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1 is a successful treatment for patients with liver failure.
2 Sepsis rate was also predictive of IFALD and liver failure.
3 a in LR and have implications for therapy of liver failure.
4 divided into hyperacute, acute and subacute liver failure.
5 Ascites is a common complication of subacute liver failure.
6 nonalcoholic steatohepatitis, fibrosis, and liver failure.
7 egenerative therapies for APAP-induced acute liver failure.
8 ry and it is the second most common cause of liver failure.
9 The treatment was not effective in acute liver failure.
10 rrounding normal liver, reducing the risk of liver failure.
11 vival in a lethal model of resection-induced liver failure.
12 hepatic fibrosis, cirrhosis, and eventually liver failure.
13 s with decompensated cirrhosis and fulminant liver failure.
14 Group 3 animals declined rapidly, with acute liver failure.
15 onic, acute-on-chronic, or acute cholestatic liver failure.
16 roliferation after hepatectomy, resulting in liver failure.
17 iculum stress, oxidative stress, and finally liver failure.
18 r decompensations including acute-on-chronic liver failure.
19 that lead to generalized infection and acute liver failure.
20 f neurological complications associated with liver failure.
21 ses residual hepatocyte function, leading to liver failure.
22 peutic option to treat posthepatectomy acute liver failure.
23 on was abandoned because of the high risk of liver failure.
24 and ultimately hepatocellular carcinoma and liver failure.
25 diet before azoxymethane (AOM)-induced acute liver failure.
26 large-scale production for the treatment of liver failure.
27 n lead to herpes simplex virus-induced acute liver failure.
28 g in patients with paracetamol-induced acute liver failure.
29 hy is a serious neurological complication of liver failure.
30 tus are strongly associated with etiology of liver failure.
31 4 changed mental status, and one death from liver failure.
32 n the neurological complications after acute liver failure.
33 isease-acute liver failure (ALF) and chronic liver failure.
34 tributing factor for cerebral edema in acute liver failure.
35 tcomes in acute acetaminophen (APAP)-related liver failure.
36 ophen overdose is the leading cause of acute liver failure.
37 re were no cases of hepatic-related death or liver failure.
38 assessment of patients with acute-on-chronic liver failure.
39 in the IDILI caused by drugs that can cause liver failure.
40 d fibrosis and may progress to cirrhosis and liver failure.
41 n is altered on monocytes from patients with liver failure.
42 is during the transition of NAFL to NASH and liver failure.
43 -4 (TLR4) pathway plays an important role in liver failure.
44 hepatectomy with less risk of post-operative liver failure.
45 n was reduced by recAP in ACLF but not acute liver failure.
46 option for prevention of ACLF but not acute liver failure.
47 ation and/or development of acute-on-chronic liver failure.
48 indicating protection from resection-induced liver failure.
49 sparing, specific and novel therapy in acute liver failure.
50 decompensated cirrhosis or acute-on-chronic liver failure.
51 ulated even in late-stage APAP-induced acute liver failure.
52 f 165 children admitted with pediatric acute liver failure, 136 met the inclusion criteria and 45 of
53 with ALF, 20 patients with acute-on-chronic liver failure, 15 patients with cirrhosis with no eviden
54 uring the postpartum period, and 4 were from liver failure (2 of the women who died from liver failur
55 e significant medical comorbidities, such as liver failure (9.9% vs 4.2%; p < 0.001), metastatic canc
56 In patients with acetaminophen-induced acute liver failure, a low serum level of CSF1 was associated
57 cirrhosis (Non-ACLF) and in acute-on-chronic liver failure (ACLF) by CCT and ROTEM including agreemen
61 ors to predict survival and acute-on-chronic liver failure (ACLF) in patients awaiting LT, as well as
63 decompensated cirrhosis and acute-on-chronic liver failure (ACLF) include susceptibility to infection
71 and prognostic criteria of acute-on-chronic liver failure (ACLF) were developed in patients with no
72 lantation for patients with acute-on-chronic liver failure (ACLF) with 3 or more failing organs (ACLF
84 llected to measure cytokines and a marker of liver failure (alanine aminotransferase); liver tissues
86 ticenter cohort of adult patients with acute liver failure (ALF) and in an acetaminophen (APAP)-induc
90 BACKGROUND DATA: Patients with severe acute liver failure (ALF) have extreme physiologic dysfunction
91 tamol) poisoning is a leading cause of acute liver failure (ALF) in humans and induces hepatocyte nec
92 (HEV) infection is a leading cause of acute liver failure (ALF) in many developing countries, yet ra
101 rity, it represents the major cause of acute liver failure (ALF) requiring liver transplantation in U
102 taminophen (APAP, paracetamol)-induced acute liver failure (ALF) showed significant differences in th
104 nts with acute liver dysfunction (e.g. acute liver failure (ALF), acute-on chronic liver failure (AoC
105 LPS) and concanavalin A (ConA)-induced acute liver failure (ALF), but the mechanism by which FK866 af
107 ant centers coordinate complex care in acute liver failure (ALF), for which liver transplant (LT) can
113 in a patient with dengue virus induced acute liver failure (ALF).((1)) Their report highlights the ca
114 eveloped hepatocellular carcinoma, and 1 had liver failure, all of whom were in the obese group.
117 nderstanding of the processes culminating in liver failure and cancer and to prioritize vaccine candi
119 24 patients with acetaminophen-induced acute liver failure and compared with 10 healthy controls.
120 TGFbeta1 signaling during AOM-induced acute liver failure and contributes to both liver pathology an
123 omising alternative therapeutic approach for liver failure and different cell sources have been teste
124 Mice given SR9009 developed less-severe liver failure and had longer survival times than mice gi
130 inophenol [APAP]) is the main cause of acute liver failure and liver transplantation in several Weste
134 yperammonemia animal models, including acute liver failure and ornithine transcarbamylase deficiency,
135 us on the current approach to neonatal acute liver failure and the progress made in the diagnosis and
136 ntation (LT) between patients with fulminant liver failure and those with cirrhosis and severe hepati
137 e hemorrhagic fever, neurological disorders, liver failure, and blindness, which could collectively b
139 haracterised by florid hepatic inflammation, liver failure, and death within 28 days in 35% of patien
141 CV develop complications, such as cirrhosis, liver failure, and hepatocellular carcinoma over a perio
146 ical record-confirmed hepatic-related death, liver failure, and other clinically significant hepatic
147 were impaired due to systemic inflammation, liver failure, anticoagulants (heparins, phenprocoumon,
148 acute liver failure (ALF), acute-on chronic liver failure (AoCLF) or decompensated chronic liver dis
151 ; RR, 0.35 [95% CI, 0.16-0.75]; P = .006) or liver failure (ARR, 0.046 [95% CI, 0.008-0.088]; RR, 0.2
154 ficant impairment of liver function or overt liver failure as the cause of death in COVID-19 rarely o
155 tly is considered a consequence of secondary liver failure because of which liver transplantation is
156 9 expression in acetaminophen-induced acute liver failure being mediated both by circulating endogen
157 previously been implicated in cirrhosis and liver failure but not in isolated portal hypertension.
161 chronic liver failure grades 1-3 and Chronic Liver Failure-C-Organ Failure liver subscore equals to 3
166 atients can develop hepatitis, coagulopathy, liver failure, central nervous system involvement, multi
167 ng survival, while in patients with advanced liver failure (Child B/C), EVL alone carries an increase
168 Failure dataset with adoption of the Chronic Liver Failure-classification resulted in similar finding
170 abase on patients with cirrhosis and chronic liver failure (CLF) from 2006 through 2014, and data on
171 ll patients with acetaminophen-induced acute liver failure compared with healthy controls (p < 0.0001
173 of 1-year mortality, independent of Chronic Liver Failure Consortium acute-on-chronic liver failure
175 oimmune hepatitis) or patients without acute liver failure (controls) collected from a DILI Biobank i
177 17 because of ALF defined by Pediatric Acute Liver Failure criteria (raised transaminases, Internatio
182 ve therapy for toxic ingestion or idiopathic liver failure (DT) in a level 1 trauma center and large
183 e, outcomes, and prognostic factors of early liver failure (ELF) after transjugular intrahepatic port
184 bilize the lost metabolic function for acute liver failure, end-stage and congenital liver diseases,
186 r complications of WRS, including repetitive liver failure episodes and poorly controlled diabetes.
189 ic steatohepatitis can lead to cirrhosis and liver failure for which there are currently no approved
191 f existing liver disease distinguishes acute liver failure from decompensated cirrhosis or acute-on-c
192 ing the progression of non-alcoholic chronic liver failure from fatty liver disease to steatohepatiti
193 compensated cirrhosis and moderate-to-severe liver failure from nine university hospitals in six Euro
195 First, 101 patients with acute-on-chronic liver failure grades 1-3 and Chronic Liver Failure-C-Org
196 liver failure (2 of the women who died from liver failure had received isoniazid [1 in each group]).
200 long-term risk for progression to cirrhosis, liver failure, hepatocellular carcinoma, and liver-relat
201 ion is a global health problem, resulting in liver failure, hepatocellular carcinoma, and liver-relat
202 ients who have been transplanted for chronic liver failure; however long-term survival is higher comp
203 been shown to contribute to HE during acute liver failure; however, TGFbeta1 must be activated to bi
204 er fibrosis leads to portal hypertension and liver failure; however, the mechanisms leading to fibros
205 , 0.21; 95% CI, 0.06-0.74), acute-on-chronic liver failure (HR, 0.29; 95% CI, 0.03-0.99), and a model
206 Cl4-treated rats; and rapidly reversed fatal liver failure in CCl4-treated animals by restoring disea
209 o presented with recurrent episodes of acute liver failure in early infancy and are affected by cereb
210 ndoPC-derived hepatocytes are able to rescue liver failure in Fah(-/-)Rag2(-/-) mice after transplant
213 for the management acute or acute on chronic liver failure in the ICU, acknowledging that most recomm
214 on the management acute or acute on chronic liver failure in the ICU, related to five groups (cardio
215 liver injury (DILI) is the leading cause of liver failure in the United States and the most common c
218 ) overdose is the most common cause of acute liver failure in the Western world, with limited treatme
221 model of resistance to Fas receptor-mediated liver failure in the wild-derived MSM strain, compared w
222 curred (2.7%): hemothorax in one patient and liver failure in two, with major portal-systemic shunts.
224 ss that occurs after liver injury, but acute liver failure is a complex and fatal disease which is di
226 iovascular diseases in patients with chronic liver failure is associated with increased morbidity and
229 l research, cell transplantation therapy for liver failure is impeded by a shortage of human primary
230 ibility to development of ACLF whereas acute liver failure is likely due to direct hepatoxicity.
231 completion of stage 2: >=96%, postoperative liver failure (ISGLS-criteria) after stage 2: <=5%, ICU
233 atients with WD who have progressed to acute liver failure, leaving liver transplantation as the only
238 tions classified as grade III or higher were liver failures occurring in patients with Child-Pugh cla
239 rtment syndrome must be suspected when acute liver failure occurs in patients with subcapsular hemato
241 was increased in acetaminophen-induced acute liver failure on day 1 compared with healthy controls (p
242 failure, whether arising directly from acute liver failure or from decompensated chronic liver diseas
244 No patient with reactivation experienced liver failure or liver-related death within 36 weeks aft
248 nuous renal replacement therapy use in acute liver failure patients and to assess its impact on hyper
249 Retrospective analysis of acute-on-chronic liver failure patients receiving either standard medical
253 the influence of acetaminophen-induced acute liver failure plasma and endogenous DNA on Toll-like rec
254 e incubated with acetaminophen-induced acute liver failure plasma with and without deoxyribonuclease-
255 stimulation with acetaminophen-induced acute liver failure plasma, which was abrogated by preincubati
257 the critical period for survival after acute liver failure, providing promising clues of integration
260 extensive liver resection, post-hepatectomy liver failure remains one of the most lethal complicatio
265 represents the most frequent cause of acute liver failure, resulting in death or liver transplantati
267 evels were measured on admission and Chronic Liver Failure-Sequential Organ Failure Assessment criter
268 tion of hiPSC-EB-HLC in a rat model of acute liver failure significantly prolonged the mean survival
269 n, used in nearly 30% of patients with acute liver failure, still provides a life-saving alternative
270 ar prognostic power as the established Acute Liver Failure Study Group index (C-statistic 0.87 vs. 0.
271 0.604 alone, 0.797 with FABP1) and the Acute Liver Failure Study Group prognostic index (early, 0.686
273 les of 681 adults enrolled in the U.S. Acute Liver Failure Study Group were tested for anti-HEV immun
275 hepatitis (AH) is a syndrome of jaundice and liver failure that occurs in a minority of heavy consume
276 lines to a Fah(-/-) Il2rg(-/-) rat model of liver failure, the rat liver stem cells engrafted into t
277 nd death associated with tyrosinemia-induced liver failure, they developed regenerating nodules simil
278 er is a central regulator of metabolism, and liver failure thus constitutes a major health burden.
279 or patients with acetaminophen-induced acute liver failure to develop sepsis, which may culminate in
280 t of patients with paracetamol-induced acute liver failure to identify those needing emergency liver
281 critically ill children with pediatric acute liver failure to provide stability and bridge to transpl
282 um ACLF score (CLIF-C ACLFs) and presence of liver failure (total bilirubin >/=12 mg/dL) at ACLF diag
283 serious liver-related adverse events such as liver failure, variceal bleeding, serious infections, sp
287 renal replacement therapy in pediatric acute liver failure were changed in 2011 following preliminary
292 ifiable factor associated with mortality and liver failure, whereas enteral autonomy correlates with
295 report a case of an adult male with EPP and liver failure who successfully underwent a sequential li
296 d, the study of the pathogenesis of subacute liver failure with ascites complication is hampered by t