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A 49-year-old female with a past history of colonic polyps was evaluated for iron deficiency anaemia. At oesophagogastroduodenoscopy (OGD), multiple variable sized sessile and pedunculated polyps (Paris Ip + Is) were identified involving the gastric body, antrum and cardia (Figure 1). The duodenum was normal. Examination with endoscopic ultrasound confirmed the polyps to be confined to the mucosal layer. Several of the larger polyps were removed without preinjection by snare cautery using a 25 mm electrosurgical snare (Olympus, SD-210U-25) and forced Coagulation 35W, effect 3 (ERBE ICC 350; Erbe Elektromedizin, Tübingen, Germany) (Figure 2). Histology revealed gastric mucosa with prominent foveolar hyperplasia and focal low-grade dysplasia, however unlike what is typically seen in Menetrier's disease, parietal cell mass appeared normal. The most striking feature was localised foveolar overgrowth, hence the polyps were considered more in keeping with hyperplastic polyposis (HPS) or juvenile polyposis (JPS) syndromes (Figure 3).

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Figure 1. Endoscopic views of the gastric antrum (A) and Cardia/Fundus (B) revealing multiple variably sized sessile and pedunculated polyps (Paris Ip + Is) with active oozing of thick mucoid material.

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Figure 2. Polypectomy of larger polyps performed with (A) placement of a 25 mm Olympus electrosurgical snare. The polyps were excised using (B) forced coagulation, 35W effect 3 and steady closure of the snare until (C) complete transection achieved.

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Figure 3. Polyp showing foveolar hyperplasia with abundant lamina propria (*) and hyperplastic epithelium with dilated crypts (#). Arrow indicates an area of focal glandular crowding and nuclear atypia consistent with low-grade dysplasia.

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After further review of the patient's history, she was free of alopecia, onycholysis, cutaneous telangiectasia or hyperpigmentation and cardiovascular manifestations. There was no significant weight loss or chronic diarrhoea. Routine laboratory data showed anaemia (haemoglobin 86 g/l) and hypoalbuminemia (Albumin 29 g/l). Serology was negative for H. pylori. There was no significant past family history of gastrointestinal polyps or malignancy. Histologically it was difficult to make a definitive diagnosis of HPS over JPS. Based on the patient's clinical findings, HPS was favoured.

Hyperplastic gastric polyposis is an uncommon disorder defined by Niv et al. as a syndrome comprising 50 or more gastric hyperplastic polyps. For the majority of cases, there have been no specific genetic abnormalities identified, however at least two case reports have suggested autosomal dominant inheritance. Both of the two families reported had an increased risk of development of diffuse gastric carcinoma; the authors suggested that patients with established dysplasia should be considered to be at increased risk for gastric cancer. However, no guidelines exist to guide screening and management of these patients. As with our patient, this syndrome has also been associated with colorectal neoplasia; both adenomas and adenocarcinomas may develop.

The patient was strongly advised to undergo total gastrectomy, however she declined surgical management and therefore underwent seven OGD sessions with polyp debulking over 14 months. This resulted in an increase in her haemoglobin from 86 g/l to 133 g/l (normal 115–165) and albumin from 29 g/l to 33 g/l (normal 33–46).

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