Editor, Gastric mucosal lesions are common in portal hypertension, occur in up to 65 % of cirrhotics, and represent an important cause of gastrointestinal (GI) blood loss. They include portal hypertensive gastropathy (PHG) and gastric vascular ectasia (GVE) [1]. The diagnosis of PHG is based on the presence of a characteristic mosaic-like pattern of the gastric mucosa on endoscopic examination. Superimposed on this mosaiclike pattern may be red spot lesions that usually are greater than 2 mm in diameter [1]. Polypoidal lesions in portal gastropathy on endoscopy have been described in two studies [2, 3]. We present eight cases of cirrhosis and portal hypertension with severe PHG and antral polyps. We prospectively evaluated patients admitted to our department, with a diagnosis of cirrhosis, between January 2011 and March 2012 and performed upper GI endoscopy. Clinical, laboratory, endoscopy, and histology data of these patients were analyzed. During the study period, 786 patients with cirrhosis underwent upper GI endoscopy. Of these, eight (1.01 %, seven male) patients, ranging in age from 43 to 70 years, had portal hypertensive polyps. Seven patients had alcoholic cirrhosis, and one patient had hepatitis B-related cirrhosis, all of Child’s C class. The CTP score ranged from 8 to 13 and model for end-stage liver disease ranged from 9 to 21. None had hepatocellular carcinoma or portal vein thrombosis. Six patients had history of upper GI bleed and had undergone esophageal variceal ligation previously. Endoscopy in all eight patients showed multiple antral polyps two to five in number and with size ranging from 0.5 to 1 cm. All patients had associated severe PHG. Two of the six patients with upper GI bleed continued to have drop in hemoglobin and stool occult blood positivity despite eradication of varices, and one had an overt bleeding polyp on endoscopy shown in Fig. 1d. These patients underwent endoscopic polypectomy once the platelet count was corrected to more than 50,000/mm and prothrombin time was corrected with plasma. On follow up, none of the patients had a drop in hemoglobin or rebleed. Small-bowel evaluation was not done in any of these patients as they did not have a drop in hemoglobin after polypectomy. Biopsy of polyps showed elongation, tortuosity, and dilatation of gastric foveolae with the surrounding stroma showing edema, mild inflammation, and scattered smooth muscle bundles. Numerous proliferating capillaries were present in the subepithelial tissue differentiating these polyps from usual hyperplastic polyps. There were no areas of dysplasia. Rapid urease test was negative, and histology and special stains did not reveal Helicobacter pylori in any of the patients. Cirrhotics with portal hypertensive polyps did not differ from cirrhotics without portal hypertensive polyps with regard to etiology or severity of cirrhosis, duration of illness, or past history of variceal eradication. Gastroscopy in PHG shows a mosaic-like pattern of the gastric mucosa with mild and superimposed discrete cherry red spots, fine pink speckling, or scarlatina-type rash when severe [1]. Biopsies show vascular ectasia and congestion in the mucosal layer without a significant degree of inflammatory infiltrate [4, 5]. Perturbations in the tissue levels of TNF-α, prostaglandins, endothelin, and nitric oxide/peroxynitrite may participate in the vascular congestion and mucosal damage characteristic of PHG [4, 5]. Some patients with cirrhosis and portal hypertension have GVE [5]. The entity is characterized by aggregates of ectatic vessels that C. Panackel (*) :H. Joshy :B. Sebastian : S. K. Mathai Department of Gastroenterology, Medical Trust Hospital, Kochi 682 016, India e-mail: charlespanackel@hotmail.com