An Unexpected Association: Might GAVE Pave the Way to How the Metabolic Syndrome Behaves

Abstract

Gastric antral vascular ectasia (GAVE) accounts for 4% of nonvariceal upper gastrointestinal bleeds (UGIBs), manifesting with iron deficiency anemia requiring recurrent blood transfusions. Patients typically present with intermittent melena and, occasionally, hematemesis. However, some present with anemia without any overt gastrointestinal blood losses. GAVE is strongly associated with chronic liver disease. In particular, 30% to 64% of individuals with GAVE have cirrhosis. [1][2][3] PaTHOGenesis OF Gave in PaTienTs wiTH CirrHOsisThe pathogenesis of GAVE disease is not well understood; the disease has been linked to mechanical stress, portal hypertension, liver dysfunction, and metabolic syndrome. Mechanical stress was once considered to be the primary reason for the formation of antral GAVE. Several studies have outlined abnormal antral motility studies in patients with GAVE and cirrhosis. 4 According to this theory, the peristalsis of gastric mucosa through the pylorus causes fibromuscular hyperplasia, leading to the formation of ectatic vessels as a by-product. However, this theory falls short in that it does not explain the formation of ectatic vessels elsewhere in the gastrointestinal tract, an occurrence that has been described in the literature. 4 Given the high association between GAVE and cirrhosis, portal hypertension was thought to be a possible cause of GAVE, similar to portal hypertensive gastropathy (PHG). 5 However, one study documented that transjugular intrahepatic portosystemic shunt (TIPS) was not associated with