ライフサイエンスコーパス: portal hypertension

1 ellular carcinoma (HCC), without evidence of portal hypertension.

2 odilation, which contributes to the onset of portal hypertension.

3 rhosis and liver failure but not in isolated portal hypertension.

4 eries of rats and mice with cirrhosis or/and portal hypertension.

5 lent option to treat severe complications of portal hypertension.

6 to vasodilators, with beneficial effects on portal hypertension.

7 but they do not accurately reflect degree of portal hypertension.

8 -MD-02 in patients with NASH, cirrhosis, and portal hypertension.

9 a specific cause of idiopathic noncirrhotic portal hypertension.

10 % [12 of 20]) underwent major resection with portal hypertension.

11 superior to liver elastography in predicting portal hypertension.

12 with protection against hepatic fibrosis and portal hypertension.

13 trary effects in cirrhotic and non-cirrhotic portal hypertension.

14 inically significant (CSPH) and severe (SPH) portal hypertension.

15 epresent risk factors for hepatic injury and portal hypertension.

16 redict altered risk of incident cirrhosis or portal hypertension.

17 ension (IPH) is a rare cause of intrahepatic portal hypertension.

18 giogenesis is implicated in fibrogenesis and portal hypertension.

19 h as swallowing difficulty, hepatomegaly and portal hypertension.

20 ccurate noninvasive technique for estimating portal hypertension.

21 uent increased portal venous inflow leads to portal hypertension.

22 hosis, and might be a therapeutic target for portal hypertension.

23 ortal inflow to contribute to development of portal hypertension.

24 ol for the diagnosis of clinically important portal hypertension.

25 asodilation, a mechanism that contributes to portal hypertension.

26 plasma-ascitic albumin gradient to diagnose portal hypertension.

27 position fails to eliminate complications of portal hypertension.

28 any signs of residual/recurrent features of portal hypertension.

29 to the arterial vasodilation associated with portal hypertension.

30 hether Nogo-B gene deletion could ameliorate portal hypertension.

31 s) modulates fibrogenesis, angiogenesis, and portal hypertension.

32 injury, with resultant sinusoidal damage and portal hypertension.

33 y 5) of developing severe liver disease with portal hypertension.

34 osis (CF) develops severe liver disease with portal hypertension.

35 chnique for detecting clinically significant portal hypertension.

36 atients with cystic fibrosis and significant portal hypertension.

37 and may be important in the pathogenesis of portal hypertension.

38 atients without liver failure or significant portal hypertension.

39 hepatorenal syndrome, or bleeding caused by portal hypertension.

40 eneficial effect of NO donors for therapy of portal hypertension.

41 progressive thrombocytopenia, suggestive of portal hypertension.

42 ntribute significantly to the development of portal hypertension.

43 bnormalities, which may lead to noncirrhotic portal hypertension.

44 patients with cirrhosis and complications of portal hypertension.

45 hospitalized patients with complications of portal hypertension.

46 namic abnormalities typical of cirrhosis and portal hypertension.

47 parameter can be used to monitor therapy of portal hypertension.

48 econdary liver changes such as cirrhosis and portal hypertension.

49 other patients (1%) developed non-cirrhotic portal hypertension.

50 lications for the pathogenesis of sinusoidal portal hypertension.

51 ted with advanced liver cirrhosis and severe portal hypertension.

52 l contributor, with no significant effect of portal hypertension.

53 y revealed no evidence of hepatic disease or portal hypertension.

54 US is needed for diagnosis and screening of portal hypertension.

55 (TIPS) creation is an accepted treatment of portal hypertension.

56 vernous transformation, and complications of portal hypertension.

57 (PAH) that can develop as a complication of portal hypertension.

58 atic inflammation, fibrosis, congestion, and portal hypertension.

59 lting in functional Budd-Chiari syndrome and portal hypertension.

60 overweight/obese patients with cirrhosis and portal hypertension.

61 l dysfunction in patients with cirrhosis and portal hypertension.

62 liary dysgenesis, portal tract fibrosis, and portal hypertension.

63 patients with alcohol-related cirrhosis and portal hypertension.

64 rt and disclosed a transudate, suggestive of portal hypertension.

65 tic portosystemic shunt (TIPS) for cirrhotic portal hypertension.

66 dy of 162 patients with NASH, cirrhosis, and portal hypertension, 1 year of biweekly infusion of bela

67 h A, 6 Child-Pugh B, and 1 Child-Pugh C) and portal hypertension (11 males, median age 54 years (rang

68 wed by cholelithiasis in liver cirrhosis and portal hypertension (18.2%) and empyema or perforated ga

69 82% were male, 78% had cirrhosis, most with portal hypertension (61%, n=46/76), and 18% had prior-LT

70 All patients had portal hypertension, 76% had varices, and 41% had a hist

71 In 5-6% of patients with portal hypertension a pathological state exists in which

72 Sinusoidal portal hypertension, a disorder characterized by liver s

73 In addition to portal hypertension, a number of other vascular syndrome

74 al IHBDD complicated with cholangitis and/or portal hypertension achieved excellent long-term patient

75 n, AQP1 promotes angiogenesis, fibrosis, and portal hypertension after bile duct ligation and is regu

76 rization, and developed less-severe forms of portal hypertension after portal vein ligation.

77 esophageal varices result almost solely from portal hypertension, although the hyperdynamic circulati

78 rom 0% to 4%, 20 patients with cirrhosis and portal hypertension and 20 healthy volunteers with no kn

79 the only procedure that completely reverses portal hypertension and addresses the primary disease wh

80 04038 increases sodium excretion and reduces portal hypertension and ascites in experimental cirrhosi

81 nts and rats with cirrhosis and ascites have portal hypertension and circulatory dysfunction.

82 ns, widely accepted in vivo animal models of portal hypertension and cirrhosis, and in vitro angiogen

83 the endogenous angioinhibitor vasohibin-1 in portal hypertension and cirrhosis.

84 e a promising novel therapeutic strategy for portal hypertension and cirrhosis.

85 nsfer exerts multifold beneficial effects in portal hypertension and cirrhosis: reduction of patholog

86 nts, ductular cell expansion correlated with portal hypertension and collagen expression.

87 onse to chronic liver injury, which leads to portal hypertension and end-stage liver disease.

88 Portal hypertension and esophageal varices needing treat

89 of hepatic fibrosis which ultimately causes portal hypertension and gastroesophageal varices.

90 childhood cirrhosis, increases the risks for portal hypertension and gastrointestinal bleeding.

91 nous engorgement that will contribute toward portal hypertension and gut edema.

92 reduced endothelial fenestrae and developed portal hypertension and hepatic angiosarcoma over time.

93 ohepatitis, NASH) associated with cirrhosis, portal hypertension and hepatocellular carcinoma, yet th

94 ary prophylaxis of bleeding in children with portal hypertension and high-risk varices.

95 ress in understanding the pathophysiology of portal hypertension and improvements in the diagnosis an

96 ic hepatitis (AH) with advanced fibrosis and portal hypertension and in experimental mouse fibrosis.

97 omes were discussed in more detail including portal hypertension and IR injury.

98 arterial (PA) hypertension in patients with portal hypertension and is associated with significant m

99 ges due to performed procedures, because the portal hypertension and it's further complications had n

100 Portal hypertension and its complications account for th

101 mice with PH associated with CCl(4)-induced portal hypertension and liver cirrhosis, but were normal

102 oteins CPEB1 and CPEB4 during development of portal hypertension and liver disease.

103 Progressive liver fibrosis leads to portal hypertension and liver failure; however, the mech

104 sfunction contributes to the pathogenesis of portal hypertension and may represent a novel therapeuti

105 In disease models such as portal hypertension and mesenteric artery high/low flow,

106 ory function and prognosis in cirrhosis with portal hypertension and normal creatinine.

107 These patients are prone to gallstones, portal hypertension and possible surgical complications

108 irrhosis with its attendant complications of portal hypertension and potentially end-stage liver dise

109 cirrhosis complications, such as early-onset portal hypertension and primary liver cancers.

110 imaging was performed in seven patients with portal hypertension and refractory ascites before and 2

111 cts on intrahepatic circulation and decrease portal hypertension and rifaximin modulates the gut micr

112 fects 10%-30% of patients with cirrhosis and portal hypertension and significantly increases mortalit

113 With improved understanding of portal hypertension and the dynamic physiology of collat

114 This was accompanied by early-onset severe portal hypertension and twofold to fourfold increase in

115 patients (LD rate, 28.6% [85 of 297]) had no portal hypertension and underwent major resections or, i

116 Approaches to the management of portal hypertension and variceal hemorrhage in pediatric

117 Complications of portal hypertension and, rarely, hepatocellular carcinom

118 on can be related to the hyperestrogenism of portal hypertension and/or to decreased testosterone res

119 scarring from any cause leads to cirrhosis, portal hypertension, and a progressive decline in renal

120 with hepatic "recompensation," reduction of portal hypertension, and eventually avoidance of liver t

121 esulting fibrosis can lead to organ failure, portal hypertension, and fatal bleeding.

122 parenchyma, leading to hepatic dysfunction, portal hypertension, and hepatomegaly.

123 The presence of ascites, portal hypertension, and higher Charlson score were inde

124 risk for HCC based on age, sex, evidence of portal hypertension, and history of blood transfusion us

125 nary arterial hypertension in the setting of portal hypertension, and is present in 5%-10% of cirrhos

126 hout (OR, 2.98; 95% CI, 1.97-4.52; P < .001) portal hypertension, and MELD score (OR, 1.79; 95% CI, 1

127 onalcoholic steatohepatitis, liver fibrosis, portal hypertension, and nodular regenerative hyperplasi

128 oalbuminemia, cardiocirculatory dysfunction, portal hypertension, and systemic inflammation in patien

129 dure corrected liver function and eliminated portal hypertension, and the patient showed substantial

130 , FAH(-/-) pigs developed liver fibrosis and portal hypertension, and thus may serve as a large-anima

131 ere hepatosplenism, periportal fibrosis with portal hypertension, and urogenital inflammation and sca

132 rding the management of the complications of portal hypertension are reviewed, including a trial of b

133 The aim of this study is to evaluate portal hypertension as an independent risk factor in gen

134 patients with compensated cirrhosis and with portal hypertension as determined by the hepatic venous

135 Recursive partitioning analysis confirmed portal hypertension as the most important factor (OR, 2.

136 significant reduction of portal fibrosis and portal hypertension as well as of liver cysts.

137 transfer on angiogenesis, fibrogenesis, and portal hypertension-associated hemodynamic alterations w

138 provides evidence that vasohibin-1 regulates portal hypertension-associated pathological angiogenesis

139 Only FIB-4 predicted portal hypertension at diagnosis (area under the receive

140 er cirrhosis is complicated by bleeding from portal hypertension but also by portal vein thrombosis (

141 Patients had cirrhosis and portal hypertension but did not have GEV.

142 213 subjects with compensated cirrhosis with portal hypertension but without GEV enrolled in a random

143 213 patients with compensated cirrhosis and portal hypertension but without varices included in a tr

144 fects 10%-30% of patients with cirrhosis and portal hypertension, but the impact on functional status

145 tients with CF and severe liver disease with portal hypertension (CFLD) from 63 CF centers in the Uni

146 ality Improvement Program (NSQIP) formed the portal hypertension cohort, and were case matched to pat

147 eNOS activity and to a dramatic increase in portal hypertension compared to BDL in wild-type mice.

148 interventional treatments for patients with portal hypertension complications as well as to highligh

149 sidered as a noninvasive technique to manage portal hypertension complications.

150 re needed to identify clinically significant portal hypertension (CSPH) and esophageal varices (EVs)

151 CLD), the presence of clinically significant portal hypertension (CSPH) and varices needing treatment

152 Whether preoperative clinically significant portal hypertension (CSPH) has or not an impact on the o

153 nty-four patients had clinically significant portal hypertension (CSPH), of whom 59 had severe portal

154 ssociated cirrhosis and clinical significant portal hypertension (CSPH, hepatic venous pressure gradi

155 t (HVPG), and predict clinically significant portal hypertension (CSPH; HVPG >/= 10 mmHg), decompensa

156 sitive) with baseline clinically significant portal hypertension (CSPH; HVPG >=10 mmHg) and SVR after

157 Patients with liver cirrhosis and portal hypertension demonstrated faster-than-normal tran

158 llnesses include connective tissue diseases, portal hypertension, diet and stimulant drug use, HIV in

159 varices, which are most commonly a result of portal hypertension, downhill esophageal varices result

160 les) with patent umbilical vein and signs of portal hypertension due to liver cirrhosis.

161 ne recipients have evidence of non-cirrhotic portal hypertension due to periportal liver fibrosis or

162 ssociated with intrahepatic angiogenesis and portal hypertension during late-stage fibrosis, and hete

163 ediating inherited and acquired noncirrhotic portal hypertension, expand the phenotypic spectrum of D

164 rices (EVs) or having clinically significant portal hypertension (for presurgical risk stratification

165 had cirrhosis with clinical complications of portal hypertension from all patients (n = 271,030) hosp

166 Patients with NASH, cirrhosis, and portal hypertension (hepatic venous pressure gradient [H

167 nrolled patients with compensated cirrhosis, portal hypertension (hepatic venous pressure gradient [H

168 lity were associated with the development of portal hypertension, hepatosplenomegaly, gastrointestina

169 SA class, anesthesia type, inpatient status, portal hypertension history, and variable complication r

170 .1; 95% CI, 2.0 to 8.3), PAH associated with portal hypertension (HR, 3.6; 95% CI, 2.4 to 5.4), modif

171 Subjects with clinically insignificant portal hypertension (HVPG < 10 mm Hg) whose PLT remained

172 ss vary differently with respect to cause of portal hypertension (ie, congestion- or cirrhosis-induce

173 eoside analogue didanosine is known to cause portal hypertension in a subset of patients and lowers d

174 LCN2 contributes to liver fibrosis and portal hypertension in AH and could represent a new ther

175 l hemorrhage is a concerning complication of portal hypertension in children, the first bleed appears

176 etwork and are correlated to the severity of portal hypertension in cirrhosis.

177 contributes to splanchnic vasodilatation and portal hypertension in cirrhosis.

178 he presence of hepatic nodules, and signs of portal hypertension in consensus.

179 Data on the impact of portal hypertension in general surgical outcomes has bee

180 ading to extracellular matrix production and portal hypertension in liver cirrhosis.

181 ) to simulate congestive hepatopathy-induced portal hypertension in mice; some mice were given subcut

182 increased intrahepatic resistance (IHR) and portal hypertension in NASH cirrhotic rats.

183 ; these events subsequently increase IHR and portal hypertension in NASH cirrhotic rats.

184 ative SHAPE to HVPG measurements to diagnose portal hypertension in participants undergoing a transju

185 sed and correlated with disease severity and portal hypertension in patients with AH.

186 t leads to better control of RA secondary to portal hypertension in patients with cirrhosis, compared

187 lications related to liver insufficiency and portal hypertension in patients with heavy alcohol intak

188 f galectin 3 that reduces liver fibrosis and portal hypertension in rats and was safe and well tolera

189 rogeneous group of diseases characterized by portal hypertension in the absence of cirrhosis.

190 nosis and management of the complications of portal hypertension in the face of an increasing burden

191 early-onset familial idiopathic noncirrhotic portal hypertension, in which Mendelian mutations may ac

192 m 66 children with major endoscopic signs of portal hypertension, including grade 3 esophageal varice

193 reased risk attributable to complications of portal hypertension, including variceal rupture.

194 In patients with idiopathic noncirrhotic portal hypertension (INCPH), data on morbidity and morta

195 utant previously identified in a family with portal hypertension indicated basal constitutive channel

196 Portal hypertension, indicated by low platelet counts, w

197 Advanced fibrosis and portal hypertension influence short-term mortality.

198 rican Society of Anesthesiologists (ASA) >2, portal hypertension, intraoperative blood transfusions,

199 Idiopathic portal hypertension (IPH) is a rare cause of intrahepati

200 Portal hypertension is a clinical syndrome characterized

201 Having complications of portal hypertension is a harbinger of decompensated cirr

202 Idiopathic noncirrhotic portal hypertension is a heterogeneous group of diseases

203 Gastrointestinal bleeding related to portal hypertension is a serious complication in patient

204 Portal hypertension is associated with a significant mor

205 The most frequent cause of portal hypertension is cirrhosis.

206 The development of portal hypertension is fundamental in the pathogenesis o

207 re gradient (HVPG) is based on the fact that portal hypertension is pathogenically related to liver i

208 Portal hypertension is responsible for most of the compl

209 rrent standard for assessing the severity of portal hypertension is the invasive acquisition of hepat

210 Portal hypertension is the main complication of cirrhosi

211 In patients with cirrhosis, portal hypertension is the main driver of cirrhosis prog

212 urs in the context of advanced cirrhosis and portal hypertension, is associated with particularly hig

213 Idiopathic EHPVT, a significant cause of portal hypertension, is surgically corrected by MRB.

214 omoting liver sinusoidal capillarization and portal hypertension, ischemic heart disease, peripheral

215 is and management of idiopathic noncirrhotic portal hypertension, its pathogenesis remains elusive.

216 ociated with the development of noncirrhotic portal hypertension, likely owing to injury to the micro

217 n damage (eg, cytopenias, liver dysfunction, portal hypertension, malabsorption, and weight loss).

218 portosystemic shunt (TIPS) in patients with portal hypertension may be considered as a rescue therap

219 ed with progressively developed fibrosis and portal hypertension (mean stiffness at 80 Hz and 48-week

220 t hepatic fibrogenesis and cirrhosis, marked portal hypertension, microcirculatory dysfunction, an en

221 Noncirrhotic portal hypertension (NCPH) is a rare but important clini

222 Noncirrhotic portal hypertension (NCPH) is a rare but potentially lif

223 nce of Nogo-B ameliorates liver fibrosis and portal hypertension, Nogo-B blockade may be a potential

224 Once portal hypertension occurred, all subjects on TG were ch

225 ght subjects from six kindreds with onset of portal hypertension of indeterminate etiology during inf

226 lustrate the potential independent effect of portal hypertension on clinical outcome outside the sett

227 To evaluate the impact of noncirrhotic portal hypertension on survival in CGD, all records from

228 ections or, in case of minor resections, had portal hypertension or a MELD score greater than 9; and

229 may underestimate complications arising from portal hypertension or infection.

230 tio [OR], 2.41; 95% CI, 1.17-4.30; P = .01), portal hypertension (OR, 2.20; 95% CI, 1.13-4.30; P = .0

231 ephalopathy, esophageal varices, ascites, or portal hypertension) or liver transplant were estimated

232 e at risk of developing liver insufficiency, portal hypertension, or bowel infarction and may experie

233 nt may be a useful measure of progression of portal hypertension over time.

234 sence of a high-flow fistula, which elevated portal hypertension, patient did not qualify for the liv

235 the standard used to determine the degree of portal hypertension (PH) and an important prognostic fac

236 arkers would be useful for the assessment of portal hypertension (PH) and esophageal varices (EV) in

237 casan is a pan-caspase inhibitor that lowers portal hypertension (PH) and improves survival in murine

238 All patients had evidence of portal hypertension (PH) at diagnosis, and 42% were symp

239 resistance (IHVR) is the primary factor for portal hypertension (PH) development.

240 Pharmacological treatment of portal hypertension (PH) has been exclusively devoted to

241 UGIB was attributed to portal hypertension (PH) in 99 (63%) patients and peptic

242 Portal hypertension (PH) is a major cause of morbidity a

243 Portal hypertension (PH) is a recognized risk factor of

244 Portal hypertension (PH) is the main driver of cirrhosis

245 hosis, and the presence of clinical signs of portal hypertension (PH) were assessed using receiver op

246 Portal hypertension (PH), a pathophysiological derangeme

247 CB(2) agonist alleviates portal hypertension (PH), severity of portosystemic coll

248 logical alterations that are associated with portal hypertension (PH).

249 sequences, including fibrosis/cirrhosis with portal hypertension (PH).

250 rs of the presence of clinically significant portal hypertension (PH).

251 interferon (IFN)-free therapies ameliorates portal hypertension (PH); however, it remains unclear wh

252 hosis but also portal vein obstruction cause portal hypertension (PHT) and angiogenesis.

253 ular resistance that is the primary cause of portal hypertension (PHT) in cirrhosis.

254 Progression of portal hypertension (PHT) was defined as the onset of va

255 ices in those with compensated cirrhosis and portal hypertension (PHT).

256 ant discoveries about the pathophysiology of portal hypertension (PHT).

257 athways in different rat models of cirrhotic portal hypertension (PHT).

258 Mechanical forces contribute to portal hypertension (PHTN) and fibrogenesis.

259 with preoperative hierarchic interaction of portal hypertension, planned extension of hepatectomy, a

260 of a normal control), ascites, splenomegaly, portal hypertension (portal vein velocity, 3.9-5.6 cm/se

261 Liver cirrhosis and portal hypertension present with three unique pulmonary

262 experienced participants with cirrhosis and portal hypertension, prior liver transplantation (LT) or

263 The portal hypertension probably could be a result of incomp

264 In patients with bleeding related to portal hypertension, prophylactic antibiotics may decrea

265 within a prospective cohort of patients with portal hypertension recruited from tertiary care centers

266 oportions of patients in the LVP+A group had portal hypertension-related bleeding (18% vs 0%; P = .01

267 of varices and the incidence and outcome of portal hypertension-related bleeding.

268 Sixteen (33%) patients had one or more portal hypertension-related complication within 3 months

269 INCPH are at high risk of major surgical and portal hypertension-related complications when they harb

270 y of ascites (P = 0.02) were associated with portal hypertension-related complications within 3 month

271 TIPS) is now a standard for the treatment of portal hypertension-related complications.

272 The potential use of terutroban for portal hypertension requires further investigation.

273 ntrahepatic bile ducts + 2 x dysmorphy + 1 x portal hypertension; score with gadolinium administratio

274 mic encephalopathy, is a consequence of both portal hypertension (shunting of blood through portosyst

275 emic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosyst

276 l hypertension (CSPH), of whom 59 had severe portal hypertension (SPH).

277 classifications; explore and illustrate new 'portal hypertension theories' of gastric variceal diseas

278 leeding have changed after the emergence of 'portal hypertension theories' of proximity, throughput,

279 Hepatic stellate cells (HSCs) contribute to portal hypertension through multiple mechanisms that inc

280 ne age; sex; performance status; presence of portal hypertension; tumor distribution; levels of bilir

281 t survival in patients with complications of portal hypertension undergoing elective placement of tra

282 cardiography (TEE) in patients with signs of portal hypertension undergoing orthotopic liver transpla

283 rts of patients with idiopathic noncirrhotic portal hypertension undergoing TIPS in seven centers bet

284 patients (LD rate, 4.9% [11 of 226]) without portal hypertension underwent minor resection with a MEL

285 transit in patients with liver cirrhosis and portal hypertension using a magnet-based Motility Tracki

286 scular diseases and is associated with liver portal hypertension, vascular shunting, and portal fibro

287 Liver injury with portal hypertension was established using bile duct liga

288 s induced in rats by bile duct ligation, and portal hypertension was induced by partial portal vein l

289 Cirrhosis was present in 157 patients (91%); portal hypertension was present in 139 patients (81%).

290 Fibrosis and portal hypertension were attenuated based on immunostain

291 Hispanics hospitalized for complications of portal hypertension were less likely to undergo a pallia

292 rences with preserved liver function, and no portal hypertension were treated with resection.

293 unt is the best predictor of the severity of portal hypertension, which has early onset but is underd

294 In patients with idiopathic noncirrhotic portal hypertension who have normal kidney function or d

295 cutive patients with severe complications of portal hypertension who received placement of TIPS from

296 Patients with mild portal hypertension whose PLT remains greater than 100,0

297 Two rodent models of portal hypertension with increased BT were used, CCl(4)-

298 All three affected subjects had stable portal hypertension with noncirrhotic liver disease for

299 After the operation portal hypertension, with splenomegaly and symptoms of t

300 ely enrolled 300 patients with cirrhosis and portal hypertension without a history of hepatic encepha