ライフサイエンスコーパス: varices

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

2 t common cause actual bleeding from downhill varices.

3 e ability to visually confirm eradication of varices.

4 al of being able to visualize eradication of varices.

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

6 s who underwent endoscopy were found to have varices.

7 liary atresia and high-risk gastroesophageal varices.

8 mber of 4.6 sessions was needed to eradicate varices.

9 ldren with portal hypertension and high-risk varices.

10 ood products among patients with and without varices.

11 s following bleeding due to malignancies and varices.

12 during OLT in patients with esophagogastric varices.

13 t increased risk of cirrhosis and esophageal varices.

14 ficantly associated with the presence of new varices.

15 best cutoff values for the detection of new varices.

16 ence the risk of developing new or enlarging varices.

17 encountered less frequently than esophageal varices.

18 nd endoscopic screening for gastroesophageal varices.

19 eening test for identifying large esophageal varices.

20 copy irrespective of the prevalence of large varices.

21 determine the optimal screening strategy for varices.

22 re endoscopic screening for large esophageal varices.

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

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

25 aging and pressure measurement of esophageal varices.

26 blished on hemodynamic physiology of gastric varices.

27 es and new modalities to evaluate esophageal varices.

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

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

30 sophageal varices and of moderate/large size varices.

31 r disease predict the presence of esophageal varices.

32 fit from endoscopic screening for esophageal varices.

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

34 hemorrhage in those found to have esophageal varices.

35 al hypertension and bleeding from esophageal varices.

36 49%), mesenteric edema; 14 (40%), mesenteric varices.

37 atients with cirrhosis with large esophageal varices.

38 t increased risk of cirrhosis and esophageal varices.

39 rvival in patients with cirrhosis with large varices.

40 c patients with actively bleeding esophageal varices.

41 88 (39.5%; 95%CI: 33.0-45.9) had esophageal varices.

42 found in groups with and without oesophageal varices.

43 ses portal hypertension and gastroesophageal varices.

44 ntity from the more common distal esophageal varices.

45 urvival times of patients who have bled from varices.

46 e independent predictors for the presence of varices.

47 elapectin did reduce HVPG and development of varices.

48 ot achieved regarding primary prophylaxis of varices.

49 nerstone of definitive treatment of downhill varices.

50 roup analysis of patients without esophageal varices, 2 mg/kg belapectin did reduce HVPG and developm

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

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

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

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

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

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

57 ongst those with history of (h/o) esophageal varices 7(41.2%) did not receive octreotide.

58 210 patients with existing gastroesophageal varices, 74 (35.2%) had variceal progression or bleeding

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

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

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

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

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

64 atopetal flow), and repeated bleeding of the varices after receiving three doses of intravascularly a

65 cal parameters in predicting the presence of varices among cirrhotic patients in northwestern Tanzani

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

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

68 ed to determine the prevalence of esophageal varices and assess the utility of clinical parameters in

69 2 situations: prevention of rebleeding from varices and control of refractory cirrhotic ascites.

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

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

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

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

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

75 adults with cirrhosis with large esophageal varices and no prior history of bleeding, with a minimum

76 atients with cirrhosis with large esophageal varices and no prior history of bleeding.

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

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

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

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

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

82 selection of patients at high risk of having varices and prioritize them for endoscopic screening and

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

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

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

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

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

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

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

90 ress syndrome and hemorrhage from esophageal varices) and seven cases of cancer (one each of prostate

91 ll patients had portal hypertension, 76% had varices, and 41% had a history of ascites (predominantly

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

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

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 respect of age, sex, presence of oesophageal varices, and the diameter of the paraumbilical vein and

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

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

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

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 Gastric varices are encountered less frequently than esophageal

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

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

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

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

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

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

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

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

112 of a subgroup of patients without esophageal varices at baseline (n = 81), 2 mg/kg belapectin was ass

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

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

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

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

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

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

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

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

121 PSDR least performed in predicting varices, (AUC: 0.382; 95%CI: 0.304-0.459; cutoff: < 640;

122 s recommend an early diagnosis of esophageal varices before incident bleeding by screening all patien

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

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

125 captured care processes for ascites (n = 5), varices/bleeding (n = 7), hepatic encephalopathy (n = 4)

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

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

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

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

130 ntional and hemodynamic diagnosis of gastric varices concerning new classifications; explore and illu

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

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

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

134 e prediction of the risk of gastroesophageal varices could spare unnecessary endoscopies in patients

135 37 had varices [CTP-A 4/14(26.6%), CTP-B 19/24(79.2%), CTP-C 14

136 Although patients with varices demonstrated a significantly longer prothrombin

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

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

139 Varices developed less frequently among patients with a

140 The presence of oesophageal varices does not correlate with age, sex, diameter of pa

141 eening and surveillance to detect esophageal varices (EV) and prevent bleeding.

142 is usually performed for bleeding esophageal varices (EV) in infants with congenital biliary atresia.

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

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

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

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

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

148 rotherapy, which can be used in all types of varices, even in those originating in the pelvis.

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

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

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

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

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

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

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

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

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

158 72.5%) of 396 analyzed patients: 130 (32.8%) varices grade I (<5 mm under insufflation) and 157 (39.6

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

160 isease progression; grade 2 = development of varices; grade 3 = bleeding alone; grade 4 = nonbleeding

161 disease progression; grade 2=development of varices; grade 3 = bleeding alone; grade 4=nonbleeding s

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

163 e noninferiority of a screening strategy for varices guided by liver and spleen stiffness measurement

164 for pediatric patients with bleeding gastric varices (GV) associated with advanced liver cirrhosis an

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

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

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

168 the macroscopic appearance of DCHR can mimic varices, haemorrhoids, polyps or proctitis.

169 Conventionally, gastric varices have been described based on the location and ex

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

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

172 history of hepatic encephalopathy, ascites, varices, hepatorenal syndrome, or spontaneous bacterial

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

174 (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

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

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

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

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

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

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

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

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

183 r management of actively bleeding esophageal varices in cirrhotic patients.

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

185 creening in detecting clinically significant varices in patients with cirrhosis.

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

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

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

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

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

191 to follow in ultrasound-guided treatments of varices in the lower limbs, as well as to provide a brie

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

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

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

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

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

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

198 Bleeding esophageal varices is a deadly complication of liver cirrhosis.

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

200 cirrhosis, the appearance of abdominal vein varices is four times more likely than the presence of b

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

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

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

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

205 Their effectiveness in preventing varices is unknown.

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

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

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

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

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

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

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

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

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

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

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

217 oduodenoscopy (EGD) screening for esophageal varices needing treatment (EVNT).

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

219 pertension (PHT) was defined as the onset of varices needing treatment (VNT) or PHT-related bleeding.

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

221 Portal hypertension and esophageal varices needing treatment could be predicted through non

222 in patients with low probability of finding varices needing treatment.

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

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

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

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

227 collateral venous circulation, first degree varices oesophagii).

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

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

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

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

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

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

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

235 inal-endoscopy (UGIE) identifies oesophageal varices (OV).

236 ine (P = .02) and reduced development of new varices (P = .03).

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

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

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

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

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

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

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

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

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

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

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

248 Gastroesophageal varices result almost solely from portal hypertension, a

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

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

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

252 ] 1.23, 95% confidence interval 1.19, 1.27), varices screening (OR 1.20 [1.13, 1.27]), use of rifaxim

253 re more likely to receive consistent HCC and varices screening over time, less likely to experience 3

254 llular carcinoma [HCC] screening, endoscopic varices screening, and use of rifaximin after hospitaliz

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

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

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

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

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

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

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

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

263 in patients with documented esophagogastric varices undergoing OLT.

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

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

266 ed elsewhere that the presence of esophageal varices varies widely among cirrhotic patients this has

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

268 50 x 10(3)/dL for the presence of esophageal varices was 6.3 (95% CI: 2.6-15.8).

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

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

271 The presence of esophageal varices was detected using endoscopic examination and as

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

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

274 ephalopathy, or jaundice) without esophageal varices was included, and 5-year outcome is reported.

275 ephalopathy, or jaundice) without esophageal varices was included, and 5-year outcome is reported.

276 The non-invasive prediction of varices was not strong enough to replace endoscopic diag

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

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

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

280 Varices were documented by esophagogastroduodenoscopy in

281 Esophageal varices were encountered in 1 patient after weaning off

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

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

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

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

286 The varices were independently associated with increased age

287 Esophageal varices were prevalent among cirrhotic patients, most of

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

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

290 Oesophageal varices were the commonest finding in patients presentin

291 0-1, and following management of esophageal varices, when present, according to institutional guidel

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

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

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

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

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

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

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

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

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