Stomach
Polyps
Hyperplastic polyp
Last author update: 1 June 2017
Last staff update: 16 September 2022
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PubMed Search: Stomach hyperplastic polyp[title]
Table of Contents
Definition / general | Essential features | Terminology | ICD coding | Epidemiology | Sites | Etiology | Clinical features | Diagnosis | Treatment | Gross description | Microscopic (histologic) description | Microscopic (histologic) images | Differential diagnosis | Board review style question #1 | Board review style answer #1Cite this page: Patil PA, Legolvan M. Hyperplastic polyp. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/stomachhyperplastic.html. Accessed May 31st, 2023.
Definition / general
- 85% associated with chronic gastritis (with or without association with H. pylori)
- Also associated with reactive gastropathy, post surgery and bile reflux gastritis (Am J Surg Pathol 2001;25:500)
- Usually < 1 cm, more than 50% are less than 0.5 cm, however very large polyps up to 12 cm can occur and mimic malignancy
- Dysplasia is more likely when > 1.0 cm (Gut Liver 2009;3:271)
- Resembles other GI dysplasia; either low grade or high grade
Essential features
- Elongated and architecturally distorted, irregular foveolar epithelium with cystic dilatations
- Corkscrew appearance can occur
- Lamina propria shows edema, congestion, variable acute and chronic inflammation
- Smooth muscle strands can be seen extending from muscularis mucosa towards surface
- Thick walled vessels may be present towards the base of the polyp
Terminology
- Synonyms: inflammatory polyp, regenerative polyp and hyperplasiogenous polyp (Tohoku J Exp Med 1984;142:125)
ICD coding
Epidemiology
- 17% of gastric polyps are hyperplastic (Am J Gastroenterol 2009;104:1524) vs. up to 70% in older reports
- This could be due to increasing use of proton pump inhibitors and detection of fundic gland polyps (World J Gastroenterol 2016;22:8883, Dig Dis Sci 2009;54:1839, Arq Gastroenterol 2007;44:14)
- Occurs equally in males and females, age range 20 to 80 years, peaks in 6th and 7th decade (World J Gastroenterol 2016;22:8883)
- Usually solitary, can be multiple in atrophic gastritis
- If multiple, must rule out juvenile polyposis, Peutz-Jeghers or familial adenomatous polyposis (FAP) syndromes
- >50 polyps suggests gastric polyposis syndrome, an entity not well established by diagnostic criteria (J Clin Diagn Res 2012;6:1428)
- Dysplasia occurs in 0.4 to 10% (Dig Dis Sci 2009;54:1839, World J Gastroenterol 2016;22:8883); risk increases with age, particularly if > 50 years
- Carcinoma reported in 0.9% (Arq Gastroenterol 2007;44:14)
Sites
- Common site is gastric antrum but can occur anywhere in the stomach, recently body has become more common due to eradication of H. pylori (Am J Gastroenterol 2009;104:1524)
- Body of stomach is the common site in autoimmune gastritis
- Hyperplastic polyps in pyloric and prepyloric regions may have features of prolapse associated polyps
- Hyperplastic polyps at gastroesophageal junction are associated with Barrett esophagus in 33% (Am J Surg Pathol 2011;35:1038)
Etiology
- Hypothesis: exaggerated mucosal response to injury and inflammation beginning with foveolar hyperplasia, which becomes polypoid and eventually develops into a discrete polyp
- Mucosal injury is due to:
- Chronic gastritis (usually Helicobacter pylori associated)
- Reactive gastropathy (chemicals, drugs, bile reflux)
- Reflux (gastroesophageal)
- Barrett esophagus
- Autoimmune gastritis
- The Helicobacter pylori CagA protein is proposed to have a direct relation to development of hyperplastic polyps, derived from an experiment on transgenic mice in which expression of CagA in gastric mucosa led to development of hyperplastic polyps (Am J Gastroenterol 2009;104:1524, Proc Natl Acad Sci USA 2008;105:1003)
- CagA can cause aberrant activation of SHP-2, a human oncoprotein, in the stomach (Proc Natl Acad Sci USA 2008;105:1003)
- Since dysplasia suggests background chronic mucosal injury, close follow up is needed to rule out dysplasia elsewhere in stomach (Gastroenterol Rep (Oxf) 2016;4:158)
Clinical features
- Chronic gastritis symptoms
- Obstructive symptoms if near pylorus or gastroesophageal junction
Diagnosis
- Histopathology
Treatment
- On follow up, 67% are stable, 27% have enlarged and 5% have become smaller
- 71% regress after eradication of H. pylori (Ann Intern Med 1998;129:712, Eur J Gastroenterol Hepatol 1999;11:727)
- 50% recur after resection by endoscopy
- The Standards of Practice Committee of the American Society for Gastrointestinal Endoscopy (ASGE) suggests polypectomy for hyperplastic polyps greater than 0.5 cm in maximum dimension; a stronger recommendation is not made due to weak evidence (Gastrointest Endosc 2013;78:216)
Gross description
- Ovoid with smooth overlying mucosa, can be polypoid of villiform
- Surface erosion may occur
- Entirely submitted to rule out dysplasia or malignancy
Microscopic (histologic) description
- Elongated, cystically dilated, architecturally distorted, irregular foveolar epithelium
- Edematous lamina propria with acute and chronic inflammation and congestion
- Inflammation is usually towards the surface, particularly when there is erosion and ulceration
- Smooth muscle strands can extend from muscularis mucosa to the surface
- Thick walled blood vessels can be seen at the base
- At gastroesophageal junction, may show intestinal metaplasia when associated with Barrett esophagus
- Regenerative epithelial changes include focal mucin depletion, prominent nucleoli and hyperchormasia
- In areas of surface ulceration or inflammation, epithelium can have brisk mitotic activity, granulation tissue may show reactive fibroblasts and endothelial cells
- Dysplasia often affects the surface; may be intestinal, foveolar or mixed
- High grade dysplasia: complex architecture with cribriform formation or budding, back to back arrangement of glands
- H. pylori associated polyps: more likely to have lymphoplasmacytic inflammation in lamina propria and neutrophils in the epithelium (Int J Surg Pathol 2016;24:704)
Microscopic (histologic) images
Contributed by Andrey Bychkov, M.D., Ph.D.
Polypoid lesion
Hemorrhagic and ulcerated
Cystic hyperplastic glands
Contributed by Pallavi Patil, M.D.
Hyperplastic polyp
Images hosted on other servers:
Hyperplastic polyps
Differential diagnosis
- Polypoid gastritis: normal architecture, no smooth muscle wisps
- Polypoid foveolar hyperplasia: no cystic dilation, no smooth muscle wisps
- Gastritis cystica profunda: entrapped, distorted, dilated glands in muscularis
- Fundic gland polyp: distorted glands and cysts lined by parietal and chief cells
- Menetrier's disease: affects gastric body only; foveolar hyperplasia, atrophy of glands, adjacent epithelium normal
- Cronkhite-Canada syndrome: affects entire stomach; foveolar hyperplasia, atrophy of glands, adjacent epithelium shows atrophy of glands and microcystic change
- Juvenile polyposis: adjacent mucosa is normal as opposed to in hyperplastic polyp which often has chronic gastritis
- Peutz-Jeghers polyposis
- Dysplasia is present at the surface; regenerative change shows surface maturation and atypia like changes only in the proliferative zones, not at the surface
- Dysplasia is typically abrupt
- Dysplasia has architecturally complex patterns (cribriform, budding and branching)
- Dysplasia has nuclear pleomorphism, elongation and hyperchromasia without prominent nucleoli
- Regenerative epithelium shows gradual change, lacks complex patterns, has hyperchromasia but with ovoid nuclei and prominent nucleoli
Board review style question #1
Which H. pylori protein is associated with a role in the development of gastric neoplasia?
- CagA
- PAR1
- SHP2
- SRC
Board review style answer #1
A. CagA in H. pylori can cause aberrant activation of SHP-2, a human oncoprotein, in the stomach (Proc Natl Acad Sci USA 2008;105:1003)
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Reference: Hyperplastic polyp
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