Hyperplastic polyp

Last author update: 1 June 2017
Last staff update: 16 September 2022

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PubMed Search: Stomach hyperplastic polyp[title]

Pallavi A. Patil, M.B.B.S.
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Cite this page: Patil PA, Legolvan M. Hyperplastic polyp. website. 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
ICD coding
  • 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)
  • 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)
  • 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
  • Histopathology
  • 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

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Hyperplastic polyps

Differential diagnosis
  • Dysplasia must be differentiated from regenerative change
    • 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?

    1. CagA
    2. PAR1
    3. SHP2
    4. 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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