Abstract

A 51-year-old man with nonalcoholic steatohepatitis (NASH) cirrhosis was evaluated for chronic iron deficiency anemia (hemoglobin, 7–8 g/dL). Occasional scant rectal bleeding could not account for the anemia. At esophagogastroduodenoscopy (EGD), many benign-appearing 3-mm antral nodules were seen as well as mild linear antral erythema (Figure A). No varices or other abnormalities were found. A 61-year-old woman with NASH cirrhosis underwent band ligation for bleeding esophageal varices. At follow-up EGD, there were small esophageal varices, portal hypertensive gastropathy, and many antral nodules (Figure B), but no active bleeding. There were no mucosal abnormalities such as red stripes or punctate erythema. A 58-year-old man with alcoholic cirrhosis had iron deficiency anemia and melena and required monthly blood transfusions. EGD showed antral nodules and punctate antral erythema in crops (Figure C) but no varices or other cause for blood loss. In each case, biopsies of the antral nodules showed the classic histologic features that define gastric antral vascular ectasia (GAVE), as illustrated: vascular ectasias (Figure D, arrow), hyperplastic foveolar (serrated) gastric epithelium (Figure E, arrow), thrombosis in venules (Figure F, arrow), fibrohyalinosis, and spindle-cell (myofibroblast) proliferation (not shown).1Ripoll C. Garcia-Tsao G. Management of gastropathy and gastric vascular ectasia in portal hypertension.Clin Liver Dis. 2010; 14: 281-294Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar GAVE commonly causes iron deficiency anemia and occasionally overt upper gastrointestinal bleeding. The cause of GAVE is unknown. Approximately 30% of GAVE patients have cirrhosis,2Selinger C.P. Ang Y.S. Gastric antral vascular ectasia (GAVE): an update on clinical presentation, pathophysiology and treatment.Digestion. 2008; 77: 131-137Crossref PubMed Scopus (97) Google Scholar although portal hypertension is not part of the pathogenesis.1Ripoll C. Garcia-Tsao G. Management of gastropathy and gastric vascular ectasia in portal hypertension.Clin Liver Dis. 2010; 14: 281-294Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar, 3Spahr L. Villeneuve J.P. Dufresne M.P. et al.Gastric antral vascular ectasia in cirrhotic patients: absence of relation with portal hypertension.Gut. 1999; 44: 739-742Crossref PubMed Scopus (144) Google Scholar Other associations include scleroderma, chronic renal failure, and bone marrow transplantation.4Burak K.W. Lee S.S. Beck P.L. Portal hypertensive gastropathy and gastric antral vascular ectasia (GAVE) syndrome.Gut. 2001; 49: 866-872Crossref PubMed Scopus (135) Google Scholar GAVE classically appears endoscopically as either (1) longitudinal red stripes in the antrum radiating proximally from the pylorus, the so-called watermelon stomach, or (2) punctate erythema in crops that is common in patients with cirrhosis (Figure C). We describe a nodular form of GAVE as a third endoscopic phenotype of this disorder that shares the classic histologic features with the striped and punctate forms of GAVE. Nodular GAVE could easily be dismissed as fundic gland, inflammatory, or hyperplastic polyps, on the basis only of endoscopic appearances. Biopsy of the antral nodules is required to make the diagnosis. Typically, GAVE is treated with argon plasma coagulation to prevent or treat bleeding,5Fuccio L. Zagari R.M. Serrani M. et al.Endoscopic argon plasma coagulation for the treatment of gastric antral vascular ectasia-related bleeding in patients with liver cirrhosis.Digestion. 2009; 79: 143-150Crossref PubMed Scopus (35) Google Scholar but unknown are the level of bleeding risk in nodular GAVE and whether thermocoagulation management is of value. In summary, we describe a third nodular variant of GAVE that can only reliably be differentiated from other gastric nodules/polyps seen endoscopically by biopsy. The prevalence and clinical course of this nodular variant have yet to be determined, because this form of GAVE has not previously been well appreciated.

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