limit of normal but almost never causes fulminant hepatic failure.
7 terial peritonitis, hepatorenal syndrome, or fulminant hepatic failure.
8 anges from mild elevations in liver tests to fulminant hepatic failure.
9 ailure is one of the few treatable causes of fulminant hepatic failure.
10 e sister presented with acute BCS leading to fulminant hepatic failure.
11 egaly, coagulopathy, hyperbilirubinemia, and fulminant hepatic failure.
12 tosis of hepatocytes is a seminal feature of fulminant hepatic failure.
13  liver allotransplantation for patients with fulminant hepatic failure.
14 d at preventing and treating viral and toxic fulminant hepatic failure.
15 eased in patients with acetaminophen-induced fulminant hepatic failure.
16 s have been developed to support patients in fulminant hepatic failure.
17 ver in patients awaiting transplantation for fulminant hepatic failure.
18 or treatment of intracranial hypertension in fulminant hepatic failure.
19 ts with cryptogenic cirrhosis and idiopathic fulminant hepatic failure.
20 l for the treatment of organic acidemias and fulminant hepatic failure.
21 disease, including cryptogenic cirrhosis and fulminant hepatic failure.
22 tion and refined selection, particularly for fulminant hepatic failure.
23 was successfully performed in a patient with fulminant hepatic failure.
24 ut may lead to acute hepatitis and rarely to fulminant hepatic failure.
25 atic encephalopathy but appears unchanged in fulminant hepatic failure.
26 to hepatic encephalopathy and brain edema in fulminant hepatic failure.
27 s, 27% (3 of 11) of patients with idiopathic fulminant hepatic failure, 18% (2 of 11) of patients wit
28                    Eight (33%) patients with fulminant hepatic failure, 97 (66%) patients with chroni
29 ver transplantation if they have evidence of fulminant hepatic failure, a life-threatening systemic c
30  not been previously reported as a cause for fulminant hepatic failure after liver transplantation.
31 on communication to prevent amplification of fulminant hepatic failure and acetaminophen-induced hepa
32 riceal bleeding, as well as in patients with fulminant hepatic failure and alcoholic hepatitis.
33 f Fas-specific antibodies into mice leads to fulminant hepatic failure and death.
34 ls are beginning to acknowledge subgroups of fulminant hepatic failure and properly randomize therapy
35 ce nodularity is commonly seen at imaging in fulminant hepatic failure and usually reflects a combina
36  who was transferred to our institution with fulminant hepatic failure and worsening hepatic encephal
37  major complications of acute liver failure (fulminant hepatic failure) and a major cause of death in
38 ients with cryptogenic cirrhosis, idiopathic fulminant hepatic failure, and patients with other forms
39         There was a trend for UNOS status 1, fulminant hepatic failure, and presence of LPD to be ass
40  more cases of sudden infant death syndrome, fulminant hepatic failure, and severe complications duri
41                               UNOS status 1, fulminant hepatic failure, and the development of Epstei
42 y patients who die from paracetamol overdose fulminant hepatic failure as accurately as King's Colleg
43 st severe cases, as well as in patients with fulminant hepatic failure at high risk for mortality who
44 ars) who underwent liver transplantation for fulminant hepatic failure at our institution during a 5-
45 ver transplantation is associated with acute fulminant hepatic failure, biliary tract necrosis and le
46 ema is a cause of morbidity and mortality in fulminant hepatic failure but has not been well document
47 ped as follows: a) chronic liver failure; b) fulminant hepatic failure; c) patients immediately statu
48      The high mortality rate associated with fulminant hepatic failure combined with the limited avai
49  seven patients, including one who developed fulminant hepatic failure complicated by cerebral edema,
50  sinusoidal endothelium and portal tracts of fulminant hepatic failure explants, whereas there were m
51                      Patients diagnosed with fulminant hepatic failure face high mortality rates.
52 with adverse outcomes of pregnancy including fulminant hepatic failure, fetal loss, premature birth,
53 tiologies of AA included non-A, non-B, non-C fulminant hepatic failure (FHF) (3 patients), graft-vers
54                                 During human fulminant hepatic failure (FHF) circulating levels of mo
55 ctive liver support system for patients with fulminant hepatic failure (FHF) continues to be unmet.
56                                Patients with fulminant hepatic failure (FHF) die with brain edema, ex
57 port a case of an adult female who developed fulminant hepatic failure (FHF) during the second trimes
58                                              Fulminant hepatic failure (FHF) in humans produces a ble
59 ce of healthy residual liver mass, otherwise fulminant hepatic failure (FHF) may arise.
60                                Patients with fulminant hepatic failure (FHF) often die awaiting liver
61            The effect of RI on patients with fulminant hepatic failure (FHF) or chronic liver disease
62  A reproducible experimental animal model of fulminant hepatic failure (FHF) resembling the clinical
63 study, patients who received transplants for fulminant hepatic failure (FHF) were stratified separate
64 ant women has a high incidence of developing fulminant hepatic failure (FHF) with significant mortali
65 f the hepatic metabolic pathways affected by fulminant hepatic failure (FHF) would help develop nutri
66 n is the only proven effective treatment for fulminant hepatic failure (FHF), but its use is limited
67 antation (OLT) is an effective treatment for fulminant hepatic failure (FHF), but postOLT mortality i
68 d as etiologic agents in non-A, non-B (NANB) fulminant hepatic failure (FHF), but the frequency of in
69       In group 1 (n = 18) were patients with fulminant hepatic failure (FHF), in group 2 (n = 3) were
70 g orthotopic liver transplantation (OLT) for fulminant hepatic failure (FHF), some patients develop c
71  outcomes following liver transplantation in fulminant hepatic failure (FHF).
72    Death occurs in half of all children with fulminant hepatic failure (FHF).
73 homas may involve the liver but rarely cause fulminant hepatic failure (FHF).
74  for extrahepatic biliary atresia (EHBA) and fulminant hepatic failure (FHF).
75 ible aetiological role of TTV in cryptogenic fulminant hepatic failure (FHF).
76 n for liver transplantation in patients with fulminant hepatic failure (FHF).
77 metabolic support for comatose patients with fulminant hepatic failure for up to 5 days.
78                            Patients dying of fulminant hepatic failure, for whom no alternative thera
79             A 25-year-old man presented with fulminant hepatic failure from an unusual peripheral T c
80 gy expenditure was markedly increased in the fulminant hepatic failure group (mean energy expenditure
81 d experimental protocol of LPS-induced acute fulminant hepatic failure (i.p. injection of low dose of
82 s into a bioartificial liver device to treat fulminant hepatic failure improved animal survival, ther
83 er, the hepatocyte-like cells rescued lethal fulminant hepatic failure in a nonobese diabetic severe
84 ied strain HC-TN (genotype 1a), which caused fulminant hepatic failure in a patient and, subsequently
85 ansplantation were biliary atresia in seven, fulminant hepatic failure in six, chronic rejection in s
86 ute, self-limiting liver disease that causes fulminant hepatic failure in specific high-risk groups o
87 be included in the differential diagnosis of fulminant hepatic failure in young patients who show no
88              The management of patients with fulminant hepatic failure is a major clinical endeavor.
89           The pathogenesis of brain edema in fulminant hepatic failure is still unresolved.
90 asmid DNA prevented endotoxin-induced lethal fulminant hepatic failure, leading to dramatically enhan
91 he patient was a 13-year-old boy with acute, fulminant hepatic failure of unknown etiology who underw
92 be included in the differential diagnosis of fulminant hepatic failure of unknown pathogenesis.
93                                           No fulminant hepatic failure or death was observed.
94       The patient died in early childhood of fulminant hepatic failure, refractory epilepsy, lactic a
95                      A 28-year-old male with fulminant hepatic failure secondary to hepatitis B was r
96                                Patients with fulminant hepatic failure should be stabilized and trans
97                              Candidates with fulminant hepatic failure (Status-1A) receive the highes
98 wo mechanisms may account for brain edema in fulminant hepatic failure: the osmotic effects of brain
99  hemofiltration may be used in patients with fulminant hepatic failure to facilitate fluid removal an
100  liver disease ranging from acute (including fulminant hepatic failure) to chronic hepatitis, cirrhos
101 e of OLT, Z scores greater than -2.0 at OLT, fulminant hepatic failure, tumor, and postOLT complicati
102 is, sclerosing cholangitis, cystic fibrosis, fulminant hepatic failure, tyrosinemia, and chronic reje
103                           Four patients with fulminant hepatic failure underwent extracorporeal liver
104 T, (iv) diagnosis of tumor, (v) diagnosis of fulminant hepatic failure, (vi) retransplantation, (vii)
105                            Ten patients with fulminant hepatic failure were excluded from the study,
106          Although rare, HSV-1 can also cause fulminant hepatic failure, which is often fatal.
107 ation should be considered for patients with fulminant hepatic failure who are appropriate transplant
108 atients suffering from acetaminophen-induced fulminant hepatic failure who were sedated, paralyzed, a
109 ith known sickle cell disease, who developed fulminant hepatic failure with subsequent extreme hyperb
110                Patients meeting criteria for fulminant hepatic failure without acetaminophen toxicity

 
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