Classify gastric polyps accurately, assess the background mucosa and inherited context, remove lesions with meaningful neoplastic risk, and apply evidence-based surveillance to atrophy, intestinal metaplasia and dysplasia without over-scoping low-risk findings.
Gastric epithelial protrusions include fundic-gland polyps, hyperplastic polyps and adenomas; subepithelial lesions and neuroendocrine tumours follow different pathways. Visual diagnosis can guide immediate management but does not replace histology when features are atypical or risk is meaningful. A high-quality report records location, number, dimensions, Paris morphology, ulceration and representative photographs, then evaluates the rest of the stomach rather than focusing only on the largest bump.
The background mucosa often contains the main risk. H. pylori causes chronic inflammation that can progress to multifocal atrophy and intestinal metaplasia. Autoimmune gastritis produces corpus-predominant atrophy and hypergastrinaemia. Hyperplastic polyps can mark either process, and adenomas frequently arise within metaplastic mucosa. Biopsies from antrum and body in separately labelled containers allow topographical risk assessment and prevent a focal sample from being misread as the whole stomach.
Sporadic and PPI-associated fundic-gland polyps are usually benign, while numerous or dysplastic lesions can signal familial adenomatous polyposis.
Hyperplastic polyps arise in H. pylori gastritis, autoimmune atrophy or reactive mucosal injury and reflect disease in the surrounding stomach.
Adenomas and dysplasia develop more often in atrophic, metaplastic mucosa and carry clinically meaningful progression risk.
Fundic glands dilate under altered acid-gastrin signalling, while chronic inflammation stimulates exaggerated foveolar regeneration and hyperplastic polyp formation.
Persistent H. pylori or autoimmune injury removes native glands and replaces them with intestinal-type epithelium vulnerable to dysplasia.
Accumulated molecular alterations allow adenomatous or flat dysplastic clones to invade and become gastric adenocarcinoma after further progression.
Multiple small, pale, smooth sessile lesions confined to fundus and body during PPI exposure suggest fundic-gland polyps. Irregular surface, ulceration, size over 1 cm or antral location makes the pattern atypical.
Carpeting polyposis, young age, dysplasia in a fundic-gland polyp, family colorectal polyposis or duodenal adenoma should prompt colonoscopic and genomic assessment rather than gastric treatment alone.
A red lobulated antral polyp in a stomach with H. pylori, atrophy or metaplasia likely represents a hyperplastic lesion; bleeding and iron deficiency can occur from surface erosion.
A solitary velvety or lobulated lesion, often in the antrum or incisura, may be an adenoma. Dysplasia grade and complete resectability require expert endoscopic and pathology review.
Dysplasia reported from apparently flat random biopsies may reflect a subtle missed lesion or interpretive uncertainty and should trigger expert pathology confirmation plus prompt enhanced repeat endoscopy.
Depression, spontaneous bleeding, ulceration, converging folds, irregular microvascular pattern or non-lifting raises invasive neoplasia concern and should stop casual snare removal in favour of expert staging.
Endoscopic probing, imaging and tissue layer assessment distinguish a true mucosal polyp from prominent folds, cysts or mesenchymal tumours.
Irregular surface, ulceration, spontaneous bleeding or depressed morphology requires expert imaging and resection planning rather than routine forceps sampling alone.
Diffuse mosaic congestion or nodular gastritis reflects background vascular or inflammatory disease rather than an isolated neoplastic polyp.
Dysplastic adenomas and high-risk atrophic or metaplastic fields can progress to invasive cancer, making pathology and background mapping inseparable.
Large, eroded or hypervascular polyps may ooze chronically or bleed after sampling, contributing to iron deficiency.
A profuse fundic-gland phenotype may reveal FAP, with important colorectal and duodenal implications for the patient and relatives.
A benign hyperplastic polyp may be less important than the extensive atrophy or metaplasia in the stomach from which it arose.
A handful of typical fundic-gland polyps during PPI use is common; numerous lesions in a young patient with dysplasia requires a polyposis lens.
Dysplasia or focal carcinoma can occupy only part of a large polyp, so a small biopsy cannot always substitute for complete resection histology.
Antral-only intestinal metaplasia and disease spanning antrum plus body do not carry equivalent risk and should not receive identical surveillance advice.
When random biopsy reports dysplasia, the next expert enhanced examination often aims to locate a subtle resectable lesion rather than merely repeat the same biopsy.
Calling every protrusion a fundic-gland polyp without recording site, size or surface pattern.
Removing a hyperplastic polyp but failing to test H. pylori or stage the surrounding atrophic mucosa.
Biopsying a gastric adenoma repeatedly instead of referring for complete expert resection.
Offering annual surveillance to all focal antral metaplasia regardless of risk and fitness to benefit.
Stopping an essential PPI abruptly because typical low-risk fundic-gland polyps were found.
Ignoring possible FAP in a young person with carpeting fundic polyposis and dysplasia.
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A 16 mm antral polyp is confirmed as a gastric adenoma with low-grade dysplasia. No invasion is seen endoscopically. Which management principle is best?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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Check interactions, allergy, pregnancy, QT risk and renal or hepatic impairment. Successful eradication does not cancel surveillance when the extent of atrophy, metaplasia or dysplasia independently warrants it.
PPI-associated fundic-gland polyps rarely require surveillance. Balance rebound acid symptoms and the original indication, and remember that PPI withdrawal does not treat adenoma or extensive premalignant mucosa.