Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) syndrome are recently characterised entities that can be associated with gastrointestinal blood loss in patients with and without cirrhosis. Up to 65% of patients with portal hypertension from cirrhosis will develop PHG but it can also occur in the setting of non-cirrhotic portal hypertension. In patients with portal hypertension, PHG is often associated with the presence of oesophageal and/or gastric varices. The mechanisms involved in the pathogenesis of PHG have not been fully elucidated. However, regulation of gastric nitric oxide, prostaglandins, tumour necrosis factor α (TNF-α), and epidermal growth factor (EGF) production may be involved.

The mechanisms involved in the development of GAVE syndrome are also unclear. The classic features of this syndrome include red, often haemorrhagic, lesions predominantly located in the gastric antrum which can result in significant blood loss. More than 70% of patients with GAVE syndrome do not have cirrhosis or portal hypertension. However, in the setting of cirrhosis, GAVE syndrome can be difficult to differentiate from PHG. This distinction is paramount in that PHG generally responds to a reduction in portal pressures whereas those with GAVE syndrome and coexisting portal hypertension generally do not respond to such therapy. This review will focus on the incidence, clinical importance, aetiology, pathophysiology, and treatment of PHG and GAVE syndrome, including differentiation between GAVE syndrome and PHG in the setting of portal hypertension.