Gastric polyps and premalignant conditions

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

Management balances prevention against procedural and surveillance burden. Typical low-risk sporadic fundic-gland polyps often need no removal or follow-up, whereas gastric adenomas need complete resection and scheduled review. Large hyperplastic lesions are removed because dysplasia and focal carcinoma risk rise with size, but H. pylori treatment may cause smaller lesions to regress. Extensive premalignant mucosa warrants surveillance if the person is fit enough to benefit; limited antral metaplasia without additional risk usually does not.

Key points

The clinically useful gastric polyp assessment combines surface pattern, size, site, number, histology and background mucosa; the word polyp alone does not determine risk.
Fundic-gland polyps are usually small, smooth and multiple in the fundus or body, often during PPI exposure, and sporadic lesions have very low malignant potential.
Numerous fundic-gland polyps in a young person, dysplasia within one, an antral location or concomitant duodenal adenoma should prompt assessment for familial adenomatous polyposis.
Hyperplastic polyps arise in an inflamed or atrophic stomach; test and eradicate H. pylori, inspect the surrounding mucosa and resect large, pedunculated, symptomatic or dysplastic lesions.
Gastric adenomas carry important malignant and synchronous-neoplasia risk and should be completely resected through an expert pathway with careful examination of the entire stomach.
Atrophy and intestinal metaplasia are premalignant fields rather than polyps; topographical biopsies establish whether disease is limited to the antrum or extends into the body.
BSG recommends three-yearly surveillance for extensive gastric atrophy or intestinal metaplasia affecting both antrum and body in suitable patients, with selected exceptions and shared decision-making.
Visible dysplasia should be staged for en-bloc endoscopic resection, while non-visible dysplasia requires expert pathology review and repeat high-quality enhanced examination to find a hidden lesion.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Fundic-gland change

Sporadic and PPI-associated fundic-gland polyps are usually benign, while numerous or dysplastic lesions can signal familial adenomatous polyposis.

Inflammatory hyperplasia

Hyperplastic polyps arise in H. pylori gastritis, autoimmune atrophy or reactive mucosal injury and reflect disease in the surrounding stomach.

Neoplastic and atrophic pathways

Adenomas and dysplasia develop more often in atrophic, metaplastic mucosa and carry clinically meaningful progression risk.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Glandular dilatation or repair
Fundic glands dilate under altered acid-gastrin signalling, while chronic inflammation stimulates exaggerated foveolar regeneration and hyperplastic polyp formation.
2
Atrophy and metaplasia
Persistent H. pylori or autoimmune injury removes native glands and replaces them with intestinal-type epithelium vulnerable to dysplasia.
3
Dysplastic clonal progression
Accumulated molecular alterations allow adenomatous or flat dysplastic clones to invade and become gastric adenocarcinoma after further progression.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Typical fundic-gland pattern

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.

Possible polyposis syndrome

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.

Hyperplastic inflammatory field

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.

Adenomatous lesion

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.

Non-visible dysplasiaRed flag

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.

Early cancer morphologyRed flag

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
High-definition enhanced upper-GI endoscopyFirst step
Why
Characterise every lesion and search systematically for synchronous neoplasia.
Interpretation and limitations
Document number, exact site, size, morphology and optical pattern with images. Enhanced imaging helps delineate dysplasia, but histology and resection specimen depth determine definitive risk.
02
Targeted polyp histology
Why
Distinguish fundic-gland, hyperplastic, adenomatous and malignant epithelial lesions.
Interpretation and limitations
Biopsy or resect according to size and optical risk. A forceps sample can miss focal dysplasia in a large lesion; complete en-bloc resection gives superior assessment when safe and indicated.
03
Topographical background biopsies
Why
Stage inflammation, atrophy and intestinal metaplasia beyond the polyp.
Interpretation and limitations
Label antrum and body separately and target abnormalities. Involvement of both compartments defines an extensive field with greater cancer risk than antral-only change.
04
H. pylori active testing
Why
Identify a reversible driver of hyperplasia and premalignant progression.
Interpretation and limitations
Use histology or urease testing with adequate site sampling, or a prepared breath or stool antigen test. Eradicate confirmed infection and verify cure when premalignant disease makes persistence consequential.
05
Expert pathology review
Why
Confirm dysplasia grade and resolve discordance before irreversible treatment.
Interpretation and limitations
Low- and high-grade dysplasia can be difficult to reproduce in inflamed mucosa. Specialist GI review should correlate the biopsy with the visible lesion and decide whether repeat sampling or resection is needed.
06
Polyposis and family assessment
Why
Detect an inherited syndrome when gastric findings are disproportionate or atypical.
Interpretation and limitations
Review age, family cancers, colorectal polyp burden and duodenal findings. Genomic testing is consented and phenotype-led; a few ordinary PPI-associated fundic-gland polyps do not diagnose FAP.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Thickened fold or subepithelial lesion

Endoscopic probing, imaging and tissue layer assessment distinguish a true mucosal polyp from prominent folds, cysts or mesenchymal tumours.

Early gastric cancer

Irregular surface, ulceration, spontaneous bleeding or depressed morphology requires expert imaging and resection planning rather than routine forceps sampling alone.

Portal hypertensive or inflammatory nodularity

Diffuse mosaic congestion or nodular gastritis reflects background vascular or inflammatory disease rather than an isolated neoplastic polyp.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01ClassifyDescribe lesion and fieldFirst stepOne or more gastric polyps or a premalignant biopsy finding is identified at endoscopy.

1Record lesion morphology, size, number and location with photographs, and use enhanced imaging to identify depression, irregular pattern or a resection boundary.
2Obtain appropriate lesion tissue while sampling antrum and body background separately when hyperplastic, adenomatous, atrophic or metaplastic disease is possible.
3Reconcile optical diagnosis, pathology, H. pylori status, PPI exposure and family phenotype in a clear final plan rather than issuing an isolated histology result.

02RemoveTreat neoplastic potentialA gastric adenoma, dysplastic polyp, suspicious visible lesion or high-risk hyperplastic polyp is confirmed.

1Refer adenomas and visible dysplasia for expert en-bloc endoscopic resection assessment, choosing EMR, ESD or surgery according to size, invasion features and local capability.
2Resect hyperplastic polyps that are over 1 cm, pedunculated, symptomatic or dysplastic and treat H. pylori, while inspecting the background for synchronous premalignant change.
3Review the complete specimen for margins, invasion and grade in the MDT, then set follow-up from final pathology rather than the pre-resection forceps biopsy.

03SurveilMatch follow-up to field riskAtrophy, intestinal metaplasia or resected gastric adenoma creates an ongoing neoplasia risk.

1Offer three-year surveillance to suitable people with extensive atrophy or metaplasia involving antrum and body, incorporating family history, persistent H. pylori and whether future treatment would be acceptable.
2After complete gastric adenoma excision, arrange endoscopy at 12 months and then ongoing surveillance according to BSG guidance, findings and local expert protocol.
3Do not routinely surveil typical sporadic fundic-gland polyps or isolated antral metaplasia without additional risk; document why follow-up is or is not planned.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Removes an important driver of hyperplastic polyps, atrophy progression and gastric cancer risk, although established metaplasia may remain.

H. pylori eradication in premalignant gastric disease

Use the current seven-day NICE and local-formulary PPI plus two-antibiotic combination, tailored to penicillin allergy, previous exposure and resistance advice, followed by a properly prepared active test of cure.

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.

Medicine review may reduce unnecessary exposure associated with fundic-gland polyps while preserving required acid control or gastroprotection.

Review of long-term proton-pump inhibitor exposure

Continue the lowest effective licensed PPI dose only for a current indication; do not stop abruptly or solely because ordinary fundic-gland polyps are present without considering reflux, ulcer and bleeding risk.

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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Gastric adenocarcinoma

Dysplastic adenomas and high-risk atrophic or metaplastic fields can progress to invasive cancer, making pathology and background mapping inseparable.

Bleeding and anaemia

Large, eroded or hypervascular polyps may ooze chronically or bleed after sampling, contributing to iron deficiency.

Synchronous inherited disease

A profuse fundic-gland phenotype may reveal FAP, with important colorectal and duodenal implications for the patient and relatives.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Maintain a lesion register with site, size, histology, resection completeness and pathology review so follow-up is attached to the correct gastric finding.
Confirm H. pylori cure after treatment in a valid testing window, particularly where hyperplastic, atrophic or metaplastic change remains.
At surveillance endoscopy, use high-quality systematic inspection and targeted plus topographical biopsy rather than repeating random sampling without reference to prior maps.
After endoscopic resection, monitor immediate and delayed bleeding, pain and perforation, then review margins, depth and lymphovascular findings before declaring cure.
Reassess family history and colorectal or duodenal findings when fundic-gland polyp burden, age or dysplasia suggests an inherited polyposis syndrome.
Stop surveillance when comorbidity, frailty or preference means detection would not lead to beneficial treatment, documenting the shared decision.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Background can matter more

A benign hyperplastic polyp may be less important than the extensive atrophy or metaplasia in the stomach from which it arose.

Carpeting changes context

A handful of typical fundic-gland polyps during PPI use is common; numerous lesions in a young patient with dysplasia requires a polyposis lens.

Forceps may under-stage

Dysplasia or focal carcinoma can occupy only part of a large polyp, so a small biopsy cannot always substitute for complete resection histology.

Extent sets field risk

Antral-only intestinal metaplasia and disease spanning antrum plus body do not carry equivalent risk and should not receive identical surveillance advice.

Dysplasia may be hidden

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.

11Common pitfallsFrequent interpretation and management errors.

01
Calling every protrusion a fundic-gland polyp without recording site, size or surface pattern.
02
Removing a hyperplastic polyp but failing to test H. pylori or stage the surrounding atrophic mucosa.
03
Biopsying a gastric adenoma repeatedly instead of referring for complete expert resection.
04
Offering annual surveillance to all focal antral metaplasia regardless of risk and fitness to benefit.
05
Stopping an essential PPI abruptly because typical low-risk fundic-gland polyps were found.
06
Ignoring possible FAP in a young person with carpeting fundic polyposis and dysplasia.