ライフサイエンスコーパス: hepatic encephalopathy

1 E covered stent-graft is higher incidence of hepatic encephalopathy.

2 ips, and those, if any, with hepatic failure/hepatic encephalopathy.

3 ved long-term rifaximin treatment to prevent hepatic encephalopathy.

4 cal for the prevention of hyperammonemia and hepatic encephalopathy.

5 ve driving performance in those with minimal hepatic encephalopathy.

6 as gastroesophageal variceal hemorrhage and hepatic encephalopathy.

7 lopment of sepsis, hepatorenal syndrome, and hepatic encephalopathy.

8 mission rates in patients with cirrhosis and hepatic encephalopathy.

9 n its clinical efficacy in the management of hepatic encephalopathy.

10 time to the first hospitalization involving hepatic encephalopathy.

11 as a therapy for hospitalized patients with hepatic encephalopathy.

12 educed the risk of hospitalization involving hepatic encephalopathy.

13 hospitalized patient with more than trivial hepatic encephalopathy.

14 he time to the first breakthrough episode of hepatic encephalopathy.

15 m burden is largely or entirely unrelated to hepatic encephalopathy.

16 toms associated with human disorders such as hepatic encephalopathy.

17 lease, produce some of the manifestations of hepatic encephalopathy.

18 pecifically variceal hemorrhage, ascites and hepatic encephalopathy.

19 and protein intake, even in the presence of hepatic encephalopathy.

20 tions, spontaneous bacterial peritonitis and hepatic encephalopathy.

21 ing effects of improved ascites and worsened hepatic encephalopathy.

22 rome, spontaneous bacterial peritonitis, and hepatic encephalopathy.

23 nary hypertension, cardiac dysfunction), and hepatic encephalopathy.

24 leeding, and a trial of synbiotic therapy in hepatic encephalopathy.

25 ALF were ventilated electively for grade IV hepatic encephalopathy.

26 hypertension in patients with ALF and severe hepatic encephalopathy.

27 ism and to contribute to the pathogenesis of hepatic encephalopathy.

28 ed the development of hyperammonemia-induced hepatic encephalopathy.

29 efore regraft due to overwhelming sepsis and hepatic encephalopathy.

30 previous ascites without increasing rates of hepatic encephalopathy.

31 lcohol-dependent patients, and patients with hepatic encephalopathy.

32 Sleep disturbance is a classic sign of hepatic encephalopathy.

33 evalence in cirrhotic patients without overt hepatic encephalopathy.

34 t assessment and had no clinical evidence of hepatic encephalopathy.

35 otect recipients from hyperammonemia-induced hepatic encephalopathy.

36 , kidney failure with a no dialysis code, or hepatic encephalopathy.

37 rtension, liver atrophy, hyperammoniemia and hepatic encephalopathy.

38 ved long-term rifaximin treatment to prevent hepatic encephalopathy.

39 acids that were previously investigated for hepatic encephalopathy.

40 ntestinal bleeding, renal injury, falls, and hepatic encephalopathy.

41 a prospective approach for the treatment of hepatic encephalopathy.

42 m stent, without increasing the incidence of hepatic encephalopathy.

43 P < 0.01), even after adjustment for MELD or hepatic encephalopathy.

44 measures to assess cerebral edema in severe hepatic encephalopathy.

45 PS was associated with higher rates of early hepatic encephalopathy.

46 ion, neutrophil exhaustion, and exacerbating hepatic encephalopathy.

47 ts rebleeding, death, treatment failure, and hepatic encephalopathy.

48 olitis in very low birth weight infants, and hepatic encephalopathy.

49 patic encephalopathy, and 32.3% ascites plus hepatic encephalopathy), 14.5% developed HCC, 2.0% under

50 Decompensation events included ascites, hepatic encephalopathy (191; 16.6%), and variceal bleedi

51 ratio [HR] 1.59 [95% CI 1.13-2.20]; p=0.01), hepatic encephalopathy (2.81 [1.72-4.42]; p=0.0004), dia

52 patients and reduced risk of recurrent overt hepatic encephalopathy (25.5% vs 46.8%) in randomized tr

53 Hepatic encephalopathy (-29.2 d, 95% CI: -30.4 to -28.0)

54 ith normal graft function who presented with hepatic encephalopathy 3 months after LT with stable liv

55 itis C virus listing diagnoses (69% vs 56%), hepatic encephalopathy (36% vs 31%), height (161.9 vs 17

56 us 30%; P = 0.001), with higher incidence of hepatic encephalopathy (50% versus 27.5%; P = 0.04), hyp

57 s. 30%; P = 0.001), with higher incidence of hepatic encephalopathy (50% vs. 27.5%; P = 0.04), hypona

58 I: -35.3 to -33.9), and combined ascites and hepatic encephalopathy (-63.8 d, 95% CI: -65.0 to -62.6)

59 to new insights into the pathophysiology of hepatic encephalopathy, a common condition that is cause

60 Postshunt hepatic encephalopathy after liver transplantation (LT)

61 le acids may play a pathological role during hepatic encephalopathy, although precisely how they dysr

62 ory mechanisms may provide new insights into hepatic encephalopathy and brain edema in fulminant hepa

63 The mechanism of hepatic encephalopathy and cerebral edema in this settin

64 Hepatic encephalopathy and cerebral oedema remain import

65 These have been variously attributed to hepatic encephalopathy and impaired hepatic melatonin me

66 ciated with some complications, particularly hepatic encephalopathy and infections.

67 of shunt-related side effects, particularly hepatic encephalopathy and insufficient cardiac response

68 Cerebral edema is common in severe hepatic encephalopathy and may be life threatening.

69 ce is frequent in cirrhotic patients without hepatic encephalopathy and may be related to abnormaliti

70 ed ratio, acute kidney injury, septic shock, hepatic encephalopathy and model for end stage liver dis

71 re severe systemic complications (high-grade hepatic encephalopathy and need for renal replacement th

72 an immune-mediated encephalopathy; lymphoma, hepatic encephalopathy and progressive multifocal leukoe

73 iew is to highlight studies used to test for hepatic encephalopathy and those utilizing specific new

74 d use of rifaximin after hospitalization for hepatic encephalopathy) and outcomes (30-day readmission

75 hepatic decompensation (46.7% ascites, 21.1% hepatic encephalopathy, and 32.3% ascites plus hepatic e

76 bumin was 3.0 g/dL, 28% had ascites, 18% had hepatic encephalopathy, and 83% were Child class B or C.

77 , portal hypertension, hypoprothrombinaemia, hepatic encephalopathy, and decreased serum concentratio

78 bowel syndrome, inflammatory bowel disease, hepatic encephalopathy, and fibromyalgia and burn injury

79 lications, including portal vein thrombosis, hepatic encephalopathy, and gastrointestinal bleeding.

80 on 2 consecutive visits, variceal bleeding, hepatic encephalopathy, and liver-related death) and his

81 Hemodynamic changes, incidence of hepatic encephalopathy, and long-term (>3 months) need f

82 mission rates in patients with cirrhosis and hepatic encephalopathy, and may improve driving performa

83 OR 3.29, 95% CI 1.44-7.50), history of overt hepatic encephalopathy (aOR 7.40, 95% CI 1.20-45.56), an

84 t strategies for patients with cirrhosis and hepatic encephalopathy appears to continue to contribute

85 patients with cirrhosis, hyperammonemia and hepatic encephalopathy are common after gastrointestinal

86 Two approaches to new therapies for hepatic encephalopathy are needed.

87 ns and the complete reversibility of minimal hepatic encephalopathy are poorly documented.

88 aximin group had a hospitalization involving hepatic encephalopathy, as compared with 22.6% of patien

89 nificantly reduced the risk of an episode of hepatic encephalopathy, as compared with placebo, over a

90 drome, spontaneous bacterial peritonitis and hepatic encephalopathy, as well as recent studies of pre

91 alignancy, previous upper abdominal surgery, hepatic encephalopathy, ascites, and Crohn's disease, wh

92 mmonly, cirrhosis with complications such as hepatic encephalopathy, ascites, hepatocellular carcinom

93 use of any number of complications including hepatic encephalopathy, ascites, hepatorenal syndrome (H

94 and mortality, mainly due to complications [hepatic encephalopathy, ascites, hepatorenal syndrome (H

95 and mortality, mainly due to complications [hepatic encephalopathy, ascites, hepatorenal syndrome (H

96 cirrhosis; >=3 Elixhauser score; presence of hepatic encephalopathy, ascites, variceal bleeding, hepa

97 ts (ASA) class >=3, and 72% had a history of hepatic encephalopathy, ascites, varices, hepatorenal sy

98 ELD-Na (AUC: 0.86), albumin (AUC: 0.77), and hepatic encephalopathy (AUC: 0.62) were retained as the

99 n age 54 y, 79.4% male), none had ascites or hepatic encephalopathy before KTA, but 15 had clinical p

100 yte, is decreased in cirrhotic patients with hepatic encephalopathy but appears unchanged in fulminan

101 is well documented in the treatment of acute hepatic encephalopathy, but its efficacy for prevention

102 Hepatic encephalopathy can be precipitated by several of

103 temic infections and lactulose treatment for hepatic encephalopathy, can impact gut microbiome compos

104 Hepatic encephalopathy causes significant cognitive impa

105 Covert hepatic encephalopathy (CHE) is clinically underrecogniz

106 loped to allow clinicians to test for covert hepatic encephalopathy (CHE).

107 Presence of subclinical hepatic encephalopathy, chronotypology profile, and indi

108 um sensitivity suggests a role for ASIC1s in hepatic encephalopathy, cirrhosis, and other neuronal di

109 onine cycle and triggers hypermethioninemia, hepatic encephalopathy, cognitive impairment, and seizur

110 to prevent variceal bleeding, lactulose for hepatic encephalopathy, combination aldosterone antagoni

111 liver cirrhosis and causally associated with hepatic encephalopathy development.

112 t can be administered safely during episodic hepatic encephalopathy due to cirrhosis and that protein

113 ocellular carcinoma, hepatic decompensation (hepatic encephalopathy, esophageal varices, ascites, or

114 .6; p < 0.05) and increased with severity of hepatic encephalopathy (grade 0-2 vs 3/4) and systemic i

115 Those patients with advanced hepatic encephalopathy (grade 3/4) or high systemic infl

116 Hepatic encephalopathy has been classified into differen

117 edictors of response to lactulose therapy in hepatic encephalopathy have been reported, along with th

118 d L-ornithine-L-aspartate therapy in minimal hepatic encephalopathy have been reported.

119 mine, such as occur in cerebral ischemia and hepatic encephalopathy, have yet to be examined.

120 severe bacterial infection (BI) (14.5%) and hepatic encephalopathy (HE) (5%).

121 EEG) is useful to objectively diagnose/grade hepatic encephalopathy (HE) across its spectrum of sever

122 Hepatic encephalopathy (HE) after Trans-jugular intrahep

123 , we studied the association of ammonia with hepatic encephalopathy (HE) and 21-day transplant-free s

124 es in intestinal microbiota that can lead to hepatic encephalopathy (HE) and infections, especially w

125 liver failure (ALF) and are associated with hepatic encephalopathy (HE) and intracranial hypertensio

126 ssociations between LFI scores, ascites, and hepatic encephalopathy (HE) and mortality.

127 and portal hypertension without a history of hepatic encephalopathy (HE) and reviewed medical and pha

128 Dementia and hepatic encephalopathy (HE) are challenging to distingui

129 The mechanisms behind the development of hepatic encephalopathy (HE) are unclear, although hypera

130 Hepatic encephalopathy (HE) can cause major morbidity de

131 Hepatic encephalopathy (HE) constitutes a neuropsychiatr

132 g rifaximin, who had experienced two or more hepatic encephalopathy (HE) events in the previous 6 mon

133 In patients with cirrhosis, hepatic encephalopathy (HE) has acute but reversible as

134 logy but its usefulness in the evaluation of hepatic encephalopathy (HE) has never been properly asse

135 The pathogenesis of hepatic encephalopathy (HE) in cirrhosis is multifactori

136 l albumin dialysis (ECAD) may improve severe hepatic encephalopathy (HE) in patients with advanced ci

137 p inhibitors (PPIs) may be a risk factor for hepatic encephalopathy (HE) in patients with cirrhosis,

138 ism plays a major role in the development of hepatic encephalopathy (HE) in patients with cirrhosis.

139 Hepatic encephalopathy (HE) is a frequent complication o

140 Recurrent hepatic encephalopathy (HE) is a leading cause of readmi

141 Progression of hepatic encephalopathy (HE) is a major determinant of ou

142 Hepatic encephalopathy (HE) is a major neurological comp

143 Hepatic encephalopathy (HE) is a prognostically relevant

144 BACKGROUND & AIMS: Hepatic encephalopathy (HE) is a serious complication of

145 Hepatic encephalopathy (HE) is a serious complication of

146 Hepatic encephalopathy (HE) is a serious neurologic comp

147 Hepatic encephalopathy (HE) is a severe complication in

148 Symptomatic postshunt hepatic encephalopathy (HE) is a very infrequent conditi

149 Cirrhosis and hepatic encephalopathy (HE) is associated with an altere

150 Hepatic encephalopathy (HE) is associated with poor qual

151 lacement can worsen cognitive dysfunction in hepatic encephalopathy (HE) patients due to toxins, incl

152 Refractory hepatic encephalopathy (HE) remains a major cause of mor

153 Hepatic encephalopathy (HE) represents a significant bur

154 disaccharides (NADs) have been used to treat hepatic encephalopathy (HE) since 1966.

155 Screening for hepatic encephalopathy (HE) that does not cause obvious

156 organ failures as 1) shock, 2) grade III/IV hepatic encephalopathy (HE), 3) need for dialysis and me

157 278 cirrhotics [39% hepatic encephalopathy (HE), 31%DM] underwent stool whil

158 485 of 1,071 patients (45.3%) had grade 3-4 hepatic encephalopathy (HE), 500 of 1,070 (46.7%) requir

159 thought to be central to the pathogenesis of hepatic encephalopathy (HE), but its prognostic role in

160 (PHES) analyses are widely used to diagnose hepatic encephalopathy (HE), but little is known about t

161 Patients may develop hepatic encephalopathy (HE), pulmonary hypertension (PaH

162 stic regression for all readmissions and for hepatic encephalopathy (HE), renal/metabolic, and infect

163 her epilepsy is a risk factor for developing hepatic encephalopathy (HE), which is a strong predictor

164 insults can lead to acute liver failure and hepatic encephalopathy (HE).

165 fect outcomes of patients with cirrhosis and hepatic encephalopathy (HE).

166 ned substances and improves hemodynamics and hepatic encephalopathy (HE).

167 PAP) acute liver failure (ALF) and grade 1-2 hepatic encephalopathy (HE).

168 d flow (CBF) in patients with cirrhosis with hepatic encephalopathy (HE).

169 atability, is being studied for treatment of hepatic encephalopathy (HE).

170 ive impairment and coma, a syndrome known as hepatic encephalopathy (HE).

171 r (BZR) appears to play an important role in hepatic encephalopathy (HE).

172 ads to neuropsychiatric complications called hepatic encephalopathy (HE).

173 elated to some complications including overt hepatic encephalopathy (HE).

174 s associated with brain dysfunction known as hepatic encephalopathy (HE).

175 tes was the most common (86.5%), followed by hepatic encephalopathy (HE; 37.8%), variceal bleeding (V

176 ute liver injury (ALI), 78% of whom also had hepatic encephalopathy (HE; ALF), were followed until da

177 Outpatients with cirrhosis (with/without hepatic encephalopathy [HE]) and controls underwent stoo

178 ent of ascites, variceal hemorrhage [VH], or hepatic encephalopathy [HE]) in patients with compensate

179 ents with cirrhosis (62% with ascites and/or hepatic encephalopathy [HE]) who were within 7 days of b

180 ver disease (ESLD) events including ascites, hepatic encephalopathy, hepatocellular carcinoma, esopha

181 t psychotropic substances, mental confusion, hepatic encephalopathy, hepatocellular carcinoma, severe

182 Treatment of hyperammonemia and hepatic encephalopathy in cirrhosis is an unmet clinical

183 zation was 215.2 days to hospitalization for hepatic encephalopathy in non-PPI users compared to 139.

184 ed liver damage and is used as a therapy for hepatic encephalopathy in patients refractory to standar

185 oration of liver function, coagulopathy, and hepatic encephalopathy in the absence of pre-existing li

186 ther than ammonia that might be important in hepatic encephalopathy, including the synergistic role o

187 Other mortality predictors include hepatic encephalopathy, intensive care unit (ICU) stay,

188 Hepatic encephalopathy is a chronically debilitating com

189 Hepatic encephalopathy is a frequent and debilitating co

190 Hepatic encephalopathy is a frequent and serious complic

191 Hepatic encephalopathy is a neuropsychiatric complicatio

192 Latent or sub-clinical hepatic encephalopathy is a recognized complication of c

193 Hepatic encephalopathy is a serious neurological complic

194 Hepatic encephalopathy is a syndrome whose pathophysiolo

195 rbidity in patients with cirrhosis; however, hepatic encephalopathy is considered a reversible syndro

196 active investigation, standard treatment for hepatic encephalopathy is lactulose and alteration of gu

197 Although hepatic encephalopathy is not a single clinical entity,

198 When hepatic encephalopathy is present, a precipitating cause

199 tus was associated with older age, dialysis, hepatic encephalopathy, longer length of stay, and highe

200 Severe hepatic encephalopathy, low body mass index (<18.5) and

201 e), copper (Wilson's disease) and manganese (hepatic encephalopathy, manganese intoxication in intrav

202 ter suggests that the effect of lactulose on hepatic encephalopathy may not be related to alteration

203 Hepatic encephalopathy may result in some irreversible c

204 At admission, 3 patients had hepatic encephalopathy; median levels of prothrombin tim

205 A simple diagnostic test to identify minimal hepatic encephalopathy (MHE) and predict future overt HE

206 Minimal hepatic encephalopathy (MHE) detection is difficult beca

207 ly diagnosis of liver cirrhosis with minimal hepatic encephalopathy (MHE) disease was developed.

208 Patients with minimal hepatic encephalopathy (MHE) have attention, response in

209 d L-ornithine-L-aspartate therapy in minimal hepatic encephalopathy (MHE) have been reported.

210 Patients with cirrhosis and minimal hepatic encephalopathy (MHE) have driving difficulties b

211 Patients with minimal hepatic encephalopathy (MHE) have impaired driving skill

212 Minimal hepatic encephalopathy (MHE) in cirrhosis is associated

213 Minimal hepatic encephalopathy (MHE) is a subclinical cognitive

214 Minimal hepatic encephalopathy (MHE) is associated with falls, t

215 Minimal hepatic encephalopathy (MHE) is difficult to diagnose.

216 Minimal hepatic encephalopathy (MHE) is the presence of neuropsy

217 nt in cirrhosis spans a continuum of minimal hepatic encephalopathy (MHE) to overt hepatic encephalop

218 esentative connectivity patterns for minimal hepatic encephalopathy (MHE) using large-scale intrinsic

219 nts with liver cirrhosis may develop minimal hepatic encephalopathy (MHE) which affects their quality

220 ognitive impairment of patients with minimal hepatic encephalopathy (MHE).

221 adverse clinical outcomes, including minimal hepatic encephalopathy (MHE).

222 g approach could be the detection of minimal hepatic encephalopathy (MHE).

223 ypothesized that patients with cirrhosis and hepatic encephalopathy might be unable, due to excessive

224 ent with rifaximin maintained remission from hepatic encephalopathy more effectively than did placebo

225 r ascites (n = 5), varices/bleeding (n = 7), hepatic encephalopathy (n = 4), hepatocellular cancer (H

226 rtezomib and dexamethasone (pneumonia [n=1], hepatic encephalopathy [n=1]).

227 A breakthrough episode of hepatic encephalopathy occurred in 22.1% of patients in

228 In multivariate analysis, hepatic encephalopathy (odds ratio [OR], 2.728; 95% conf

229 with fulminant hepatic failure and worsening hepatic encephalopathy of unknown etiology for considera

230 n patients with cirrhosis and bouts of overt hepatic encephalopathy (OHE) are missing.

231 ents as primary prophylaxis to prevent overt hepatic encephalopathy (OHE) episodes.

232 ric tests [SPT]) for MHE diagnosis and overt hepatic encephalopathy (OHE) prediction.

233 rt of 1,000 cirrhosis patients without overt hepatic encephalopathy (OHE), from entry into treatment,

234 alidity and their predictive value for overt hepatic encephalopathy (oHE), rehospitalization, and dea

235 inimal hepatic encephalopathy (MHE) to overt hepatic encephalopathy (OHE), the pathophysiology of whi

236 t because of an increased incidence of overt hepatic encephalopathy (OHE).

237 cant portal hypertension but may cause overt hepatic encephalopathy (oHE).

238 (NonHep E) which is not considered as overt hepatic encephalopathy (OHE).

239 th cirrhosis (with or without previous overt hepatic encephalopathy; OHE) and age-matched controls fr

240 n reported, along with the effect of minimal hepatic encephalopathy on driving.

241 h regard to the effects of various models of hepatic encephalopathy on the blood-brain barrier (BBB)

242 tacaval anastomosis (PCA), a type B model of hepatic encephalopathy, on the peripheral pharmacokineti

243 when they present with complications such as hepatic encephalopathy or ascites.

244 n, even with portal hypertension but without hepatic encephalopathy or ascites.

245 are often contraindicated by the presence of hepatic encephalopathy or hepatorenal syndrome.

246 27]), use of rifaximin after a discharge for hepatic encephalopathy (OR 2.09 [1.80, 2.43]), and reduc

247 95% confidence interval [CI]: 1.06-1.47) and hepatic encephalopathy (OR = 36.94, 95% CI: 5.07-269.28)

248 patients who developed hepatorenal syndrome, hepatic encephalopathy, or sepsis were lower in group A

249 presence of ascites, esophageal varices, or hepatic encephalopathy, or when ESLD was stated as a cau

250 In univariate analysis, history of hepatic encephalopathy (P = 0.033), immunosuppressant tr

251 osine was lower in the alcohol-dependent and hepatic encephalopathy patients than in the healthy subj

252 cently detoxified alcohol-dependent and five hepatic encephalopathy patients with alcohol and non-alc

253 ms are altered in both alcohol-dependent and hepatic encephalopathy patients.

254 xperienced clinical events (39% ascites, 24% hepatic encephalopathy); patients who progressed had hig

255 was defined as bleeding esophageal varices, hepatic encephalopathy, persistent ascites, or death exc

256 Antecedents of hepatic encephalopathy, pre-LT sodium serum levels, and

257 ciated risk factors: cause of liver disease, hepatic encephalopathy, preoperative, intraoperative, an

258 The patient developed hepatic encephalopathy, renal failure, and profound coag

259 d the mechanisms by which infection triggers hepatic encephalopathy require further investigation.

260 Competing effects of hepatic encephalopathy, requirement for repeated LVP, an

261 atients who were in remission from recurrent hepatic encephalopathy resulting from chronic liver dise

262 cal flicker frequency (CFF) and psychometric hepatic encephalopathy score (PHES) analyses are widely

263 ess the predictive value of the Psychometric Hepatic Encephalopathy Score (PHES) in identifying patie

264 CHE was diagnosed using the Psychometric Hepatic Encephalopathy Score (PHES) with an abnormality

265 erwent clinical evaluation, the Psychometric Hepatic Encephalopathy Score (PHES), and EEG recording w

266 bnormal is MHE, gold standard), psychometric hepatic encephalopathy score (PHES), and inhibitory cont

267 athy-Syndrome-Test yielding the psychometric hepatic encephalopathy score (PHES), Animal Naming Test

268 n attention tests and/or in the Psychometric Hepatic Encephalopathy Score (PHES).

269 cirrhosis were administered the Psychometric Hepatic Encephalopathy Score and animal naming test to d

270 try, MHE was diagnosed when the Psychometric Hepatic Encephalopathy Score was <=-4.

271 me (PT), total bilirubin, serum ammonia, and hepatic encephalopathy score were also significantly imp

272 in time, serum albumin and bilirubin levels, hepatic encephalopathy score, and duration of survival.

273 MHE was diagnosed through the Psychometric Hepatic Encephalopathy Score.

274 Psychometric hepatic encephalopathy scores did not correlate with sur

275 licker frequency (CFF) test and psychometric hepatic encephalopathy scores were used to detect MHE.

276 Affected patients develop hepatic encephalopathy, seizures, and severe cognitive i

277 atio, 1.9; P < .001) and higher frequency of hepatic encephalopathy (subdistribution hazard ratio, 2.

278 Guidelines for the treatment of hepatic encephalopathy suggest ammonia reduction as the

279 of post-TIPS OHE and to compare Psychometric Hepatic Encephalopathy Sum Score(PHES) and the Critical

280 evere AH (discriminant function >/=32 and/or hepatic encephalopathy) that compared the efficacy of ac

281 ctivity, which might also reduce the risk of hepatic encephalopathy through an increase in skeletal m

282 ions such as ascites, variceal bleeding, and hepatic encephalopathy, underscoring its clinical signif

283 ic saline decreases cerebral edema in severe hepatic encephalopathy utilizing a quantitative techniqu

284 was defined by the development of: ascites, hepatic encephalopathy, variceal bleeding, prothrombin <

285 ion ICD-9-CM or ICD-10-CM code (ie, ascites, hepatic encephalopathy, variceal hemorrhage [VH], and he

286 ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, variceal hemorrhage, hepatocellu

287 outpatient resource use, and the presence of hepatic encephalopathy was an additional predictor of hi

288 Ascites and hepatic encephalopathy was documented in 26% and 7% of p

289 dy was to determine whether pre-TIPS minimal hepatic encephalopathy was predictive of post-TIPS OHE a

290 Post-TIPS overt hepatic encephalopathy was present in 14 patients (34%).

291 Overall, hepatic encephalopathy was similar in both groups (45 of

292 or use, renal replacement therapy, grade 3/4 hepatic encephalopathy, WBC count, and albumin.

293 n stratified by AD, patients with ascites or hepatic encephalopathy were significantly more likely to

294 (international normalized ratio 2.0 without hepatic encephalopathy) were used to determine levels of

295 ABA-Ergic drugs can favor the development of hepatic encephalopathy, whereas drugs undergoing extensi

296 mpensation (ascites, variceal hemorrhage and hepatic encephalopathy), which defines the transition fr

297 ing is recommended in patients with advanced hepatic encephalopathy who are awaiting orthotopic liver

298 y of the disorder, especially in relation to hepatic encephalopathy, will probably soon lead to furth

299 Early hepatic encephalopathy (within 1 year) was significantly

300 rug-induced ALF (defined as coagulopathy and hepatic encephalopathy without underlying chronic liver