PORTAL-HYPERTENSIVE GASTROPATHY

In the present article we describe updated information concerning the clinical feature of portal-hypertensive gastropathy (PHG), which is ch aracterized by mucosal and submucosal vascular dilatation without infl ammation. Although this lesion represents non-variceal bleeding, there is a wide variation of its prevalence. Portal pressure and some humor al factors may play important roles in its pathogenesis. Gastric acid secretory activity is reduced, whereas the gastric mucosal barrier is impaired. With regard to gastric mucosal haemodynamics, whether 'overf low' (i.e. active congestion) or 'stasis' (i.e. passive congestion) ca use gastric mucosal hyperaemia is not known. A severe lesion is a pote ntial source of bleeding, while mild lesions are of little clinical si gnificance and endoscopic variceal obliteration aggravates PHG in some patients. In the treatment of PHG, pharmacological (e.g. propranolol) , surgical (e.g. portosystemic shunt) and radiological (e.g. transjugu lar intrahepatic portosystemic shunt) procedures may be useful in prev enting bleeding from PHG.