ライフサイエンスコーパス: esophageal varices

1 r bleeding ulcers, two receiving therapy for esophageal varices).

2 initial screening test for identifying large esophageal varices.

3 hosis require endoscopic screening for large esophageal varices.

4 images from lymph nodes, the azygos vein, or esophageal varices.

5 invasive imaging and pressure measurement of esophageal varices.

6 ageal varices and new modalities to evaluate esophageal varices.

7 vanced liver disease predict the presence of esophageal varices.

8 ely to benefit from endoscopic screening for esophageal varices.

9 cholangitis (PSC) may develop and bleed from esophageal varices.

10 nt initial hemorrhage in those found to have esophageal varices.

11 distinct entity from the more common distal esophageal varices.

12 lts in portal hypertension and bleeding from esophageal varices.

13 tive intervention for patients with bleeding esophageal varices.

14 not be used to treat patients with bleeding esophageal varices.

15 raphic measurement and endoscopic grading of esophageal varices.

16 sophagoscopy for the detection and sizing of esophageal varices.

17 producible method of determining the size of esophageal varices.

18 n alone in patients with major bleeding from esophageal varices.

19 Most patients (75%) had esophageal varices, 21% were Child-B, and 29% had at lea

20 (1.95; 95% CI: 1.14-3.68) and development of esophageal varices (3.11; 95% CI: 1.57-10.65) were signi

21 atients with cirrhosis require screening for esophageal varices and for liver cancer.

22 to enroll patients in screening programs for esophageal varices and hepatocellular carcinoma.

23 rediction of variceal bleeding, treatment of esophageal varices and new modalities to evaluate esopha

24 For patients with cirrhosis with high-risk esophageal varices and no history of variceal hemorrhage

25 e areas of endoluminal ultrasound imaging of esophageal varices and noninvasive pressure measurement

26 alyzed to identify independent predictors of esophageal varices and of moderate/large size varices.

27 Untreated patients with newly diagnosed esophageal varices and practicing gastroenterologists we

28 gnificantly and the pharmacologic therapy of esophageal varices and the prophylaxis of the initial va

29 ers, and worsening liver disease (cirrhosis, esophageal varices, and deterioration in liver function)

30 significant number of gastric varices, peri-esophageal varices, and extraluminal pathology were iden

31 platelet count, higher alkaline phosphatase, esophageal varices, and smoking was developed to predict

32 Downhill esophageal varices are a distinct entity from the more c

33 Proximal or 'downhill' esophageal varices are a rare cause of upper gastrointes

34 ause the pathophysiology and hemodynamics of esophageal varices are not well understood.

35 logic disease were independent predictors of esophageal varices (area under the receiver operator cha

36 atic decompensation (hepatic encephalopathy, esophageal varices, ascites, or portal hypertension) or

37 varices and we excluded 26 patients who had esophageal varices at baseline so that predictors of new

38 cally significant PH (HVPG >/= 10 mm Hg) and esophageal varices at high risk of bleeding.

39 Emergency treatment of bleeding esophageal varices (BEV) consists mainly of endoscopic a

40 ely 90% sensitivity in the identification of esophageal varices determined to be large on endoscopy,

41 e assessment of portal hypertension (PH) and esophageal varices (EV) in patients with cirrhosis.

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

43 rrhosis without (stage 1) and with (stage 2) esophageal varices (EV).

44 ; HVPG values correlate with the presence of esophageal varices (EV).

45 n either in isolation or in combination with esophageal varices (EV).

46 y significant portal hypertension (CSPH) and esophageal varices (EVs) in patients with compensated ci

47 s with low likelihood of harboring high-risk esophageal varices (EVs) or having clinically significan

48 tients with cirrhosis with moderate to large esophageal varices (EVs), the more cost-effective option

49 liver disease such as refractory ascites and esophageal varices for patients awaiting liver transplan

50 In those with small esophageal varices, growth to LEVs was observed in 13%,

51 copic treatments for strictures and bleeding esophageal varices have been proposed and may improve ou

52 ESLD was defined as bleeding esophageal varices, hepatic encephalopathy, persistent a

53 ase severity were worse and the frequency of esophageal varices higher with increasing Ishak stage (P

54 um albumin (HR 0.97; 95% CI: 0.94-0.99), and esophageal varices (HR 1.70; 95% CI: 1.21-2.38) but not

55 Performance status, AST, abdominal pain, and esophageal varices improved the discriminatory ability o

56 atients showed no varices in 52 (34%), small esophageal varices in 28 (19%), large esophageal varices

57 ography (HRES) was used to image and measure esophageal varices in control subjects and patients with

58 Our aim was to determine the prevalence of esophageal varices in patients with PSC and the variable

59 However, the exact prevalence of esophageal varices in patients with PSC remains unknown

60 in the endoscopic and radiologic therapy of esophageal varices in the past few years.

61 remains unknown and potential predictors of esophageal varices in this population have not been iden

62 rty-six percent (102 of 283) of patients had esophageal varices including 56% (57 of 102) with modera

63 This update and review of esophageal varices is given in five sections: new develo

64 small esophageal varices in 28 (19%), large esophageal varices (LEVs) in 60 (40%), and gastric varic

65 t, and were case matched to patients without esophageal varices (NEV) based on sex, age, surgery type

66 and major risk factors for bleeding, such as esophageal varices or a low platelet count, are frequent

67 ence or absence of PH defined as presence of esophageal varices or ascites or low platelet count and

68 ns of portal hypertension, including grade 3 esophageal varices or grade 2 varices with red wale mark

69 ates and defined by the presence of ascites, esophageal varices, or hepatic encephalopathy, or when E

70 following clinical characteristics: ascites, esophageal varices, or total bilirubin greater than 2 mg

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

72 T was independently associated with baseline esophageal varices (P = 0.01) and prothrombin time (P =

73 esophageal variceal bleeding, screening for esophageal varices, prediction of variceal bleeding, tre

74 Hemorrhage from esophageal varices remains a substantial management prob

75 ly a result of portal hypertension, downhill esophageal varices result from vascular obstruction of t

76 re significantly less likely to rebleed from esophageal varices than patients receiving sclerotherapy

77 te analysis identified bilirubin, cirrhosis, esophageal varices, tumor size, and macrovascular invasi

78 less than 150 x 10(3)/dL for the presence of esophageal varices was 6.3 (95% CI: 2.6-15.8).

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

80 Esophageal varices were encountered in 1 patient after w

81 Child-Pugh score, tumor number, and esophageal varices were independent predictors of surviv

82 Patients with bleeding esophageal varices were randomized into ligation or comb

83 l, 62 patients with cirrhosis with high-risk esophageal varices were randomized to propranolol (titra

84 Unlike the much more common distal esophageal varices, which are most commonly a result of

85 should be considered for patients with large esophageal varices who cannot tolerate beta-blockers.

86 upper endoscopy revealed multiple 'downhill' esophageal varices with stigmata of recent hemorrhage.

87 Child-Pugh class, or the presence/absence of esophageal varices with the postmeal delta increase in L

88 In patients with esophageal varices without bleeding, prophylaxis with va