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1 and controlling bleeding from esophageal and gastric varices.
2 ch, established on hemodynamic physiology of gastric varices.
3 enal malignancy (48 and 32 respectively) and gastric varices aetiologies (2.8) when compared with oth
4 s (aHR, 0.4; 95% CI, 0.2-0.9; P = 0.048), or gastric varices (aHR, 0.5; 95% CI, 0.3-0.7; P = 0.022) p
6 TIPS) on portal hemodynamics, esophageal and gastric varices, and hepatic function have not been full
7 g, ascites, thrombocytopenia, esophageal and gastric varices, anemia, and increased levels of liver e
9 intestinal bleedings from ulcers or esophago-gastric varices are life threatening medical conditions
12 he conventional and hemodynamic diagnosis of gastric varices concerning new classifications; explore
13 h actively bleeding esophageal or contiguous gastric varices despite sclerotherapy were assessed for
14 of radiology files revealed 86 patients with gastric varices diagnosed during double-contrast upper g
16 ocedure for pediatric patients with bleeding gastric varices (GV) associated with advanced liver cirr
18 oup, patients with ascites and/or esophageal/gastric varices had lower serum RvD1 levels compared to
24 e of the characteristic features of tumorous gastric varices on double-contrast studies so that they
25 cksonville location with esophageal varices, gastric varices, or both seen on CT abdomen and pelvis,
29 ents with EV regardless of the size and with gastric varices since these patients display clinically
30 dhesive agents for the treatment of bleeding gastric varices, the successful treatment of early gastr
31 rade 2 varices with red wale markings and/or gastric varices, treated consecutively from February 200
33 ers were invalid (n = 239), if esophageal or gastric varices were not reported (n = 25), varices othe
36 vity of CT scans in detecting esophageal and gastric varices when compared to the gold standard of EG