Gastric hyperplastic polyp is the most common type of gastric polyp (75-90%), a benign epithelial lesion developing from reactive hyperplasia of the mucosa. Typically found in the fundus or corpus as small (<1 cm), multiple, smooth-surfaced polyps. Shows strong association with Helicobacter pylori infection, chronic gastritis, and atrophic gastritis — spontaneous regression may occur after H. pylori eradication. Malignancy risk is low (<2%) but increases in >1 cm polyps and with dysplasia. On CT, they appear as small, smooth-contoured mucosal polypoid lesions. Differentiation from fundic gland polyps (proton pump inhibitor-associated) and adenomatous polyps is made clinically and histopathologically.
Age Range
40-80
Peak Age
65
Gender
Female predominant
Prevalence
Common
Hyperplastic polyp develops as a reactive lesion resulting from chronic mucosal damage and repair process. Chronic inflammation triggered by Helicobacter pylori infection causes mucosal epithelial damage and compensatory hyperplasia response. IL-1beta, TNF-alpha, and other proinflammatory cytokines stimulate excessive proliferation of foveolar epithelial cells — this exaggerated but not uncontrolled regeneration creates elongated foveolar structures and cystic dilations. Histologically, elongated, tortuous foveolar glands, edematous lamina propria, and chronic inflammatory infiltrate are characteristic. Small size and smooth contour on CT reflect the lesion's regular glandular structure. Enhancement is moderate, deriving from capillary proliferation induced by chronic inflammation but not as prominent as neovascularization in adenomatous polyps. Polyp regression after H. pylori eradication reflects the dampening of hyperplastic response with removal of inflammatory stimulus. Rare dysplasia development (1-2%) is explained by chronic inflammation increasing genetic instability and p53 mutation accumulation.
Small (<1 cm), smooth-surfaced, multiple mucosal polypoid lesions in gastric fundus or corpus — suggestive of hyperplastic polyps on chronic gastritis background. Location and morphology are critical for differentiation from antral, lobulated, large polyps (adenomatous).
In CT arterial phase, small (<1 cm), smooth-contoured, homogeneously moderately enhancing polypoid lesions are observed in the fundal or corporal mucosa. Usually multiple. Best detected when gastric lumen is filled with fluid.
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[Number] smooth-contoured, moderately enhancing mucosal polypoid lesions, largest [size] mm, are identified in the gastric [fundus/corpus] mucosa.
In portal venous phase, polyps maintain mild enhancement. May not show significant difference from surrounding normal mucosa — causing small polyps to be missed in this phase.
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In portal venous phase, polypoid lesions show enhancement similar to surrounding mucosa, making definitive delineation difficult.
On EUS, small, well-defined, iso-hyperechoic polypoid lesions originating from the mucosal layer are observed. Submucosa and muscularis propria are intact. Smooth surface morphology is visible. Minimal vascularity on color Doppler.
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On EUS, [number] smooth-surfaced, iso-hyperechoic polypoid lesions, largest [size] mm, in the gastric mucosa with intact deep layers.
On T2-weighted sequences, small, smooth-contoured polypoid lesions show intermediate signal intensity. May be mildly hyperintense due to edematous stroma. Small polyps may not be detectable with inadequate gastric wall distension.
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On MRI T2-weighted sequence, small, smooth-contoured polypoid lesions of intermediate signal intensity are observed in the gastric mucosa.
On non-contrast CT, small hyperplastic polyps are isodense to gastric mucosa and generally undetectable. However, larger polyps may be visible as intraluminal protrusions when gastric lumen is filled with air.
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On non-contrast CT, no definite polypoid lesion assessable in the gastric mucosa is identified.
On DWI, hyperplastic polyps generally show no significant diffusion restriction. ADC values are preserved and higher than adenomatous polyps — reflecting low cellularity and absence of dysplasia.
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On DWI, no significant diffusion restriction in polypoid lesions with preserved ADC values.
Criteria
Foveolar hyperplasia + edematous lamina propria + chronic inflammation. <1 cm, multiple.
Distinct Features
Potential regression after H. pylori eradication. Very low malignancy risk.
Criteria
>2 cm size. Bleeding, obstruction symptoms. Increased dysplasia risk.
Distinct Features
Appears as prominent polypoid mass on CT. May require endoscopic resection or surgery. Surface erosion and ulceration may be seen.
Criteria
Focal dysplasia focus within hyperplastic polyp. More frequent in >1 cm polyps.
Distinct Features
Endoscopic morphology may be indistinguishable from classic type. Diagnosis only by histopathology. Complete polypectomy and close follow-up required.
Distinguishing Feature
Adenomatous polyp lobulated surface, antral, usually solitary and larger; hyperplastic polyp smooth surface, fundal/corporeal, multiple and small
Distinguishing Feature
Carcinoma wall thickening, irregular contour, perigastric invasion; hyperplastic polyp mucosal-confined, smooth contour
Distinguishing Feature
GIST submucosal/muscularis propria origin, larger; hyperplastic polyp mucosal origin, small
Distinguishing Feature
Carcinoid submucosal, hypervascular, chromogranin positive; hyperplastic polyp mucosal, moderate vascularity, epithelial marker positive
Urgency
routineManagement
conservativeBiopsy
NeededFollow-up
12-monthFor small (<1 cm) hyperplastic polyps, H. pylori treatment and follow-up is sufficient after biopsy excludes dysplasia. Endoscopic polypectomy recommended for >1 cm polyps. Polyp regression expected after H. pylori eradication — follow-up endoscopy at 6-12 months. If dysplasia detected, complete polypectomy and 6-month endoscopic surveillance initiated. Increased polyp frequency in FAP, Peutz-Jeghers, or Cowden syndrome requiring systemic evaluation.
Hyperplastic polyps are generally benign. Polyps >1 cm or symptomatic ones are removed by endoscopic polypectomy. H. pylori eradication may lead to polyp regression.