ライフサイエンスコーパス: variceal

1 We also assessed variceal and nonvariceal bleeding.

2 ers (18%) than in nonresponders who received variceal band ligation (31%) (P = .06).

3 patic portosystemic stent-shunt (TIPSS) with variceal band ligation (VBL) in the secondary prophylaxi

4 With the advent of variceal band ligation and transjugular intrahepatic por

5 Variceal band ligation may be used to temporize acute va

6 nt options for secondary prophylaxis include variceal band ligation, beta blockers, a combination of

7 of patients had injection sclerotherapy and variceal band ligation, respectively.

8 f choice for esophageal variceal bleeding is variceal band ligation.

9 e drugs whereas nonresponders underwent only variceal band ligation.

10 Since its introduction, endoscopic variceal banding has been shown to be superior to needle

11 splant, and two were stable after esophageal variceal banding or diuretic therapy of ascites.

12 Patients who have had one variceal bleed are at high risk of rebleeding.

13 n, 9.3% versus 3.4%, P = 0.048, or who had a variceal bleed as the index presentation of AIH, 20% ver

14 lockers, ligation reduces the risk for first variceal bleed but has no effect on mortality.

15 atic portosystemic shunt, almost every acute variceal bleed can be controlled.

16 s causes of death in individuals after a non-variceal bleed compared with deaths in a matched sample

17 l varices and the prophylaxis of the initial variceal bleed has lagged behind these other interventio

18 c variceal ligation (EVL) to prevent a first variceal bleed have not been empirically studied.

19 A non-variceal bleed may therefore warrant a careful assessmen

20 y cost an incremental $12,408 per additional variceal bleed prevented.

21 -blocker therapy, the relative risk of first variceal bleed was 0.48 (0.24-0.96), with NNT of 13; how

22 nsitivity and specificity for detection of a variceal bleed were 67% and 75%, respectively.

23 ients with cirrhosis and a recent esophageal variceal bleed were randomized to either endoscopic band

24 prophylaxis or that prevention of a sentinel variceal bleed will ultimately improve survival; therefo

25 d, including one in the standard care group (variceal bleed) and two in the G-CSF and stem-cell infus

26 ne or more of the following events: varices, variceal bleed, ascites, encephalopathy, liver transplan

27 untreated controls, relative risks of first variceal bleed, bleed-related mortality, and all-cause m

28 d the number needed to treat (NNT) for first variceal bleed, bleed-related mortality, and all-cause m

29 nical features such as history of esophageal variceal bleed, encephalopathy or ascites, and laborator

30 rred in 11% of patients, including one fatal variceal bleed.

31 Among variceal bleeders, the odds ratio of death for AAs was 1

32 Death resulted from variceal bleeding (5 patients in the TIPS group and 3 in

33 Patients with cirrhosis with acute variceal bleeding (AVB) have high mortality rates (15%-2

34 proved effective in the prophylaxis of acute variceal bleeding (AVB).

35 Esophageal variceal bleeding (EVB) is a serious and common complica

36 rrhosis and massive or refractory esophageal variceal bleeding (EVB), but is frequently associated wi

37 Indications for TIPS were recurrent variceal bleeding (n = 25) and refractory ascites (n = 1

38 atients who had undergone TIPS placement for variceal bleeding (n = 28) or intractable ascites (n = 1

39 ons were intractable ascites (n = 14), acute variceal bleeding (n = 3), and hydrothorax (n = 2).

40 in comparison to that for the management of variceal bleeding (P =.001).

41 tions reviewed in this paper are varices and variceal bleeding (primary prophylaxis, treatment of the

42 tions reviewed in this paper are varices and variceal bleeding (primary prophylaxis, treatment of the

43 ons discussed in this review are varices and variceal bleeding (primary prophylaxis, treatment of the

44 ion (EVL) are used for primary prevention of variceal bleeding (VB) in patients with cirrhosis with m

45 Outcome of variceal bleeding (VB) in patients with hepatocellular c

46 Variceal bleeding (VB) was the most common manifestation

47 46 +/- 26 months) for primary end points of variceal bleeding and encephalopathy and secondary end p

48 uggest a new pathophysiology in the cause of variceal bleeding and imply new methods to prevent and t

49 rrhotic patients with acute gastroesophageal variceal bleeding and is an independent factor to predic

50 , prophylactic ligation reduces the risks of variceal bleeding and mortality.

51 ection is associated with failure to control variceal bleeding and needs to be evaluated in the plann

52 MRB for primary and secondary prophylaxis of variceal bleeding and other complications, if appropriat

53 bdominal and chest varices, gastroesophageal variceal bleeding and refractory ascites than sub-acute

54 Overall, only 2 patients (4%) had gastric variceal bleeding and required splenectomy.

55 igation plus nadolol in preventing recurrent variceal bleeding and several meta-analyses on trials co

56 in/terlipressin in the control of esophageal variceal bleeding and suggest it is a safe and effective

57 osis results in a high likelihood of gastric variceal bleeding and that splenectomy should be perform

58 novel ideas regarding the pathophysiology of variceal bleeding are described.

59 tient with refractory esophagogastroduodenal variceal bleeding as a result of diffuse portomesenteric

60 on developed refractory duodenal and jejunal variceal bleeding as a result of diffuse visceral splanc

61 fewer than one fifth of these patients have variceal bleeding before or after surgery.

62 patients with cirrhosis admitted with acute variceal bleeding between 2001 and 2010 were prospective

63 y than the 629 nonusers to have a history of variceal bleeding but less likely to have Child-Pugh cla

64 Gastric variceal bleeding from pancreatitis-induced splenic vein

65 n of beta blockers for primary prevention of variceal bleeding has become standard practice.

66 Prophylaxis against the first variceal bleeding has been proposed to reduce morbidity

67 Yet, the mortality rate from variceal bleeding has not changed significantly and the

68 al failure, when other treatment options for variceal bleeding have failed, particularly in a younger

69 From them, 163 admissions for variceal bleeding in 137 patients were included in the m

70 ion test in 157 episodes of gastroesophageal variceal bleeding in 143 patients with cirrhosis.

71 rly efficacious in the control of refractory variceal bleeding in Child-Pugh class A and B patients.

72 ll tolerated and greatly reduces the risk of variceal bleeding in children with biliary atresia and h

73 ylactically in one patient with a history of variceal bleeding in order to prevent this complication

74 Gastroesophageal variceal bleeding in patients with cirrhosis is associat

75 rapy could reduce rebleeding and death after variceal bleeding in patients with cirrhosis.

76 during the first 5 days after the episode of variceal bleeding in relation to the diagnosis of bacter

77 r clinical experience suggested that gastric variceal bleeding in these patients was uncommon.

78 to all patients with cirrhosis with previous variceal bleeding irrespective of prognostic stage.

79 Variceal bleeding is a life-threatening complication of

80 Variceal bleeding is a major complication of IPH.

81 Variceal bleeding is a severe complication of LC.

82 Variceal bleeding is difficult to treat in these patient

83 atment for primary prophylaxis of esophageal variceal bleeding is nonselective beta blockers.

84 igation sessions for treatment of esophageal variceal bleeding is uncertain.

85 ndoscopic treatment of choice for esophageal variceal bleeding is variceal band ligation.

86 Postoperative variceal bleeding necessitated splenectomy and gastric d

87 ed with a lower risk of recurrent or de novo variceal bleeding or ascites (hazard ratio, 0.11; 95% co

88 ct were more often correlated with recurrent variceal bleeding or ascites than were hepatic vein sten

89 onth intervals and for symptoms of recurrent variceal bleeding or ascites.

90 red as a rescue therapy in case of recurrent variceal bleeding or failure of endoscopic management.

91 PS) are sometimes used to reduce the risk of variceal bleeding or treat intractable ascites before or

92 udy was to compare the cost-effectiveness of variceal bleeding prophylaxis with propranolol, scleroth

93 copic therapy, TIPS leads to lower recurrent variceal bleeding rates and it is more cost effective in

94 Variceal bleeding refractory to medical treatment with b

95 e of a patient with massive gastroesophageal variceal bleeding refractory to numerous endoscopic trea

96 ts with cirrhosis and acute gastroesophageal variceal bleeding remains unknown.

97 lity in patients with cirrhosis and previous variceal bleeding stratified by cirrhosis severity (Chil

98 This risk of variceal bleeding was 5% for patients with CT-identified

99 withdrawal of propranolol, the freedom from variceal bleeding was not significantly different betwee

100 Since the procedure, no recurrent variceal bleeding was reported and the shunt remained pa

101 Variceal bleeding was the initial manifestation in 27 (1

102 AAs with variceal bleeding were more likely to have endoscopic va

103 Patients with cirrhosis with controlled variceal bleeding were randomized to an HVPG-guided ther

104 -Pugh class A and B cirrhosis and refractory variceal bleeding were randomized to DSRS or TIPS.

105 role in treatment of selected patients with variceal bleeding who are not present or future transpla

106 patients hospitalized with acute esophageal variceal bleeding who had successful ligation at present

107 that of 180 adult patients with a history of variceal bleeding who underwent transplantation soon aft

108 patients successfully treated for esophageal variceal bleeding with endoscopic sclerotherapy who rece

109 decompensation (ascites, encephalopathy, and variceal bleeding), hepatocellular carcinoma, liver tran

110 For variceal bleeding, 15 (28.8%) and 21 (40.4%) of patients

111 second episode of gastric and/or esophageal variceal bleeding, after hemodynamic stabilization upon

112 ergency portacaval shunt permanently stopped variceal bleeding, almost never became occluded, accompl

113 Five had variceal bleeding, and 2 had portosystemic shunts.

114 TIPS volume of </= 20 TIPS/year, variceal bleeding, and nosocomial infections were indepe

115 band ligation may be used to temporize acute variceal bleeding, and should be applied on the proximal

116 atorenal syndrome, hepatocellular carcinoma, variceal bleeding, and spontaneous bacterial peritonitis

117 patients with cirrhosis who have infections, variceal bleeding, as well as in patients with fulminant

118 ortality and coincided with hospitalization, variceal bleeding, bacterial infection, and/or developme

119 ng events, total days of hospitalization for variceal bleeding, blood transfusion requirements after

120 therapies have a role in temporizing active variceal bleeding, but relief of the underlying SVC obst

121 re, Child-Pugh score, serum sodium, previous variceal bleeding, cirrhosis etiology, and ascites sever

122 derwent successful endoscopic hemostasis for variceal bleeding, covered TIPS was superior to EVL + be

123 fter excluding 28 patients with a history of variceal bleeding, data on 183 patients were analyzed to

124 Major complications of cirrhosis, such as variceal bleeding, encephalopathy, and hepatorenal syndr

125 ly) on liver decompensation events (ascites, variceal bleeding, encephalopathy, and/or hepatocellular

126 tion in the development of ascites, varices, variceal bleeding, encephalopathy, liver transplantation

127 significant increases in the RR of ascites, variceal bleeding, encephalopathy, or death between the

128 te-Pugh score >or=7 on 2 consecutive visits, variceal bleeding, hepatic encephalopathy, and liver-rel

129 indications but also further decompensation (variceal bleeding, hepatorenal syndrome) and improves su

130 After variceal bleeding, long-term maintenance of hemodynamic

131 five AMA positive patients without ascites, variceal bleeding, or encephalopathy; a serum bilirubin

132 lopment of: ascites, hepatic encephalopathy, variceal bleeding, prothrombin <45%, serum bilirubin >45

133 outcomes [CTP > 7, ascites, encephalopathy, variceal bleeding, SBP, HCC, death] had significantly hi

134 opments in the pathophysiology of esophageal variceal bleeding, screening for esophageal varices, pre

135 elated adverse events such as liver failure, variceal bleeding, serious infections, spontaneous bacte

136 For the prevention of recurrent esophageal variceal bleeding, studies show that patients treated wi

137 good-risk patients underwent operations for variceal bleeding, the incidence of postoperative enceph

138 In conclusion, in patients with variceal bleeding, TIPS compared with ET reduces the reb

139 eening for esophageal varices, prediction of variceal bleeding, treatment of esophageal varices and n

140 158 patients) reported rates of spontaneous variceal bleeding, which occurred in a significantly low

141 or and minor bleedings and less incidence of variceal bleeding.

142 rates than TIPS in management of refractory variceal bleeding.

143 g and imply new methods to prevent and treat variceal bleeding.

144 n made in the area of the pathophysiology of variceal bleeding.

145 patient with decompensated cirrhosis died of variceal bleeding.

146 shunts are widely used for the management of variceal bleeding.

147 m for the prevention of recurrent esophageal variceal bleeding.

148 ns of portal hypertension such as ascites or variceal bleeding.

149 n for the prevention of recurrent esophageal variceal bleeding.

150 nd aspartate aminotransferase and history of variceal bleeding.

151 ood hepatic reserve for long-term control of variceal bleeding.

152 survival for patients treated surgically for variceal bleeding.

153 a median 51 (8-280) months, only one due to variceal bleeding.

154 se may lead to lethal complications, such as variceal bleeding.

155 ng sodium retention, ascites recurrence, and variceal bleeding.

156 patients with cirrhosis and gastroesophageal variceal bleeding.

157 Four presented with cholangitis and one with variceal bleeding.

158 The key inclusion criteria were: 1) variceal bleeding; 2) cirrhosis; 3) no need to modify th

159 hout liver transplantation; transplantation; variceal bleeding; development of ascites, encephalopath

160 register were used to define a cohort of non-variceal bleeds between 1997 and 2010.

161 he management of refractory ascites (RA) and variceal bleeds.

162 In combination group patients, each variceal column was ligated distally and 1 mL of ethanol

163 ers and endoscopic therapy can be managed by variceal decompression with either surgical shunts or tr

164 and beta-blockers do not reduce the risk of variceal development or progression.

165 of preprimary prophylaxis (PPP) is to avoid variceal development, and therefore it necessarily deals

166 -hemodynamic improvements, avoiding not only variceal development, but also other PH-related complica

167 The optimal interval would provide variceal eradication as rapidly as possible to lessen ea

168 endpoint was the proportion of patients with variceal eradication at 4 weeks.

169 Four-week variceal eradication occurred more often in the 1-week t

170 VBL was performed weekly until variceal eradication, and then at 3 months, 6 months, an

171 e and predictors of de novo gastroesophageal variceal formation and progression in a large cohort of

172 eters were analyzed as predictors of de novo variceal formation and variceal progression.

173 the hyperdynamic circulation contributes to variceal growth and hemorrhage.

174 the hyperdynamic circulation contributes to variceal growth and hemorrhage.

175 otic patients undergoing TIPSS insertion for variceal haemorrhage and correlate this with outcome.

176 e that bacterial infections in patients with variceal haemorrhage may be the critical factor that tri

177 26 patients with alcoholic cirrhosis and variceal haemorrhage were studied prior to and 1-hour af

178 n of these two effects leads to the onset of variceal haemorrhage.

179 ), pneumonia (7%), hemobilia (7%), esophagus variceal hemorrhage (3%), and vascular diseases (10%).

180 ranolol than banding patients had esophageal variceal hemorrhage (4/31 vs. 0/31; difference, 12.9%; P

181 jects who developed liver failure (7 vs. 3), variceal hemorrhage (5 vs. 8), or acute renal failure (3

182 opranolol, 24 former placebo), 9 experienced variceal hemorrhage (6 former propranolol, 3 former plac

183 Esophageal variceal hemorrhage (EVH) is a serious and expensive seq

184 , hepatorenal syndrome (HRS), and esophageal variceal hemorrhage (EVH).

185 , hepatorenal syndrome (HRS), and esophageal variceal hemorrhage (EVH)].

186 s, hepatorenal syndrome (HRS) and esophageal variceal hemorrhage (EVH)].

187 Patients at increased risk for variceal hemorrhage (HVPG >/= 12 mm Hg) had a significan

188 tion (defined as the development of ascites, variceal hemorrhage [VH], or hepatic encephalopathy [HE]

189 to 23 months after placement, with recurrent variceal hemorrhage and failed TIPS revision.

190 thal complications, such as gastroesophageal variceal hemorrhage and hepatic encephalopathy.

191 esponders to pharmacological therapy after a variceal hemorrhage are adequately protected from reblee

192 late may decrease the probability of gastric variceal hemorrhage compared to nonselective beta-blocke

193 Octreotide improved control of esophageal variceal hemorrhage compared with all alternative therap

194 late may decrease the probability of gastric variceal hemorrhage compared with nonselective beta-bloc

195 The frequency of variceal hemorrhage decreased from 3.5 to 0.5 episodes p

196 entified randomized trials of octreotide for variceal hemorrhage from computerized databases, scienti

197 Patients with cirrhosis and variceal hemorrhage have a high risk of rebleeding.

198 ction and the role of primary prophylaxis of variceal hemorrhage in children.

199 ) in the secondary prophylaxis of esophageal variceal hemorrhage in patients with cirrhosis.

200 rior to VBL for the secondary prophylaxis of variceal hemorrhage in patients with cirrhosis.

201 BBs) reduce portal pressure and the risk for variceal hemorrhage in patients with cirrhosis.

202 to the management of portal hypertension and variceal hemorrhage in pediatrics remain controversial,

203 in Asia, and drug or alcoholic hepatitis and variceal hemorrhage in the West.

204 Although variceal hemorrhage is a concerning complication of port

205 ocker therapy for the primary prophylaxis of variceal hemorrhage is a cost-effective measure, as the

206 dard care for prevention of first esophageal variceal hemorrhage is beta-blockade, but this may be in

207 spective studies on beta blockers to prevent variceal hemorrhage lack long-term follow-up, and indefi

208 was used to adjust trends in nonvariceal and variceal hemorrhage mortality for age, sex, and comorbid

209 the development of endoscopically documented variceal hemorrhage or a severe medical complication req

210 ain outcome measure was the cost per initial variceal hemorrhage prevented.

211 g they should be continued for prevention of variceal hemorrhage remains unknown.

212 Variceal hemorrhage requiring emergent TIPS placement (h

213 1 variables available before TIPS placement, variceal hemorrhage requiring emergent TIPS placement (r

214 When propranolol is withdrawn, the risk of variceal hemorrhage returns to what would be expected in

215 01 for spontaneous bacterial peritonitis and variceal hemorrhage to ascites: 0.01-0.03).

216 ere assigned randomly more than 5 days after variceal hemorrhage to groups given a small covered tran

217 ts and physicians for primary prophylaxis of variceal hemorrhage vary significantly.

218 The mortality following variceal hemorrhage was reduced from 24.6% to 20.9% (una

219 No episodes of repeat variceal hemorrhage were noted.

220 esented with the first episode of esophageal variceal hemorrhage were randomized to TIPSS (31) or VBL

221 of propranolol for the primary prevention of variceal hemorrhage were tapered off of propranolol and

222 Fifty-six patients had TIPS placement for variceal hemorrhage, 49 for refractory ascites, and 24 f

223 ions associated with cirrhosis, specifically variceal hemorrhage, ascites and hepatic encephalopathy.

224 sponsible for its most common complications: variceal hemorrhage, ascites, and portosystemic encephal

225 sponsible for its most common complications: variceal hemorrhage, ascites, and portosystemic encephal

226 spontaneous bacterial peritonitis, varices, variceal hemorrhage, encephalopathy).

227 ding 10 (56%) of 18 patients with refractory variceal hemorrhage, had thrombus in the portal venous s

228 cterial peritonitis, hepatic encephalopathy, variceal hemorrhage, hepatocellular carcinoma, and morta

229 r disease, and it predisposes the patient to variceal hemorrhage, hepatorenal syndrome, hepatopulmona

230 the protective effect of propranolol against variceal hemorrhage, noted previously, was no longer pre

231 gh-risk esophageal varices and no history of variceal hemorrhage, propranolol-treated patients had si

232 on, muscle wasting, ascites, esophagogastric variceal hemorrhage, spontaneous bacterial peritonitis,

233 ies potential risk of esophageal and gastric variceal hemorrhage.

234 ll (76.4%) and only 1% of patients developed variceal hemorrhage.

235 aneous bacterial peritonitis, and esophageal variceal hemorrhage.

236 h patients requiring primary prophylaxis for variceal hemorrhage.

237 and physicians for the primary prevention of variceal hemorrhage.

238 lockers decrease portal pressure and prevent variceal hemorrhage.

239 e development of gastroesophageal varices or variceal hemorrhage.

240 n (EVL) is performed to decrease the risk of variceal hemorrhage.

241 ing with propranolol for prevention of first variceal hemorrhage.

242 ty and efficacy of octreotide for esophageal variceal hemorrhage.

243 cological therapy of portal hypertension and variceal hemorrhage.

244 eon's 18-year experience with operations for variceal hemorrhage.

245 me Child-Pugh A or B patients with recurrent variceal hemorrhage.

246 ystem are common in patients with refractory variceal hemorrhage.

247 for acute (2) or sclerotherapy-resistant (3) variceal hemorrhage.

248 quently diagnosed in cirrhotic patients with variceal hemorrhage.

249 e use of portal decompression as therapy for variceal hemorrhage.

250 taneous bacterial peritonitis, or esophageal variceal hemorrhage.

251 taneous bacterial peritonitis, or esophageal variceal hemorrhage.

252 e both effective for primary prophylaxis for variceal hemorrhage; however, the route of administratio

253 bleeding were more likely to have endoscopic variceal hemostasis delayed more than 24 hours after adm

254 Endoscopic variceal ligation (EVL) and nonselective beta-blockers (

255 hough both beta-blockade (BB) and endoscopic variceal ligation (EVL) are used for primary prevention

256 Elective esophageal variceal ligation (EVL) is performed to decrease the ris

257 enter randomized trial, long-term endoscopic variceal ligation (EVL) or glue injection + beta-blocker

258 selective beta-blockers (BBs) and endoscopic variceal ligation (EVL) to prevent a first variceal blee

259 l varices without bleeding, prophylaxis with variceal ligation or beta-blockers was similar in terms

260 Endoscopic variceal ligation plus beta-blockers (EVL+BB) is current

261 of varices, a randomized trial of endoscopic variceal ligation plus nadolol in preventing recurrent v

262 macologic therapy, development of endoscopic variceal ligation, and the maturing of liver transplanta

263 tion for primary prophylaxis with endoscopic variceal ligation, sclerotherapy, or nonspecific beta-bl

264 of several randomized trials of prophylactic variceal ligation, the effect on bleeding-related outcom

265 ce of variceal rebleeding (41.9% vs. 42.9%), variceal obliteration (41.9% vs. 40.0%), hospital days,

266 safe and effective adjunctive therapy after variceal obliteration techniques.

267 ent of bleeding fundal varices is endoscopic variceal obturation.

268 The first regards increased variceal pressure during peristaltic contraction.

269 The second describes increased variceal pressure with increasing intraabdominal pressur

270 counts (P = .0002) were at greatest risk of variceal progression (area under the receiver operating

271 ing gastroesophageal varices, 74 (35.2%) had variceal progression or bleeding during follow-up.

272 predictors of de novo variceal formation and variceal progression.

273 reatment groups were similar in incidence of variceal rebleeding (41.9% vs. 42.9%), variceal oblitera

274 7 (0%) patients in the TIPS group, developed variceal rebleeding (P = 0.001).

275 ug therapy accurately stratifies the risk of variceal rebleeding (VRB).

276 nts, 173 had the procedure for prevention of variceal rebleeding and 58 for treatment of refractory a

277 and cost-effectiveness for the prevention of variceal rebleeding and patient survival at 1-year follo

278 treatment (ET) is frequently used to prevent variceal rebleeding but this still occurs in about 50% o

279 Outcomes of therapies to prevent variceal rebleeding differ depending on cirrhosis severi

280 varices, rebleeding from varices, number of variceal rebleeding events, total days of hospitalizatio

281 vered TIPS was straightforward and prevented variceal rebleeding in patients with Child A or B cirrho

282 During follow-up (mean 27 +/- 29 months), variceal rebleeding occurred in 7/25 (28%), including th

283 oing elective TIPS, either for prevention of variceal rebleeding or for treatment of refractory ascit

284 owing elective TIPS for either prevention of variceal rebleeding or for treatment of refractory ascit

285 EL and ES had similar cost/variceal rebleeding prevented ($28,678 vs. $29,093) and

286 ockers (EVL+BB) is currently recommended for variceal rebleeding prophylaxis, a recommendation that e

287 are is relevant, and in published studies on variceal rebleeding prophylaxis, there is a lack of info

288 The frequency and the severity of variceal rebleeding was significantly lower in the TIPSS

289 Variceal rebleeding was significantly more frequent with

290 f antibiotic prophylaxis in preventing early variceal rebleeding, and a trial of synbiotic therapy in

291 In the prevention of variceal rebleeding, beta-blockers +/- nitrates are as e

292 ligation is the standard approach to prevent variceal rebleeding, but bleeding recurs and mortality i

293 erior to EVL + beta-blocker for reduction of variceal rebleeding, but did not improve survival.

294 the first choice treatment for prevention of variceal rebleeding.

295 The primary end point was variceal rebleeding.

296 ffects of TIPS on portal pressures and flow, variceal resolution, and hepatic function.

297 plications of portal hypertension, including variceal rupture.

298 16,355 patients with a non-variceal upper gastrointestinal bleed were matched to 81

299 ents with liver cirrhosis, patients with non-variceal upper gastrointestinal bleeding, and patients w

300 ty in England following both nonvariceal and variceal upper gastrointestinal hemorrhage decreased fro