ライフサイエンスコーパス: varices

1 lesser curve) or GOV2 (esophageal and fundal varices).

2 ulcers, two receiving therapy for esophageal varices).

3 entified by both EGD and HRES as grade I (no varices).

4 ntity from the more common distal esophageal varices.

5 s following bleeding due to malignancies and varices.

6 during OLT in patients with esophagogastric varices.

7 ficantly associated with the presence of new varices.

8 best cutoff values for the detection of new varices.

9 ence the risk of developing new or enlarging varices.

10 nd endoscopic screening for gastroesophageal varices.

11 eening test for identifying large esophageal varices.

12 urvival times of patients who have bled from varices.

13 copy irrespective of the prevalence of large varices.

14 determine the optimal screening strategy for varices.

15 re endoscopic screening for large esophageal varices.

16 ating the use of beta-blockers in preventing varices.

17 lymph nodes, the azygos vein, or esophageal varices.

18 aging and pressure measurement of esophageal varices.

19 es and new modalities to evaluate esophageal varices.

20 ncluding 56% (57 of 102) with moderate/large varices.

21 dentified varices and 18% for EGD-identified varices.

22 sophageal varices and of moderate/large size varices.

23 r disease predict the presence of esophageal varices.

24 fit from endoscopic screening for esophageal varices.

25 (PSC) may develop and bleed from esophageal varices.

26 hemorrhage in those found to have esophageal varices.

27 e independent predictors for the presence of varices.

28 al hypertension and bleeding from esophageal varices.

29 49%), mesenteric edema; 14 (40%), mesenteric varices.

30 a conglomerate mass of varices, or tumorous varices.

31 albumin levels but not with splenomegaly or varices.

32 rolling bleeding from esophageal and gastric varices.

33 ot achieved regarding primary prophylaxis of varices.

34 thods that would enable rapid eradication of varices.

35 TIPS is higher than after HGPCS for bleeding varices.

36 ention for patients with bleeding esophageal varices.

37 d to treat patients with bleeding esophageal varices.

38 urement and endoscopic grading of esophageal varices.

39 y for the detection and sizing of esophageal varices.

40 method of determining the size of esophageal varices.

41 patients with major bleeding from esophageal varices.

42 nerstone of definitive treatment of downhill varices.

43 t common cause actual bleeding from downhill varices.

44 e ability to visually confirm eradication of varices.

45 al of being able to visualize eradication of varices.

46 djusted for Child-Pugh stage and presence of varices.

47 s who underwent endoscopy were found to have varices.

48 liary atresia and high-risk gastroesophageal varices.

49 mber of 4.6 sessions was needed to eradicate varices.

50 ldren with portal hypertension and high-risk varices.

51 ood products among patients with and without varices.

52 By the end of the study, 25 patients had new varices (20.2%).

53 Most patients (75%) had esophageal varices, 21% were Child-B, and 29% had at least 1 previo

54 CI: 1.14-3.68) and development of esophageal varices (3.11; 95% CI: 1.57-10.65) were significantly hi

55 one versus 35%, P = 0.002), gastroesophageal varices (5% versus 30%, P = 0.03), and stage III/IV dise

56 malignancy (95% died within three years) and varices (52%).

57 ulcer was the most common cause, followed by varices [52 (18.1%)] and gastritis [51 (17.1%)].

58 ents who underwent endoscopy was oesophageal varices (57%), followed by peptic ulcer disease (18%) an

59 210 patients with existing gastroesophageal varices, 74 (35.2%) had variceal progression or bleeding

60 Most varices (82.2%) were documented in the esophagus, 4.2% i

61 trial of beta-blockers in the prevention of varices, a randomized trial of endoscopic variceal ligat

62 rial of beta-blockers in patients with small varices, a randomized trial of transjugular intrahepatic

63 ; development of ascites, encephalopathy, or varices; a doubling of serum bilirubin to 2.5 mg/dL or g

64 ignancy (48 and 32 respectively) and gastric varices aetiologies (2.8) when compared with other bleed

65 eding was 5% for patients with CT-identified varices and 18% for EGD-identified varices.

66 In patients with large varices and a high wall tension, the release of endotoxi

67 CT can demonstrate varices and ascites before frank cirrhosis is evident an

68 .013, .002, respectively), and the number of varices and collateral vessels increased significantly (

69 our, iron or fat deposition, and presence of varices and collateral vessels.

70 2 situations: prevention of rebleeding from varices and control of refractory cirrhotic ascites.

71 atment for a standardized patient with large varices and examined the influence of treatment characte

72 Five of the 12 patients had proved gastric varices and five were presumed to have varices on the ba

73 h cirrhosis require screening for esophageal varices and for liver cancer.

74 All patients had bleeding varices and had failed nonoperative management.

75 atients in screening programs for esophageal varices and hepatocellular carcinoma.

76 f variceal bleeding, treatment of esophageal varices and new modalities to evaluate esophageal varice

77 nts with cirrhosis with high-risk esophageal varices and no history of variceal hemorrhage, propranol

78 endoluminal ultrasound imaging of esophageal varices and noninvasive pressure measurement that progre

79 dentify independent predictors of esophageal varices and of moderate/large size varices.

80 ineffective in preventing the development of varices and other complications of PH.

81 further investigate the relationship between varices and PLT at the time of endoscopy, (2) investigat

82 ted patients with newly diagnosed esophageal varices and practicing gastroenterologists were enrolled

83 In obliterating varices and reducing rebleeding events from esophageal v

84 Endpoints were development and growth of varices and the incidence and outcome of portal hyperten

85 and the pharmacologic therapy of esophageal varices and the prophylaxis of the initial variceal blee

86 nt symptom of decompensated liver cirrhosis, varices and ulcerations in the upper gastrointestinal tr

87 fic complications reviewed in this paper are varices and variceal bleeding (primary prophylaxis, trea

88 fic complications reviewed in this paper are varices and variceal bleeding (primary prophylaxis, trea

89 c complications discussed in this review are varices and variceal bleeding (primary prophylaxis, trea

90 nts enrolled were reviewed for predictors of varices and we excluded 26 patients who had esophageal v

91 rsening liver disease (cirrhosis, esophageal varices, and deterioration in liver function).

92 t number of gastric varices, peri-esophageal varices, and extraluminal pathology were identified by C

93 portal hemodynamics, esophageal and gastric varices, and hepatic function have not been fully define

94 unt, higher alkaline phosphatase, esophageal varices, and smoking was developed to predict the risk o

95 h a small heterogeneously attenuating liver, varices, and splenomegaly.

96 ychological comorbid conditions, presence of varices, and the absence of decompensated liver disease

97 refer a patient for endoscopic screening for varices, and to enroll patients in a screening program f

98 Risk of CSPH, varices, and VNT was modeled with logistic regression.

99 es, thrombocytopenia, esophageal and gastric varices, anemia, and increased levels of liver enzymes,

100 Viewed in profile, the varices appeared as smooth submucosal masses with undula

101 Downhill esophageal varices are a distinct entity from the more common dista

102 Proximal or 'downhill' esophageal varices are a rare cause of upper gastrointestinal hemor

103 al bleedings from ulcers or esophago-gastric varices are life threatening medical conditions which re

104 thophysiology and hemodynamics of esophageal varices are not well understood.

105 high risk patients followed by BB therapy if varices are present (sEGD-->BB), (4) selective screening

106 d by beta-blocker (BB) therapy (EGD-->BB) if varices are present, (2) EGD followed by endoscopic band

107 ndoscopic band ligation (EBL) (EGD-->EBL) if varices are present, (3) selective screening endoscopy (

108 ng endoscopy followed by EBL (sEGD-->EBL) if varices are present, (5) empiric beta-blocker therapy in

109 se were independent predictors of esophageal varices (area under the receiver operator characteristic

110 progression to cirrhosis; the development of varices, ascites, or encephalopathy; sustained quadrupli

111 ensation (hepatic encephalopathy, esophageal varices, ascites, or portal hypertension) or liver trans

112 Patients with varices at baseline also had an endoscopy at 2 years.

113 to define the predictors for the presence of varices at baseline and for newly developing varices in

114 d we excluded 26 patients who had esophageal varices at baseline so that predictors of newly developi

115 those without bleeding at diagnosis, 74% had varices at first endoscopy.

116 ficant PH (HVPG >/= 10 mm Hg) and esophageal varices at high risk of bleeding.

117 ignificantly associated with the presence of varices at initial endoscopy (odds ratio = 1.9 and 3.9).

118 ignificantly associated with the presence of varices at initial endoscopy.

119 obstruction result in bleeding from downhill varices at such a high rate, despite being a less common

120 d trial comparing TIPS to HGPCS for bleeding varices began in 1993.

121 Emergency treatment of bleeding esophageal varices (BEV) consists mainly of endoscopic and pharmaco

122 leeding in patients with cirrhosis and large varices but not to prevent the development of varices in

123 st patients bleed from esophageal or gastric varices, but bleeding from ectopic varices or portal hyp

124 fied patients with very low risk of all-size varices, but both LSPS and a model combining TE and plat

125 come measures were development of cirrhosis, varices, cholangiocarcinoma, liver transplantation, or d

126 MR images showed pretibial varices connected to an enlarged vessel in the tibia tha

127 ageal varices, prevention of rebleeding from varices, control of refractory cirrhotic ascites and hep

128 dominal CT as the initial screening test for varices could be cost-effective.

129 eline so that predictors of newly developing varices could be determined.

130 Although patients with varices demonstrated a significantly longer prothrombin

131 ly bleeding esophageal or contiguous gastric varices despite sclerotherapy were assessed for risk of

132 sitivity in the identification of esophageal varices determined to be large on endoscopy, but only ab

133 De novo varices developed in 157 of the 598 (26.2%) patients.

134 Varices developed less frequently among patients with a

135 logy files revealed 86 patients with gastric varices diagnosed during double-contrast upper gastroint

136 st-line therapy in the treatment of bleeding varices due to portal hypertension, although they have n

137 bus, lesions suggestive of tumor, mesenteric varices, edema, or splenorenal shunt were recorded.

138 important disease (endometriosis and pelvic varices, endometriosis, adenomyosis, or pelvic adhesions

139 t of portal hypertension (PH) and esophageal varices (EV) in patients with cirrhosis.

140 From 2005 to 2012, patients with esophageal varices (EV) in the National Surgical Quality Improvemen

141 isolation or in combination with esophageal varices (EV).

142 hout (stage 1) and with (stage 2) esophageal varices (EV).

143 es correlate with the presence of esophageal varices (EV).

144 es were identified in 41 patients (77%) with varices evident on computed tomography (CT) in 40 of 53

145 nt portal hypertension (CSPH) and esophageal varices (EVs) in patients with compensated cirrhosis.

146 likelihood of harboring high-risk esophageal varices (EVs) or having clinically significant portal hy

147 cirrhosis with moderate to large esophageal varices (EVs), the more cost-effective option is uncerta

148 Fundic gastric varices failed to resolve in 6 of 12 cases.

149 se such as refractory ascites and esophageal varices for patients awaiting liver transplantation.

150 whereas a lower rate of abdominal and chest varices, gastroesophageal variceal bleeding and refracto

151 ith cirrhosis to screen for gastroesophageal varices (GEV).

152 o assess the development of gastroesophageal varices (GEV).

153 Gastroesophageal varices (GOV) are classified as GOV1 (EV extending down

154 oderate hepatic fibrosis or gastroesophageal varices (GOV) at oesophago-gastroduodenoscopy (OGD) has

155 72.5%) of 396 analyzed patients: 130 (32.8%) varices grade I (<5 mm under insufflation) and 157 (39.6

156 I (<5 mm under insufflation) and 157 (39.6%) varices grade II (>5 mm under insufflation).

157 In those with small esophageal varices, growth to LEVs was observed in 13%, 40%, and 54

158 Gastric varices (GV) occur in 20% of patients with portal hypert

159 Tumorous varices had a mean size of 6.8 cm (range, 3-11 cm).

160 sibly related to sunitinib], one oesophageal varices haemorrhage [possibly related to sunitinib], one

161 (one case each of renal failure, oesophageal varices haemorrhage, circulatory collapse, wound infecti

162 ments for strictures and bleeding esophageal varices have been proposed and may improve outcomes, alt

163 ESLD was defined as bleeding esophageal varices, hepatic encephalopathy, persistent ascites, or

164 y were worse and the frequency of esophageal varices higher with increasing Ishak stage (P < 0.0001).

165 (HR 0.97; 95% CI: 0.94-0.99), and esophageal varices (HR 1.70; 95% CI: 1.21-2.38) but not with the pr

166 10 patients with no varices seen on EGD had varices identified by HRES.

167 Isolated gastric varices (IGV) may be located in the fundus (IGV1) or els

168 status, AST, abdominal pain, and esophageal varices improved the discriminatory ability of CLIP.

169 There was evidence of perigastric varices in 16 of 65 (25%) patients who had follow-up ima

170 wed no varices in 52 (34%), small esophageal varices in 28 (19%), large esophageal varices (LEVs) in

171 copy in the remaining 151 patients showed no varices in 52 (34%), small esophageal varices in 28 (19%

172 We assessed the course of gastroesophageal varices in a large cohort of patients with chronic PVT.

173 were no clinical consequences of perigastric varices in any patient during a follow-up period of up t

174 The course of varices in chronic noncirrhotic, nontumoral PVT appears

175 ES) was used to image and measure esophageal varices in control subjects and patients with portal hyp

176 Development of varices in patients with chronic hepatitis C is associat

177 The predictors for developing varices in patients with primary sclerosing cholangitis

178 as to determine the prevalence of esophageal varices in patients with PSC and the variables that pred

179 However, the exact prevalence of esophageal varices in patients with PSC remains unknown and potenti

180 varices at baseline and for newly developing varices in patients with PSC.

181 ted with an increased risk of developing new varices in patients with PSC.

182 oscopic and radiologic therapy of esophageal varices in the past few years.

183 known and potential predictors of esophageal varices in this population have not been identified.

184 arices but not to prevent the development of varices in those with compensated cirrhosis and portal h

185 beta-blockers are ineffective in preventing varices in unselected patients with cirrhosis and portal

186 irrhosis and portal hypertension but without varices included in a trial evaluating the use of beta-b

187 cent (102 of 283) of patients had esophageal varices including 56% (57 of 102) with moderate/large va

188 First-line treatment of bleeding fundal varices is endoscopic variceal obturation.

189 This update and review of esophageal varices is given in five sections: new developments in t

190 m portal hypertensive gastropathy or ectopic varices is less common.

191 y for endoscopic screening and management of varices is the same as in cirrhosis.

192 Bleeding from gastric varices is treated by injection with cyanoacrylate.

193 Their effectiveness in preventing varices is unknown.

194 radiologists was good regarding the size of varices (Kappa = 0.56), and exceeded agreement between e

195 Fundal varices, large GV (>5 mm), presence of a red spot, and C

196 hageal varices in 28 (19%), large esophageal varices (LEVs) in 60 (40%), and gastric varices without

197 e progression (the development of cirrhosis, varices, liver transplantation, or death) tended to have

198 tis, benign and malignant esophageal tumors, varices, lower esophageal rings, diverticula, and esopha

199 Tumorous gastric varices manifest as remarkably similar findings on doubl

200 Viewed en face, the varices manifested as a conglomerate of thickened, tortu

201 Orbital varices may be recurrent, even after n-butyl cyanoacryla

202 atter of concern especially in case of large varices (more than 1 cm).

203 ]), with either no varices (n = 80) or small varices (n = 114), and 79 had an HVPG >5 and <10 mm Hg (

204 ng of the hilum (n = 137) or extensive hilar varices (n = 18) were encountered.

205 ts with less advanced disease frequently had varices (n = 33 [62%]) and ascites (n = 13 [24%]).

206 ally significant PHT [CSPH]), with either no varices (n = 80) or small varices (n = 114), and 79 had

207 y significant portal hypertension (CSPH) and varices needing treatment (VNT) bears prognostic and the

208 of patients at very low risk (<5%) of having varices needing treatment (VNT).

209 case matched to patients without esophageal varices (NEV) based on sex, age, surgery type, and year

210 ber of 4.2 sessions were needed to eradicate varices; no bleeding from gastroesophageal varices was o

211 wo patients of Child's class C with bleeding varices not amenable to endoscopic sclerotherapy or band

212 ful obliteration of varices, rebleeding from varices, number of variceal rebleeding events, total day

213 Higher vWF-Ag levels were associated with varices (odds ratio [OR] = 3.27; P < 0.001), ascites (OR

214 Fundic gastric varices often fail to disappear after TIPS.

215 characteristic features of tumorous gastric varices on double-contrast studies so that they are not

216 stric varices and five were presumed to have varices on the basis of additional diagnostic test resul

217 isk factors for bleeding, such as esophageal varices or a low platelet count, are frequently present

218 ence of PH defined as presence of esophageal varices or ascites or low platelet count and splenomegal

219 l hypertension, including grade 3 esophageal varices or grade 2 varices with red wale markings and/or

220 r gastric varices, but bleeding from ectopic varices or portal hypertensive gastropathy is also possi

221 oint was the development of gastroesophageal varices or variceal hemorrhage.

222 ectively every 3 months until development of varices or VH or end of study.

223 fined by the presence of ascites, esophageal varices, or hepatic encephalopathy, or when ESLD was sta

224 linical characteristics: ascites, esophageal varices, or total bilirubin greater than 2 mg/dL.

225 atients, 12 (14%) had a conglomerate mass of varices, or tumorous varices.

226 ies of patients who presented with pretibial varices over an 8-year period were collected from four i

227 with and those without high-risk esophageal varices (P = .09-.42).

228 endently associated with baseline esophageal varices (P = 0.01) and prothrombin time (P = 0.002), but

229 In addition, a significant number of gastric varices, peri-esophageal varices, and extraluminal patho

230 vo development or aggravation of preexisting varices, portal hypertensive gastropathy, or ascites.

231 ma, ascites, pleural effusion, splenomegaly, varices, portal venous thrombosis, and serum albumin lev

232 variceal bleeding, screening for esophageal varices, prediction of variceal bleeding, treatment of e

233 s include actively bleeding gastroesophageal varices, prevention of rebleeding from varices, control

234 In patients with gastric varices, primary prophylaxis with cyanoacrylate may decr

235 In patients with gastric varices, primary prophylaxis with cyanoacrylate may decr

236 Varices reappeared in 37% of children, and 97% survived

237 Varices reappeared in 45%, and 10% had breakthrough blee

238 ion of follow-up, successful obliteration of varices, rebleeding from varices, number of variceal reb

239 been exclusively devoted to gastroesophageal varices-related events at different frameworks, includin

240 Patients who have bled from varices remain at risk for rebleeding.

241 Hemorrhage from esophageal varices remains a substantial management problem.

242 Gastroesophageal varices result almost solely from portal hypertension, a

243 Gastroesophageal varices result almost solely from portal hypertension, a

244 of portal hypertension, downhill esophageal varices result from vascular obstruction of the superior

245 Analyses of the varices risk score and LSPS were superior to all other n

246 tatistical models: the PH risk score and the varices risk score.

247 Eight of the 10 patients with no varices seen on EGD had varices identified by HRES.

248 of ascites and prevention of rebleeding from varices should be limited to a select group of patients.

249 erotherapy will allow quicker eradication of varices than either modality alone.

250 antly less likely to rebleed from esophageal varices than patients receiving sclerotherapy (3 of 24 c

251 In those with large varices, the 1-year probability of first bleeding despit

252 In patients without varices, the probability of developing them was 2%, 22%,

253 agents for the treatment of bleeding gastric varices, the successful treatment of early gastric cance

254 the alternative pathophysiology of downhill varices, they require a unique approach to management.

255 ; P = .008), less frequent gastroesophageal varices (three of 19 [16%] vs 20 of 41 [49%], P = .021),

256 arices with red wale markings and/or gastric varices, treated consecutively from February 2001 throug

257 identified bilirubin, cirrhosis, esophageal varices, tumor size, and macrovascular invasion to be st

258 in patients with documented esophagogastric varices undergoing OLT.

259 ment of one or more of the following events: varices, variceal bleed, ascites, encephalopathy, liver

260 ual reduction in the development of ascites, varices, variceal bleeding, encephalopathy, liver transp

261 (ascites, spontaneous bacterial peritonitis, varices, variceal hemorrhage, encephalopathy).

262 l rebleeding rate for endoscopic therapy for varices was 16.7%.

263 50 x 10(3)/dL for the presence of esophageal varices was 6.3 (95% CI: 2.6-15.8).

264 The sensitivity of CT in detecting gastric varices was 87%.

265 The likelihood of developing varices was associated with subject race (Hispanic > Cau

266 , and between endoscopists regarding size of varices was determined using kappa statistic.

267 iologic evidence of asymptomatic perigastric varices was identified in 25% of patients.

268 e varices; no bleeding from gastroesophageal varices was observed after eradication.

269 tial screening modality for the detection of varices was significantly more cost-effective compared t

270 natural history of cirrhosis with esophageal varices was simulated using a Markov model.

271 due to UGIB in 4 patients (2.4%) Oesophageal varices was the most common cause of UGIB.

272 Varices were assessed by endoscopy and angiography.

273 Varices were documented by esophagogastroduodenoscopy in

274 Esophageal varices were encountered in 1 patient after weaning off

275 was performed at the assigned interval until varices were eradicated and then at 3 and 9 months after

276 or =25%) or banding (performed monthly until varices were eradicated) and were followed up on the sam

277 essions were at 7- to 14-day intervals until varices were eradicated.

278 Treatment was repeated weekly until varices were eradicated.

279 Gastrosplenic varices were identified in 41 patients (77%) with varice

280 ild-Pugh score, tumor number, and esophageal varices were independent predictors of survival (P<0.05)

281 Varices were obliterated more reliably by TIPS than by s

282 Patients with bleeding esophageal varices were randomized into ligation or combination the

283 nts with cirrhosis with high-risk esophageal varices were randomized to propranolol (titrated to redu

284 s in six symptomatic patients with pretibial varices were retrospectively reviewed.

285 Most of the new varices were small (76.4%) and only 1% of patients devel

286 Oesophageal varices were the commonest finding in patients presentin

287 nlike the much more common distal esophageal varices, which are most commonly a result of portal hype

288 onsidered for patients with large esophageal varices who cannot tolerate beta-blockers.

289 However, there is a risk that varices will recur, therefore continued endoscopic surve

290 .3 +/- .4 (range, 1-7) sessions to eradicate varices with ligation and 4.1 +/- .6 (1-7) with combinat

291 luding grade 3 esophageal varices or grade 2 varices with red wale markings and/or gastric varices, t

292 copy revealed multiple 'downhill' esophageal varices with stigmata of recent hemorrhage.

293 class, or the presence/absence of esophageal varices with the postmeal delta increase in LS was infer

294 s at 3 months after treatment of primary GSV varices; with neither modality proving superior.

295 In patients with esophageal varices without bleeding, prophylaxis with variceal liga

296 geal varices (LEVs) in 60 (40%), and gastric varices without LEVs in 11 (7%).