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 osorbide-mononitrate (ISMN), carvedilol, and variceal band ligation (VBL), alone or in combination, w

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 opathy, hepatocellular carcinoma, esophageal variceal bleed, and spontaneous bacterial peritonitis.

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

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

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

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

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

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

33 langitis (31%), synthetic failure (25%), and variceal bleeding (14%).

34 Patients admitted with acute variceal bleeding (AVB) and Child-Pugh C score (CP-C) or

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

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

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

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

39 e conventional arm (4.0%) developed incident variceal bleeding (log-rank test P = 0.724).

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

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

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

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

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

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

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

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

48 Variceal bleeding (VB) was the most common manifestation

49 During follow-up, 45 patients had variceal bleeding and 61 died.

50 46 +/- 26 months) for primary end points of variceal bleeding and encephalopathy and secondary end p

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

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

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

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

55 atients recruited in this trial for incident variceal bleeding and other hepatic events.

56 proaches in primary prevention of esophageal variceal bleeding and overall survival in patients with

57 Clinical outcome measures included survival, variceal bleeding and rebleeding, early-stage HCC, liver

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

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

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

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

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

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

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

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

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

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

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

69 s significantly higher within admissions for variceal bleeding compared with nonelective ICU admissio

70 tcome of this prospective study was incident variceal bleeding confirmed with upper endoscopy.

71 The proportion of ICU admissions for variceal bleeding fell significantly from 0.8% (83/42,56

72 Gastric variceal bleeding from pancreatitis-induced splenic vein

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

74 ICU and mortality of cirrhotic patients with variceal bleeding has declined significantly over time c

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

76 vascular procedures in patients with gastric variceal bleeding have changed after the emergence of 'p

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

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

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

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

81 ICU admissions for variceal bleeding in cirrhotic patients accounted for 4,

82 Gastroesophageal variceal bleeding in patients with cirrhosis is associat

83 se all-cause mortality and the risk of first variceal bleeding in patients with cirrhosis with large

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

85 ening were at similarly low risk of incident variceal bleeding in the future; patients with cirrhosis

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

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

88 Variceal bleeding is a life-threatening complication of

89 Variceal bleeding is a major complication of IPH.

90 Variceal bleeding is a severe complication of LC.

91 Variceal bleeding is a worrisome and potentially fatal c

92 Variceal bleeding is difficult to treat in these patient

93 Nonetheless, gastric variceal bleeding is more severe and associated with wor

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

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

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

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

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

99 ifference in the reduction in mortality from variceal bleeding over time between liver transplant and

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

101 Variceal bleeding refractory to medical treatment with b

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

103 The management of acute esophageal variceal bleeding remains a clinical challenge.

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

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

106 ed to simplify the risk stratification after variceal bleeding using clinical data and HVPG.

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

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

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

110 Variceal bleeding was the initial manifestation in 27 (1

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

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

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

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

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

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

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

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

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

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

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

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

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

124 f cirrhotic patients admitted to the ICU for variceal bleeding, and to compare it to the outcomes of

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

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

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

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

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

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

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

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

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

134 presence of hepatic encephalopathy, ascites, variceal bleeding, hepatocellular carcinoma, paracentesi

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

136 After variceal bleeding, long-term maintenance of hemodynamic

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

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

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

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

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

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

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

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

145 158 patients) reported rates of spontaneous variceal bleeding, which occurred in a significantly low

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

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

148 patients with cirrhosis and gastroesophageal variceal bleeding.

149 Four presented with cholangitis and one with variceal bleeding.

150 rates than TIPS in management of refractory variceal bleeding.

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

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

153 cause mortality and prevention of esophageal variceal bleeding.

154 patient with decompensated cirrhosis died of variceal bleeding.

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

156 m for the prevention of recurrent esophageal variceal bleeding.

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

158 n for the prevention of recurrent esophageal variceal bleeding.

159 nd aspartate aminotransferase and history of variceal bleeding.

160 (0.64; 0.38-1.07) for primary prevention of variceal bleeding.

161 proach for primary prophylaxis of esophageal variceal bleeding.

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

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

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

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

166 ACLF type; I: drug, infection, surgery, and variceal bleeding; R: systemic inflammatory response syn

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

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

169 hysiology of collateral circulation, gastric variceal classification has been refined to include infl

170 ve endovascular treatments such as shunt and variceal complex embolization with or without transjugul

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

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

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

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

175 ew 'portal hypertension theories' of gastric variceal disease and corresponding management and shed l

176 an improvement in the management of gastric variceal disease through newer modalities of treatment s

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

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

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

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

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

182 the hyperdynamic circulation contributes to variceal growth and hemorrhage.

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

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

185 26 patients with alcoholic cirrhosis and variceal haemorrhage were studied prior to and 1-hour af

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

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

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

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

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

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

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

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

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

195 Participants at increased risk for variceal hemorrhage (HVPG >=12 mm Hg) had a higher mean

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

197 elopment of hepatic decompensation (ascites, variceal hemorrhage and hepatic encephalopathy), which d

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

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

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

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

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

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

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

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

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

207 t and for the treatment of gastro-esophageal variceal hemorrhage in patients with decompensated cirrh

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

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

210 Although variceal hemorrhage is a concerning complication of port

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

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

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

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

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

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

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

218 Variceal hemorrhage requiring emergent TIPS placement (h

219 1 variables available before TIPS placement, variceal hemorrhage requiring emergent TIPS placement (r

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

221 01 for spontaneous bacterial peritonitis and variceal hemorrhage to ascites: 0.01-0.03).

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

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

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

225 No episodes of repeat variceal hemorrhage were noted.

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

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

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

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

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

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

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

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

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

235 ndpoint was hepatic decompensation (ascites, variceal hemorrhage, or encephalopathy).

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

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

238 resence of extrahepatic biliary disease, and variceal hemorrhage, which predicted 2-year and 10-year

239 taneous bacterial peritonitis, or esophageal variceal hemorrhage.

240 taneous bacterial peritonitis, or esophageal variceal hemorrhage.

241 ies potential risk of esophageal and gastric variceal hemorrhage.

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

243 aneous bacterial peritonitis, and esophageal variceal hemorrhage.

244 h patients requiring primary prophylaxis for variceal hemorrhage.

245 and physicians for the primary prevention of variceal hemorrhage.

246 lockers decrease portal pressure and prevent variceal hemorrhage.

247 e development of gastroesophageal varices or variceal hemorrhage.

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

249 ing with propranolol for prevention of first variceal hemorrhage.

250 ty and efficacy of octreotide for esophageal variceal hemorrhage.

251 cological therapy of portal hypertension and 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 oracentesis, and routine upper endoscopy for variceal ligation in patients with hepatic synthetic dys

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

284 Variceal rebleeding was significantly more frequent with

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

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

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

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

289 the first choice treatment for prevention of variceal rebleeding.

290 The primary end point was variceal rebleeding.

291 plications of portal hypertension, including variceal rupture.

292 iver cirrhosis who had undergone LSSM-guided variceal screening were at similarly low risk of inciden

293 surveillance (HR, 0.92; 95% CI, 0.90-0.95), variceal surveillance (HR, 0.93; 95% CI, 0.89-0.99), and

294 outpatient access to specialty care was 71%, variceal surveillance was 32%, and early postdischarge c

295 care, hepatocellular carcinoma surveillance, variceal surveillance, quality of inpatient care for upp

296 16,355 patients with a non-variceal upper gastrointestinal bleed were matched to 81

297 d teaching others to treat patients with non-variceal upper gastrointestinal bleeding (NVUGIB).

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

299 opic therapies in treating patients with non-variceal upper gastrointestinal bleeding.

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