Do alterations in the rate of gastric emptying after injection sclerotherapy for oesophageal varices play any role in the development of portal hypertensive gastropathy? Academic Article uri icon


MeSH Major

  • Esophageal and Gastric Varices
  • Gastric Emptying
  • Gastrointestinal Hemorrhage
  • Hypertension, Portal
  • Sclerotherapy


  • Bleeding from portal hypertensive gastropathy (PHG) has been estimated to account for up to 30% of all upper gastrointestinal haemorrhage in patients with cirrhosis and portal hypertension. Although portal hypertension seems to be an essential prerequisite, the precise mechanisms responsible for the development of PHG are unknown. The aim of this study was to examine the role of injection sclerotherapy of oesophageal varices in the development of PHG. Gastric emptying was studied using a radionuclide test meal with the emptying characteristics of a slow liquid in 57 patients with cirrhosis and/or portal hypertension (median age 53 yrs), of whom 34 had received injection sclerotherapy for their oesophageal varices and 20 normal healthy volunteers (median age 42 yrs). As vagal damage is associated with more rapid emptying of liquids, despite hold up of solids, this technique might be expected to demonstrate such damage if gastric emptying was accelerated. The results indicated that there was no difference in the rate of gastric emptying between normal healthy volunteers and portal hypertensive patients. However, patients who had received injection sclerotherapy emptied their stomachs faster than those who had not (p < 0.05). Furthermore, the speed of gastric emptying correlated directly with the number of injections (r = 0.41; p = 0.02) and the volume of sclerosant injected (r = 0.39; p = 0.03). These observations suggest that injection sclerotherapy for oesophageal varices results in disturbances of gastric emptying that may contribute to the pathogenesis of portal hypertensive gastropathy.

publication date

  • May 5, 1999



  • Academic Article



  • eng

PubMed Central ID

  • PMC2423968

PubMed ID

  • 10371058

Additional Document Info

start page

  • 141

end page

  • 8; discussion 148-50


  • 11


  • 3