ライフサイエンスコーパス: ascites

1 0.809 (if female) x 0.92 (if moderate/severe ascites).

2 0.809 (if female) x 0.92 (if moderate/severe ascites).

3 dmitted with acute anaemia and recurrence of ascites.

4 t liver, hepatic lymph node (LN), blood, and ascites.

5 , at least in part, for the formation of the ascites.

6 al event recorded, the occurrence of minimal ascites.

7 so highlight it as a rare cause of high SAAG ascites.

8 ated to INCPH, and 16 (36%) had a history of ascites.

9 association of liver macrohemodynamics with ascites.

10 ment shall be undertaken in cases of massive ascites.

11 ociated with decreased IL-10 and IL-6 in the ascites.

12 f surgical gastrointestinal resection and/or ascites.

13 ty, enhanced liver regeneration, and reduced ascites.

14 ons as potential quantitative trait loci for ascites.

15 oxicity in the presence of immunosuppressive ascites.

16 an increase in IL10 levels in both serum and ascites.

17 ng to a technique validated in patients with ascites.

18 es of patients with cirrhosis and refractory ascites.

19 ort an unidentified growth factor present in ascites.

20 the gallbladder wall, pleural effusion, and ascites.

21 al mortality in culture negative neutrocytic ascites.

22 increased RNA abundance when grown in human ascites.

23 associated with reduced risk of bleeding and ascites.

24 th diagnosis of culture negative neutrocytic ascites.

25 associated with culture negativeneutrocytic ascites.

26 es of patients with cirrhosis and refractory ascites.

27 ffect (FE 204038) in rats with cirrhosis and ascites.

28 ll populations into primary tumors and their ascites.

29 c, avascular tumors typical of patients with ascites.

30 ncrease mortality in cirrhosis patients with ascites.

31 edictors for ELF in patients with refractory ascites.

32 of HE or SBP in patients with cirrhosis with ascites.

33 ass C cirrhosis, hyponatremia, or refractory ascites.

34 als of satavaptan in cirrhosis patients with ascites.

35 of control rats and rats with cirrhosis and ascites.

36 tient, on dialysis, were ventilated, or with ascites.

37 follow-up evaluation, mainly for refractory ascites.

38 ization and leakiness culminating in massive ascites.

39 es of 6 untreated rabbits, and it eliminated ascites.

40 nt of malignant and non-malignant refractory ascites.

41 ed as body mass index (BMI) >35 adjusted for ascites.

42 s robustly, generating exclusively malignant ascites.

43 ents with subacute liver failure, especially ascites.

44 % and the survival mice developed noticeable ascites.

45 e of patients in either treatment group were ascites (13 [5%] of 277 patients treated with ramuciruma

46 TIPS creation was primarily performed for ascites (159 of 334 patients, 48%), gastrointestinal ble

47 was 15, serum albumin was 3.0 g/dL, 28% had ascites, 18% had hepatic encephalopathy, and 83% were Ch

48 Of the 1120 cirrhosis patients with ascites, 21 (1.9 %) were diagnosed with epilepsy.

49 sease, 7.3% experienced clinical events (39% ascites, 24% hepatic encephalopathy); patients who progr

50 Larger proportions of frail patients with ascites (29%) or HE (30%) died while on the waitlist com

51 inal pain (in 18% of patients), nausea (8%), ascites (3%), fatigue (3%), gastric stenosis (3%), hepat

52 ents, 38%), or a combination of bleeding and ascites (38 of 334 patients, 11%).

53 Of study subjects, 36% had ascites, 41% had HE, and 25% were frail.

54 frequent indication for TIPS was refractory ascites (50 of 54; 93%).

55 in the subgroup of patients with refractory ascites (588 patients, adjusted hazard ratio = 1.02, 95%

56 substudy, EIVPD was higher in patients with ascites (6.5 [5.4-8.5] versus 4.0 [3.9-5.1] mm Hg, P = 0

57 33.9%, P = 0.004) and refractory hydrothorax/ascites (6.9% vs. 16.5%, P = 0.019) in the experimental

58 arian cancer is the development of malignant ascites accompanied by widespread peritoneal metastasis.

59 dds of frailty were higher for patients with ascites (adjusted odd ratio 1.56, 95% confidence interva

60 -, heart-, and liver: body weight ratios and ascites after circumflex coronary artery ligation in rab

61 h poor survival was the development of early ascites after DEB-TACE-1 (median OS, 17 months), which w

62 considered in renal transplant patients with ascites, after all other sources have been ruled out.

63 Her serum ascites albumin gradient (SAAG) was greater than 1.1, su

64 History of ascites, albumin and hemoglobin are major determinants o

65 which was closely related to the history of ascites, albumin and hemoglobin but not to tumour load o

66 ing immune cells, as found in ovarian cancer ascites, AMG655-induced apoptosis was not enabled to any

67 splenomegaly (52/67), fever (33/64), oedema, ascites, anasarca, or a combination (29/37), elevated so

68 nts who were not frail (17% of patients with ascites and 20% with HE).

69 nomegaly with multiple granulomas as well as ascites and a left-sided pleural effusion.

70 histopathology, culminating in haemorrhagic ascites and a median survival period of 7.5 weeks.

71 Her physical examination revealed tense ascites and abdominal collateral veins.

72 al normalized ratio at waitlisting, and less ascites and encephalopathy.

73 in levels, as well as presence or absence of ascites and encephalopathy.

74 ion to pulmonary, cardiac and renal failure, ascites and encephalopathy.

75 list mortality (sHR 1.82, 95% CI 1.31-2.52); ascites and HE were not.

76 in 16 of 95 (16.8%) patients with refractory ascites and in four of 121 (3.3%) patients with other in

77 Patients with septated ascites and intraperitoneal adhesions are at potential h

78 Presence of ascites and MELD score were identified as independent ri

79 h significantly increased stromal expansion, ascites and metastases.

80 linked to their use, are self-management of ascites and palliative care at home.

81 eloped liver insufficiency manifested by new ascites and peripheral edema, treated with diuretics, a

82 Large-scale ascites and PHLF remain clinical challenges after major

83 a) were analyzed as predictive biomarkers of ascites and PHLF using Fisher exact, t test, or Wilcoxon

84 Here, we report that small EVs found in the ascites and plasma of OvCa patients contain ARG1.

85 can help identify chylous versus nonchylous ascites and pleural effusions through use of multipoint

86 ve differentiation of chylous and nonchylous ascites and pleural effusions.

87 th varying levels of instability observed in ascites and pleural fluid.

88 hild class A [69.4% sessions (n = 77)] or B; ascites and portal vein invasion was present in 18 (16.2

89 Further evaluations revealed a mild ascites and portal vein thrombosis although the patient

90 also other PH-related complications, such as ascites and portosystemic encephalopathy.

91 macrohemodynamics and their association with ascites and posthepatectomy liver failure (PHLF) after m

92 nction had recovered, with resolution of her ascites and PS of 2.

93 sive replicative capacity, derived from both ascites and solid biopsies.

94 r cell carcinoma model which forms malignant ascites and solid peritoneal tumors upon intraperitoneal

95 Ascites and splenomegaly were independent predictors for

96 s; one treated with 1.00 mg mAb/kg developed ascites and was euthanized 136 d after HCT.

97 response was measured only in patients with ascites and/or HE and baseline HVPG > 16 mm Hg.

98 tal of 193 patients with cirrhosis (62% with ascites and/or hepatic encephalopathy [HE]) who were wit

99 rapeutic targets-ranging between 0 (thyroid, ascites) and 8.48 months (breast cancers)-and were somet

100 atocellular carcinoma diagnosis, presence of ascites, and beta-blocker use.

101 ormal Ratio levels were lower, splenomegaly, ascites, and cirrhosis were more common (all P < 0.01).

102 nvestigated associations between LFI scores, ascites, and hepatic encephalopathy (HE) and mortality.

103 Adult patients with cirrhosis, ascites, and HRS-1 (based on the 2007 International Club

104 atic conditions related to INCPH, history of ascites, and serum creatinine >= 100 mumol/L: 5% of the

105 nchorage-free growth in peritoneal fluid and ascites, and to colonize remote sites, are poorly define

106 y mass index, liver iron deposition, massive ascites, and use of 3.0 T were significantly associated

107 Serum creatinine (P = 0.005), ascites as indication for TIPS (P = 0.04), and the prese

108 ates with the absence of further bleeding or ascites at follow-up examinations of patients with cirrh

109 ted with stage, preoperative CA125 level and ascites at surgery.

110 e 4.6 and 4.3 in the patient with refractory ascites at the two post-TIPS time points, respectively.

111 ents with portal hypertension and refractory ascites before and 2 and 12 weeks after TIPS placement b

112 nd promotes macrophage proliferation in mice ascites, both of which improve innate immunity.

113 ng (eg, alpha = .78 for pleural effusion and ascites) but was lower for others (eg, alpha = .08 for i

114 l of hvKP1Deltapeg-344 was observed in human ascites, but resistance to the bactericidal activity of

115 icient to proteins and reduced the volume of ascites by over 50%.

116 recapitulating their native configuration in ascites) by downregulating protein synthesis via mTORC1

117 Chylous ascites (CA) is an extremely rare complication after lap

118 for age; and (4) the presence and volume of ascites can be categorised as mild (minimal fluid by liv

119 ma tumors, secondary omental metastases, and ascites cells isolated from serous ovarian cancer patien

120 n the composition and functional programs of ascites cells, including immunomodulatory fibroblast sub

121 were examined from patient derived malignant ascites cells.

122 ities associated with failure to rescue were ascites, chronic obstructive pulmonary disease, and diab

123 pathogenesis of subacute liver failure with ascites complication is hampered by the lack of experime

124 a mouse model of subacute liver failure with ascites complication.

125 pathogenesis of subacute liver failure with ascites complication.

126 a from three 1-year trials of satavaptan for ascites control.

127 S-1 (based on the 2007 International Club of Ascites criteria of rapidly deteriorating renal function

128 suppressive tumor microenvironment (TME) and ascites-derived spheroids in ovarian cancer (OC) facilit

129 , two primary HGSOC tumors and three patient ascites-derived xenograft models.

130 (TDCM) effectively inhibits tumor growth and ascites development in a mouse model of aggressive mamma

131 mor-bearing mice suppressed tumor growth and ascites development, significantly prolonging lifespan.

132 ly inhibited peritoneal EL4 tumor growth and ascites development.

133 ncluded: fatty or cryptogenic liver disease, ascites, diabetes mellitus, and obesity.

134 Ascites drainage led to a reduction of TP53MAF concentra

135 The ascites drainage was inserted in order to reduce the int

136 toneal drainage in a patient with refractory ascites due to liver cirrhosis.

137 To comprehensively characterize the HGSOC ascites ecosystem, we used single-cell RNA sequencing to

138 s was defined as current or past evidence of ascites, either by clinical examination or by ultrasonog

139 lity were older age, smoking, liver disease, ascites, emergency or semiurgent repair, and need for in

140 ristics (high MELD score, low serum albumin, ascites, encephalopathy), surgery-related characteristic

141 endpoints defined as hepatic decompensation (ascites, encephalopathy, and variceal bleeding), hepatoc

142 ge, male gender, black race, the presence of ascites, encephalopathy, hepatocellular carcinoma, and h

143 e of opioids, ribavirin use, the presence of ascites, encephalopathy, insomnia, and depression.

144 ss who undergo TIPS placement for refractory ascites (especially in patients with MELD of 11 or 12) a

145 nd higher concentrations of soluble CD206 in ascites fluid (>0.53 mg/L) were less likely to survive f

146 d multicellular aggregates (MCAs) present in ascites fluid adhere to the peritoneum and induce retrac

147 Application of our enzymatic toolkit to ascites fluid and tissue slices from patients with ovari

148 pro-inflammatory cytokines and chemokines in ascites fluid as compared with plasma.

149 sociated mucins from cultured cells and from ascites fluid derived from patients with ovarian cancer.

150 Analysis of serial ascites fluid from patients with SBP revealed loss of LP

151 ovarian tumor growth and the development of ascites fluid in vivo.

152 Co-incubation of ovarian cancer cells with ascites fluid significantly increased sN4 shedding, whic

153 In human ascites fluid supplemented with exogenous siderophores,

154 patients, we detected 2-20-fold more sN4 in ascites fluid than serum.

155 am stain as well as multiple cultures of her ascites fluid were both negative.

156 To study this, matched peripheral blood and ascites fluid were collected from 35 patients with decom

157 cid, a signaling lipid abundant in blood and ascites fluid, is both a mitogen and chemoattractant for

158 In contrast, in ascites fluid, MAIT cells were significantly increased t

159 ession, as they are constantly secreted into ascites fluids.

160 08 and included 1198 cirrhosis patients with ascites followed for 1 year.

161 rubinemia, coagulopathy, encephalopathy, and ascites formation.

162 reduces both the incidence and the amount of ascites formed; and (iv) our retrospective analysis reve

163 Common grade 3 or worse adverse events were ascites (four [5%]) and anaemia (three [4%]); the only t

164 e adverse event in both treatment groups was ascites (four [7%] of 59 patients receiving placebo and

165 Malignant abdominal fluid (ascites) frequently develops in women with advanced high

166 202 patients with compensated cirrhosis (no ascites, gastrointestinal bleeding, encephalopathy, or j

167 inception cohort of 202 patients with CC (no ascites, gastrointestinal bleeding, encephalopathy, or j

168 Patients with culture negative neutrocytic ascites have a mortality rate comparable to spontaneous

169 Fifty-four cases of chyle leak/ascites have been reported after LDN in literature to da

170 Patients and rats with cirrhosis and ascites have portal hypertension and circulatory dysfunc

171 of recurrent or de novo variceal bleeding or ascites (hazard ratio, 0.11; 95% confidence interval, 0.

172 In contrast, among patients with ascites/HE and baseline HVPG > 16 mm Hg, only the HVPG r

173 stricting HVPG measurements to patients with ascites/HE and measuring HVPG response only if the patie

174 Among the patients with ascites/HE, those with baseline HVPG <= 16 mm Hg (n = 16

175 -stage liver disease (ESLD) events including ascites, hepatic encephalopathy, hepatocellular carcinom

176 ll bladder wall thickness, pleural effusion, ascites, hepatomegaly, and splenomegaly are highly sugge

177 liver: body weight ratios and prevalence of ascites in 8 rabbits with HF relative to indices for 13

178 associated with culture negativeneutrocytic ascites in a larger sample population.

179 xcretion and reduces portal hypertension and ascites in experimental cirrhosis.

180 peritoneal tumors and induce accumulation of ascites in mice.

181 Coronary ligation caused ascites in most rabbits, significantly increased lung-,

182 nt related], and treatment-related worsening ascites in one patient) and three with relapsed or refra

183 ment-mediated bactericidal activity in human ascites in the presence and absence of opsonization.

184 tional cohort of patients with cirrhosis and ascites in their last year of life.

185 Sterile cerebrospinal fluid ascites in which no known infectious etiology is identif

186 ce died at 15-18 days after hepatectomy with ascites, increased plasma ammonia, and very small livers

187 The effect of ascites-induced changes in IPP on OvCa progression is la

188 ely, these findings elucidate a new role for ascites-induced compression in promoting metastatic OvCa

189 rein we model the functional consequences of ascites-induced compression on ovarian tumor cells and c

190 Massive ascites, iron deposition, and high body mass index were

191 Malignant ascites is a common complication in the late stages of e

192 Ascites is a common complication of subacute liver failu

193 ype 1 (HRS-1) in patients with cirrhosis and ascites is a functional, potentially reversible, form of

194 Malignant ascites is a known consequence of vascular dysfunction,

195 Sterile cerebrospinal fluid ascites is a rare clinical entity that has only been rep

196 Chylous ascites is a rare complication after donor nephrectomy i

197 Cerebrospinal fluid ascites is a rare complication of ventriculoperitoneal s

198 Culture negative neutrocytic ascites is a variant of spontaneous bacterial peritoniti

199 f debris-stimulated ovarian tumor growth and ascites leading to sustained survival over 120 days post

200 Ascites, liver disease, diabetes, obesity, and primary s

201 , presence and size of pleural effusions and ascites, lymphadenopathy, and distant metastases.

202 There was suggestion that TIPS creation for ascites might be an underlying risk factor.

203 nt variceal bleeding (n = 25) and refractory ascites (n = 16).

204 2; 8%), and combined chylothorax and chylous ascites (n = 4; 16%).

205 process measures captured care processes for ascites (n = 5), varices/bleeding (n = 7), hepatic encep

206 tivariable analysis showed TIPS creation for ascites (odds ratio, 1.7; 95% CI: 1.04, 2.7; P = .03) an

207 ithelial and two mesenchymal cell lines from ascites of a bladder cancer patient (i.e. cells already

208 of PD-1(bright) NK cells were higher in the ascites of a cohort of patients with ovarian carcinoma,

209 Malignant cells were obtained from the ascites of a patient with advanced recurrent epithelial

210 afe and effective means to control malignant ascites of EOC.

211 nt and in tumor cells derived from malignant ascites of high-grade serous adenocarcinoma patients.

212 idic acid (LPA), a lipid mediator present in ascites of ovarian cancer patients, induced expression o

213 igation of the immune compartment present in ascites of patients with decompensated liver cirrhosis,

214 nt, was evaluated after developing new-onset ascites of unclear etiology after abdominal surgery for

215 and Wnt5a is found in high concentrations in ascites of women with ovarian cancer.

216 the interstitium (edema) and the peritoneum (ascites) of nephrotic patients is classically thought to

217 ve defects that subsequently lead to chylous ascites or chylothorax.

218 no stigmata of chronic liver disease, and no ascites or encephalopathy or other associated clinical s

219 s to assess associations between frailty and ascites or HE and competing risk regression analyses (wi

220 is observed more frequently in patients with ascites or HE and independently associated with waitlist

221 When stratified by AD, patients with ascites or hepatic encephalopathy were significantly mor

222 defined as presence of esophageal varices or ascites or low platelet count and splenomegaly.

223 Donors with massive ascites or requiring frequent large-volume paracentesis

224 ecrease the ex vivo growth/survival in human ascites or serum or decrease virulence in the in vivo in

225 Primary ovarian cancer cells from patient ascites or solid tumors sorted for alpha2-6 sialylation

226 -blockers (NSBB) in patients with refractory ascites or spontaneous bacterial peritonitis while other

227 Lastly, in tumor spheroids from malignant ascites or tissues of patients with advanced-stage ovari

228 (OR:1.2; 95%CI: 1.07-1.4; p = 0.003), having ascites (OR: 3.0; 95%CI: 1.01-8.7; p = 0.046), and advan

229 atic conditions related to INCPH, history of ascites, or increased serum creatinine.

230 (hepatic encephalopathy, esophageal varices, ascites, or portal hypertension) or liver transplant wer

231 al symptoms, bilirubin, ulcer, pancreatitis, ascites, or radioembolization-induced liver disease occu

232 Marked ascites out of proportion to peripheral edema usually de

233 On univariate analysis, ascites (P = .02), liver disease (P = .02), diabetes (P

234 s related to INCPH (P = 0.03) and history of ascites (P = 0.02) were associated with portal hypertens

235 g benefit in preventing further bleeding and ascites, p-TIPS could be a good treatment strategy for C

236 iously identified as significantly affecting ascites phenotype.

237 pistatic interaction with the CPQ region for ascites phenotype.

238 F that were defined by the presence of fetal ascites, pleural or pericardial effusions, skin edema, c

239 The presence of ascites, portal hypertension, and higher Charlson score

240 Early ascites post-DEB-TACE is associated with the survival of

241 jor determinants of the development of early ascites post-DEB-TACE.

242 Algorithms that included diagnosis codes for ascites (PPV 75%; 95% CI 63-86%), cirrhosis (PPV 60%; 47

243 n, 76% had varices, and 41% had a history of ascites (predominantly well controlled).

244 came normalized and sera from GW2580-treated ascites protected against endothelial permeability.

245 s of patients with cirrhosis with refractory ascites (RA).

246 sia are characterized by severe, symptomatic ascites refractory to attempts at medical and surgical m

247 Ascites resolved in six of seven patients.

248 er subclassified into iMCD-thrombocytopenia, ascites, reticulin fibrosis, renal dysfunction, organome

249 hemodynamics in patients with cirrhosis and ascites; rifaximin did not affect glomerular filtration

250 ed in granularity and maturation markers, in ascites samples from patients with cirrhosis.

251 We isolated PMs from ascites samples of 66 patients with decompensated cirrho

252 We used ascites samples of a separate cohort of 111 patients wit

253 osis, chronic obstructive pulmonary disease, ascites, sepsis, smoking, steroid, congestive heart fail

254 s variceal bleeding, cirrhosis etiology, and ascites severity.

255 ed jugular venous pressure and those without ascites showed directional favorability of tolvaptan ove

256 ocol use of NSBBs in cirrhosis patients with ascites shows that NSBBs did not increase mortality; the

257 In univariable analysis, ascites (sHR 1.52, 95% CI 1.14-2.05), HE (sHR 1.84, 95%

258 sequencing to profile ~11,000 cells from 22 ascites specimens from 11 patients with HGSOC.

259 0 s compared with that of a normal control), ascites, splenomegaly, portal hypertension (portal vein

260 marginally more patients with prior sepsis, ascites, steroid use, bleeding disorders, and disseminat

261 essed genes (DEGs) associated with resistant-ascites syndrome (resistant-AS), we used innovative tech

262 Ascites syndrome is a hypertensive, multifactorial, mult

263 oesophageal variceal bleeding and refractory ascites than sub-acute group (P < 0.001).

264 ally via the peritoneal fluid, and later via ascites that accumulates as a result of disruption of th

265 In those with resolved ascites, the TIPS-to-PV flow ratio was 0.8 +/- 0.2 and 0

266 In rats with cirrhosis with ascites, this state was associated with epithelial junct

267 zed 54 stable outpatients with cirrhosis and ascites to rifaximin 550 mg twice a day (n = 36) or plac

268 volume were lower in rats with cirrhosis and ascites treated with FE 204038.

269 AscH(-) significantly decreased formation of ascites, tumor burden over time, circulating tumor cells

270 univariate analysis were albumin, bilirubin, ascites, tumor size 5 cm or smaller, focality, distribut

271 tors of overall survival to be bilirubin, no ascites, tumor size 5 cm or smaller, solitary lesion, ba

272 Biodistribution study in mice with Ehrlich ascites tumors showed that (99m)Tc-DMA achieved its high

273 HCC patients pre-procedure serum bilirubin, ascites, tumour size and female gender predicted PEF pos

274 p, one of whom was admitted to hospital with ascites twice), sepsis (four patients in the G-CSF plus

275 The most common serious adverse events were ascites (two patients in the G-CSF group and two patient

276 itionally collected samples, including three ascites, two primary HGSOC tumors and three patient asci

277 y mass index, liver iron deposition, massive ascites, use of 3.0 T, presence of cirrhosis, and alcoho

278 39% of the 865 patients with cirrhosis with ascites used PPIs, 52% used them at some point during th

279 reverse the vascular pathology of malignant ascites using fluid from human patients and an immunocom

280 r score; presence of hepatic encephalopathy, ascites, variceal bleeding, hepatocellular carcinoma, pa

281 n and development of hepatic decompensation (ascites, variceal hemorrhage and hepatic encephalopathy)

282 The endpoint was hepatic decompensation (ascites, variceal hemorrhage, or encephalopathy).

283 72% had a history of hepatic encephalopathy, ascites, varices, hepatorenal syndrome, or spontaneous b

284 arterial pressure, cardiac output, SVR, and ascites volume were also measured after 6 days.

285 SVR was higher and cardiac output and ascites volume were lower in rats with cirrhosis and asc

286 (M2) macrophages and dramatically decreased ascites volume.

287 rtality rate in culture negative neutrocytic ascites was 39.41% (n = 67).

288 ceptor expression in rats with cirrhosis and ascites was markedly enhanced in the mesenteric circulat

289 hages' role in the pathogenesis of malignant ascites, we blocked macrophage function in ID8 mice usin

290 cs closely resembling those found in vivo in ascites, we show that IRF4 and MAFB were critical regula

291 ltivariable regression analysis, obesity and ascites were associated with significantly increased odd

292 Tumor biopsies or malignant ascites were collected from patients before treatment (d

293 this correlation improved when patients with ascites were excluded (r = 0.82).

294 proved when patients with recent drainage of ascites were excluded.

295 Further, myeloid and lymphoid cells in ascites were predominantly linked to tumor and blood ori

296 ly found to have sterile cerebrospinal fluid ascites which was treated successfully with a peritoneov

297 ion of patients with cirrhosis and recurrent ascites who survive transplantation-free for 1 year, com

298 r gastrointestinal bleeding, and low-protein ascites with associated poor liver function.

299 rent ovarian cancer (OvCa) develop malignant ascites with volumes that can reach > 2 L.

300 elopment of de novo or worsening of previous ascites without increasing rates of hepatic encephalopat