Watermelon Stomach Without Cirrhosis: A Rare Cause of Transfusion-Dependent GI Bleeding
Underlined: presenting author
Background
Gastric antral vascular ectasia (GAVE) is an uncommon but important cause of chronic gastrointestinal blood loss and nonvariceal upper GI bleeding. It is frequently misdiagnosed as hemorrhagic gastritis and, despite requiring neither cirrhosis nor portal hypertension, is often mistaken for portal hypertensive gastropathy (PHG). Unlike GAVE, PHG is a distinct entity with different endoscopic location, histology, and treatment. This case highlights GAVE as an underrecognized driver of transfusion-dependent anemia in an elderly patient without liver disease.
Case Presentation
An 82-year-old woman with coronary artery disease, paroxysmal atrial fibrillation (not anticoagulated), hypertension, and hypothyroidism presented after outpatient labs showed hemoglobin 4.5 g/dL. She described several days of progressive dizziness without hematemesis, melena, hematochezia, chest pain, or dyspnea. She was hemodynamically stable with pallor and no abdominal tenderness. She had biopsy-confirmed antral GAVE on serial endoscopies since 2022, with four prior sessions of argon plasma coagulation (APC), a nadir hemoglobin of 3.1 g/dL, and at least eight transfusion episodes despite continuous oral iron.
Findings
Admission hemoglobin was 5.2 g/dL with MCV 86, RDW 15.3, and normal leukocyte and platelet counts. Iron studies (iron 38, TIBC 242, transferrin saturation 15.7%, ferritin 49.5 ng/mL) with normal folate and B12 were consistent with iron deficiency from chronic GI blood loss. Repeat endoscopy re-demonstrated antral GAVE with a normal esophagus and duodenum and no varices; APC was performed. She received 3 units of packed red cells, with hemoglobin rising to 9.8 g/dL and resolution of dizziness. She was discharged on sucralfate, pantoprazole, and iron, with endoscopic follow-up in eight weeks.
Discussion & Conclusion
Three features are instructive. First, GAVE typically bleeds occultly rather than overtly. Normal vital signs and a benign abdomen coexisted with a hemoglobin of 4.5 g/dL, so hemodynamic stability should not be falsely reassuring. Second, GAVE and PHG are distinct entities that are commonly confused. GAVE occupies the antrum with tortuous ectatic columns and shows fibrin thrombi with fibromuscular hyperplasia, whereas PHG affects the fundus and body with a mosaic snakeskin pattern and reflects portal hypertension. The distinction matters because PHG responds to portal pressure reduction with nonselective beta-blockers, whereas GAVE requires endoscopic therapy. Third, transfusion dependence is common and multifactorial. All patients warrant iron repletion, and modality selection is individualized. APC has historically been first-line, but recent meta-analyses demonstrate superior efficacy with endoscopic band ligation, including higher eradication rates, lower bleeding recurrence, fewer required sessions, and reduced transfusion requirements.
GAVE should be considered in any patient with unexplained transfusion-dependent iron deficiency anemia, including those without cirrhosis or portal hypertension. Accurate endoscopic and histologic distinction from PHG, paired with sustained iron repletion, is essential to appropriate management.