A 75-year-old man presented with steadily increasing upper abdominal pain, worse after meals, over 6 weeks. He also described anorexia, early satiety, intermittent postprandial nausea and bilious vomiting, as well as bilateral ankle edema and an unintentional 10-lb weight loss, despite daily use of lansoprazole and furosemide. He described no heartburn, dysphagia, melena, hematemesis, diarrhea, fevers, night sweats, or other cardiopulmonary or urinary symptoms. His past medical history was notable for mild gastroesophageal reflux, hypertension, depression, and benign prostatic hyperplasia. Current medications included lansoprazole, valsartan, furosemide, and escitalopram. He had a negative family history and did not smoke or drink alcohol. Physical examination was normal except for 2? bilateral pitting edema to the knees. Laboratory studies were notable mainly for an albumin level of 1.5 g/dl. His white blood cell count was 10,800/ mm (54% neutrophils, 22% lymphocytes, 22% eosinophils), hematocrit 42%, and platelets 338,000/mm. Other liver function tests and serum chemistries were normal except for calcium of 6.9 mg/dl. Urinalysis was normal. Chest X-ray was normal, as was his electrocardiogram. IgA and IgG for Helicobacter pylori were positive. Abdominal computed tomography (CT) after intravenous and oral contrast showed significant thickening of the proximal gastric body and fundus with associated engorgement of the perigastric vessels and no mass (Fig. 1). The distal stomach wall was normal. Endoscopy revealed markedly thickened gastric folds with nodularity, erythema, and exudate involving the proximal stomach (Fig. 2a, b), but sparing the antrum and pylorus. The stomach was poorly distensible, and a small hiatal hernia was seen. Multiple superficial cold forceps biopsies revealed no evidence for active H. pylori infection and failed to show eosinophilia, viral inclusions, epithelial malignancy, or lymphoma. Interestingly, there were elongated gastric foveolae, many of which exhibited a corkscrew-like appearance. These hyperplastic foveolae were lined by gastric epithelium without regenerative features or mucin depletion. Atrophy of the parietal cell layer and mild lamina propria chronic inflammation were also noted. The patient was treated empirically for H. pylori with a 14day course of amoxicillin, clarithromycin, and lansoprazole based on the positive H. pylori serologies. After treatment, he continued taking a proton pump inhibitor twice daily but his symptoms did not change. He was also prescribed a brief course of prednisone that improved his peripheral eosinophilia; however, his symptoms continued to worsen. Full-thickness gastric biopsies, obtained using a jumbo forceps during a repeat endoscopy, showed foveolar hyperplasia with tortuous, corkscrew shapes and dilated mucin-filled gastric pits, atrophy of the parietal cell layer, and mild chronic inflammation of the lamina propria (Fig. 3). Some foveolar cells exhibited mucin depletion. There were no H. pylori organisms or cytomegalovirus M. Rothenberg (&) Division of Gastroenterology and Hepatology, Stanford University Medical Center, 300 Pasteur Drive, MC: 5187, Stanford, CA 94305-5187, USA e-mail: rothenbergmike@gmail.com