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1 n lead to herpes simplex virus-induced acute liver failure.
2 g in patients with paracetamol-induced acute liver failure.
3 hy is a serious neurological complication of liver failure.
4 4 changed mental status, and one death from liver failure.
5 n the neurological complications after acute liver failure.
6 isease-acute liver failure (ALF) and chronic liver failure.
7 tcomes in acute acetaminophen (APAP)-related liver failure.
8 rrounding normal liver, reducing the risk of liver failure.
9 ophen overdose is the leading cause of acute liver failure.
10 re were no cases of hepatic-related death or liver failure.
11 assessment of patients with acute-on-chronic liver failure.
12 in the IDILI caused by drugs that can cause liver failure.
13 d fibrosis and may progress to cirrhosis and liver failure.
14 n is altered on monocytes from patients with liver failure.
15 uding steatosis, cholestasis, cirrhosis, and liver failure.
16 importance of these variants in human acute liver failure.
17 demonstrated in patients with cirrhosis and liver failure.
18 vival in a lethal model of resection-induced liver failure.
19 threatening complications, such as secondary liver failure.
20 considered the effective approaches to treat liver failure.
21 ry and it is the second most common cause of liver failure.
22 drug-induced idiosyncratic liver injury and liver failure.
23 egenerative therapies for APAP-induced acute liver failure.
24 patitis E may lead to life-threatening acute liver failure.
25 out how to select a proper CBT for different liver failure.
26 nalogue (fialuridine [FIAU]) developed acute liver failure.
27 cytes represents a key event in the cause of liver failure.
28 e, a paradigm for glutathione-mediated acute liver failure.
29 ent in sera of 15 of 19 cases of INH-induced liver failure.
30 drug induced liver injury resulting in acute liver failure.
31 tokine assays 12 h after initiation of acute liver failure.
32 in consecutive patients admitted with acute liver failure.
33 herapy (ART) protects against HCV-associated liver failure.
34 de C, and 136.5% (P < .001) in those without liver failure.
35 dentify patients at risk for postresectional liver failure.
36 tients with end-stage liver disease or acute liver failure.
37 tion but also albumin function is reduced in liver failure.
38 motes liver regeneration, thereby preventing liver failure.
39 hepatic fibrosis, cirrhosis, and eventually liver failure.
40 s with decompensated cirrhosis and fulminant liver failure.
41 Group 3 animals declined rapidly, with acute liver failure.
42 onic, acute-on-chronic, or acute cholestatic liver failure.
43 roliferation after hepatectomy, resulting in liver failure.
44 iculum stress, oxidative stress, and finally liver failure.
45 r decompensations including acute-on-chronic liver failure.
46 that lead to generalized infection and acute liver failure.
47 f neurological complications associated with liver failure.
48 ses residual hepatocyte function, leading to liver failure.
49 peutic option to treat posthepatectomy acute liver failure.
50 on was abandoned because of the high risk of liver failure.
51 and ultimately hepatocellular carcinoma and liver failure.
52 diet before azoxymethane (AOM)-induced acute liver failure.
53 e assays showed pronounced features of acute liver failure 12 h after application of acetaminophen (A
54 f 165 children admitted with pediatric acute liver failure, 136 met the inclusion criteria and 45 of
56 with ALF, 20 patients with acute-on-chronic liver failure, 15 patients with cirrhosis with no eviden
57 BCS of unknown origin (2 patients), chronic liver failure (4 patients), and solitary hepatocellular
58 e significant medical comorbidities, such as liver failure (9.9% vs 4.2%; p < 0.001), metastatic canc
59 In patients with acetaminophen-induced acute liver failure, a low serum level of CSF1 was associated
61 ntly associated with a higher probability of liver failure according to ISGLS classification (P = .00
63 was inversely related to the probability of liver failure according to the 50-50 (P = .02) and ISGLS
68 decompensated cirrhosis and acute-on-chronic liver failure (ACLF) include susceptibility to infection
74 and prognostic criteria of acute-on-chronic liver failure (ACLF) were developed in patients with no
76 78 patients with acetaminophen-induced acute liver failure admitted to the Royal Infirmary Edinburgh
79 llected to measure cytokines and a marker of liver failure (alanine aminotransferase); liver tissues
82 n, overwhelming liver damage can cause acute liver failure (ALF) and death without emergent liver tra
83 dults with nonacetaminophen (non-APAP) acute liver failure (ALF) and grade 1-2 hepatic encephalopathy
86 BACKGROUND DATA: Patients with severe acute liver failure (ALF) have extreme physiologic dysfunction
87 tamol) poisoning is a leading cause of acute liver failure (ALF) in humans and induces hepatocyte nec
89 (HEV) infection is a leading cause of acute liver failure (ALF) in many developing countries, yet ra
100 s the most suitable source of CBTs for acute liver failure (ALF) or chronic liver failure (CLF) remai
103 lity to developing sepsis is common in acute liver failure (ALF) resulting in tissue damage and organ
104 taminophen (APAP, paracetamol)-induced acute liver failure (ALF) showed significant differences in th
105 LPS) and concanavalin A (ConA)-induced acute liver failure (ALF), but the mechanism by which FK866 af
115 eveloped hepatocellular carcinoma, and 1 had liver failure, all of whom were in the obese group.
116 f NAFLD and NASH to cirrhosis and ultimately liver failure, along with gaps in knowledge regarding di
117 c injury other than hepatic-related death or liver failure among duloxetine initiators compared to ve
118 dden cardiac deaths and no deaths related to liver failure among patients who received treatment with
120 nderstanding of the processes culminating in liver failure and cancer and to prioritize vaccine candi
122 AT can be a promising therapy to treat acute liver failure and clinical studies to explore this treat
123 24 patients with acetaminophen-induced acute liver failure and compared with 10 healthy controls.
126 omising alternative therapeutic approach for liver failure and different cell sources have been teste
127 into mice with concanavalin-A-induced acute liver failure and fatal metabolic liver disease due to f
129 Mice given SR9009 developed less-severe liver failure and had longer survival times than mice gi
133 V) infection is one of the leading causes of liver failure and liver cancer, affecting around 3% of t
134 tion to prevent progress of life-threatening liver failure and liver transplantation in patients with
136 yperammonemia animal models, including acute liver failure and ornithine transcarbamylase deficiency,
137 ar dedifferentiation likely mediate terminal liver failure and suggest reinstatement of this network
138 n overdose is the most common cause of acute liver failure and the leading cause of chronic liver dam
139 s and cirrhosis, which eventually results in liver failure and the need for liver transplantation.
140 the only definitive treatment for end stage liver failure and the shortage of donor organs severely
141 ntation (LT) between patients with fulminant liver failure and those with cirrhosis and severe hepati
143 world's population and is a leading cause of liver failures and the need for liver transplantation.
144 e hemorrhagic fever, neurological disorders, liver failure, and blindness, which could collectively b
145 e events including recurrence of HCC, death, liver failure, and complications of cirrhosis were recor
147 haracterised by florid hepatic inflammation, liver failure, and death within 28 days in 35% of patien
149 e survival in patients with acute-on-chronic liver failure, and erythropoietin promoted hepatic regen
150 Hypoxemia is a feared complication of acute liver failure, and high oxygen requirements will frequen
152 ical record-confirmed hepatic-related death, liver failure, and other clinically significant hepatic
155 acute respiratory distress syndrome in acute liver failure are scant and hypoxemia being a commonly e
156 ; 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
159 9 expression in acetaminophen-induced acute liver failure being mediated both by circulating endogen
161 previously been implicated in cirrhosis and liver failure but not in isolated portal hypertension.
163 tly the only effective therapy for fulminant liver failure, but its use is limited by the scarcity of
165 21 may thus be therapeutically beneficial in liver failure by preventing apoptosis and by inducing li
166 chronic liver failure grades 1-3 and Chronic Liver Failure-C-Organ Failure liver subscore equals to 3
171 ng survival, while in patients with advanced liver failure (Child B/C), EVL alone carries an increase
172 Failure dataset with adoption of the Chronic Liver Failure-classification resulted in similar finding
174 abase on patients with cirrhosis and chronic liver failure (CLF) from 2006 through 2014, and data on
179 ll patients with acetaminophen-induced acute liver failure compared with healthy controls (p < 0.0001
181 oimmune hepatitis) or patients without acute liver failure (controls) collected from a DILI Biobank i
186 nial pressure monitor in acetaminophen acute liver failure did not confer a significant 21-day mortal
188 ve therapy for toxic ingestion or idiopathic liver failure (DT) in a level 1 trauma center and large
189 rates of up to 50% have been reported after liver failure due to drug-induced hepatotoxicity and cer
192 e, outcomes, and prognostic factors of early liver failure (ELF) after transjugular intrahepatic port
193 bilize the lost metabolic function for acute liver failure, end-stage and congenital liver diseases,
195 ic steatohepatitis can lead to cirrhosis and liver failure for which there are currently no approved
198 First, 101 patients with acute-on-chronic liver failure grades 1-3 and Chronic Liver Failure-C-Org
200 er, predicting whether or not a patient with liver failure has reversible kidney disease, and therefo
201 ion is a global health problem, resulting in liver failure, hepatocellular carcinoma, and liver-relat
202 long-term risk for progression to cirrhosis, liver failure, hepatocellular carcinoma, and liver-relat
203 er fibrosis leads to portal hypertension and liver failure; however, the mechanisms leading to fibros
204 rvival in infection-related acute-on-chronic liver failure (I-ACLF) derived from multicenter studies
205 nto an immune-deficient mouse model of human liver failure, iMPC-Heps proliferated extensively and ac
207 Cl4-treated rats; and rapidly reversed fatal liver failure in CCl4-treated animals by restoring disea
210 o presented with recurrent episodes of acute liver failure in early infancy and are affected by cereb
211 ndoPC-derived hepatocytes are able to rescue liver failure in Fah(-/-)Rag2(-/-) mice after transplant
212 cause it is among the common causes of acute liver failure in intensive care units and in light of it
216 meliorates the effects of APAP-induced acute liver failure in the mouse and therefore may provide new
217 TS13 activity is associated with progressive liver failure in the patient cohort, which might be attr
218 is a major cause of hepatotoxicity and acute liver failure in the U.S., but the pathophysiology is in
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.
223 ct from death in a lethal model of fulminant liver failure induced by intraperitoneal injection of D-
225 anial pressure monitored patients with acute liver failure, intracranial hypertension is commonly obs
226 ss that occurs after liver injury, but acute liver failure is a complex and fatal disease which is di
228 y benefit, whereas in nonacetaminophen acute liver failure, it may be associated with worse outcomes.
229 atients with WD who have progressed to acute liver failure, leaving liver transplantation as the only
234 ria, RLE was 112.5% in patients with grade A liver failure (n = 20), 88.4% in patients with grade B (
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
240 was increased in acetaminophen-induced acute liver failure on day 1 compared with healthy controls (p
241 an excellent outcome for patients with acute liver failure or complications of end-stage liver diseas
243 al alternatives to organ transplantation for liver failure or dysfunction but are compromised by inef
244 ack in acute intermittent porphyria or acute liver failure or end-stage chronic liver disease in eryt
245 failure, whether arising directly from acute liver failure or from decompensated chronic liver diseas
246 No patient with reactivation experienced liver failure or liver-related death within 36 weeks aft
248 in patients with acetaminophen-induced acute liver failure (p = 0.042) at the time of liver transplan
250 een children and adults, the Pediatric Acute Liver Failure (PALF) Study Group evaluated NAC in non-AP
251 l pressure monitoring in patients with acute liver failure, patient selection and ancillary assessmen
252 Retrospective analysis of acute-on-chronic liver failure patients receiving either standard medical
257 phases of human acetaminophen-induced acute liver failure, peaking on day 1 of hospital admission, a
258 the influence of acetaminophen-induced acute liver failure plasma and endogenous DNA on Toll-like rec
259 e incubated with acetaminophen-induced acute liver failure plasma with and without deoxyribonuclease-
260 stimulation with acetaminophen-induced acute liver failure plasma, which was abrogated by preincubati
262 the critical period for survival after acute liver failure, providing promising clues of integration
263 onditions are known to cause recurrent acute liver failure (RALF), and in about 50% of cases, the und
265 extensive liver resection, post-hepatectomy liver failure remains one of the most lethal complicatio
269 s with organ failure (defined by the chronic liver failure-sequential organ failure assessment [CLIF-
270 tion of hiPSC-EB-HLC in a rat model of acute liver failure significantly prolonged the mean survival
273 0.604 alone, 0.797 with FABP1) and the Acute Liver Failure Study Group prognostic index (early, 0.686
275 les of 681 adults enrolled in the U.S. Acute Liver Failure Study Group were tested for anti-HEV immun
277 Well-established preclinical models of acute liver failure such as the Jo2 FAS/CD95 activating model
278 hepatitis (AH) is a syndrome of jaundice and liver failure that occurs in a minority of heavy consume
279 lines to a Fah(-/-) Il2rg(-/-) rat model of liver failure, the rat liver stem cells engrafted into t
280 er is a central regulator of metabolism, and liver failure thus constitutes a major health burden.
281 or patients with acetaminophen-induced acute liver failure to develop sepsis, which may culminate in
282 t of patients with paracetamol-induced acute liver failure to identify those needing emergency liver
283 critically ill children with pediatric acute liver failure to provide stability and bridge to transpl
284 um ACLF score (CLIF-C ACLFs) and presence of liver failure (total bilirubin >/=12 mg/dL) at ACLF diag
285 iprazole for MI, and telithromycin for acute liver failure) using Medicaid Analytic eXtracts (from al
286 serious liver-related adverse events such as liver failure, variceal bleeding, serious infections, sp
288 neostigmine diminishes liver damage in acute liver failure via the cholinergic anti-inflammatory path
290 renal replacement therapy in pediatric acute liver failure were changed in 2011 following preliminary
295 ce of lung injury is relatively low in acute liver failure, where 21% fulfilled acute respiratory dis
298 report a case of an adult male with EPP and liver failure who successfully underwent a sequential li
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