ライフサイエンスコーパス: hepatic encephalopathy

1 ve driving performance in those with minimal hepatic encephalopathy.

2 as gastroesophageal variceal hemorrhage and hepatic encephalopathy.

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

4 mission rates in patients with cirrhosis and hepatic encephalopathy.

5 time to the first hospitalization involving hepatic encephalopathy.

6 as a therapy for hospitalized patients with hepatic encephalopathy.

7 educed the risk of hospitalization involving hepatic encephalopathy.

8 hospitalized patient with more than trivial hepatic encephalopathy.

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

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

11 toms associated with human disorders such as hepatic encephalopathy.

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

13 pecifically variceal hemorrhage, ascites and hepatic encephalopathy.

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

15 ing effects of improved ascites and worsened hepatic encephalopathy.

16 rome, spontaneous bacterial peritonitis, and hepatic encephalopathy.

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

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

19 ALF were ventilated electively for grade IV hepatic encephalopathy.

20 hypertension in patients with ALF and severe hepatic encephalopathy.

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

22 ed the development of hyperammonemia-induced hepatic encephalopathy.

23 efore regraft due to overwhelming sepsis and hepatic encephalopathy.

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

25 Sleep disturbance is a classic sign of hepatic encephalopathy.

26 evalence in cirrhotic patients without overt hepatic encephalopathy.

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

28 otect recipients from hyperammonemia-induced hepatic encephalopathy.

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

30 measures to assess cerebral edema in severe hepatic encephalopathy.

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

32 ion, neutrophil exhaustion, and exacerbating hepatic encephalopathy.

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

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

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

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

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

38 cal for the prevention of hyperammonemia and hepatic encephalopathy.

39 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

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

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

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

43 Postshunt hepatic encephalopathy after liver transplantation (LT)

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

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

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

47 Hepatic encephalopathy and cerebral oedema remain import

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 Hepatic encephalopathy can be precipitated by several of

75 Hepatic encephalopathy causes significant cognitive impa

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

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

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

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

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

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

82 .6; p < 0.05) and increased with severity of hepatic encephalopathy (grade 0-2 vs 3/4) and systemic i

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

84 Hepatic encephalopathy has been classified into differen

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

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

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

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

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

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

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

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

93 Hepatic encephalopathy (HE) constitutes a neuropsychiatr

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

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

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

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

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

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

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

101 Hepatic encephalopathy (HE) is a frequent complication o

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

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

104 Hepatic encephalopathy (HE) is a major neurological comp

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

106 Hepatic encephalopathy (HE) is a serious complication of

107 Hepatic encephalopathy (HE) is a severe complication in

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

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

110 Hepatic encephalopathy (HE) represents a significant bur

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

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

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

114 278 cirrhotics [39% hepatic encephalopathy (HE), 31%DM] underwent stool whil

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Hepatic encephalopathy is a chronically debilitating com

135 Hepatic encephalopathy is a frequent and serious complic

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

137 Hepatic encephalopathy is a serious neurological complic

138 Hepatic encephalopathy is a syndrome whose pathophysiolo

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

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

141 Although hepatic encephalopathy is not a single clinical entity,

142 When hepatic encephalopathy is present, a precipitating cause

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

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

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

146 Hepatic encephalopathy may result in some irreversible c

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

148 Minimal hepatic encephalopathy (MHE) detection is difficult beca

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

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

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

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

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

154 Minimal hepatic encephalopathy (MHE) in cirrhosis is associated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 Psychometric hepatic encephalopathy scores did not correlate with sur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 Early hepatic encephalopathy (within 1 year) was significantly

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