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Gastric Polyps

para>2/3 of gastric polyps are in patients >60 years old.  

ETIOLOGY AND PATHOPHYSIOLOGY


  • Fundic gland polyp
    • Sessile lesion usually <0.5 cm; found throughout the stomach (1)
    • Very low risk for malignancy (3)
    • Associated with long-term PPI use (4).
    • Histology shows dilated oxyntic glands, lined by flattened parietal and mucous cells (4).
  • Hyperplastic polyp
    • Smooth, rounded (typically multiple) lesions, usually in the antrum (5)
    • 0.5 to 1.5 cm-can be much larger (4)
    • Hyperregenerative response of epithelium in response to chronic inflammation (most commonly H. pylori).
    • Low risk for malignancy
      • Hyperplastic polyps >1 cm may indicate neoplasm. Loss of p16 and increased Ki-67 expression may be markers for dysplasia in hyperplastic polyps (6).
  • Adenomatous polyp (raised intraepithelial neoplasia)
    • Typically arise in the background of chronic, atrophic gastritis (4)
    • Velvety, lobulated, usually solitary lesion; most often found in the antrum; <2 cm (4)
    • Considered to be premalignant (2)
      • Malignant potential depends on size (>2 cm with 40-50% risk of malignant transformation) and degree of dysplasia and villous component.
  • Carcinoid polyp
    • Clusters of enterochromaffin cells in the mucosa; most often in the corpus or fundus (1)
    • Risk for metastasis depends on size.
    • Three distinct subtypes: Types 1 and 2 is associated with hypergastrinemia (1,2).
  • Xanthoma
    • Small, yellow nodules or plaques that protrude from the surrounding pink gastric mucosa.
    • Lipid-laden macrophages containing cholesterol and neutral fat loosely embedded in the lamina propria
    • No malignant potential
  • GIST
    • Neoplastic proliferations of interstitial cells of Cajal (or their precursors) (4)
    • Well-circumscribed, submucosal lesions; most often in the fundus; median size 6 cm (1,4)
    • Varying malignant potential based on size and mitotic activity (1).
    • 50% of patients with GISTs >2 cm have metastatic disease at the time of presentation (usually liver) (4).
  • Inflammatory fibroid polyp
    • Originates from submucosa; frequently with central depression or ulceration; 1 to 5 cm (4)
    • No malignant potential
  • Hyperplastic and adenomatous polyps: associated with any inflammatory process causing chronic cell turnover
  • Hamartomas
    • Abnormal formation and overgrowth of otherwise normal tissue
    • Benign; rarely invade or compress surrounding structures
  • All others: no known causes

Genetics
  • Most have no known hereditary component.
  • Fundic gland polyps are associated with familial adenomatous polyposis (FAP) arising from APC gene mutation (7).

RISK FACTORS


  • Increased incidence with age
  • Chronic gastritis: hyperplastic polyps (5)
    • Including NSAID use, increased gastric secretions, erosions, or ulcers
  • Long-term PPI use: fundic gland polyps (4)
  • H. pylori: hyperplastic and adenomatous polyps (4)
  • BRAF inhibitors used to treat melanoma may increase the risk for hypertrophic gastric polyps.

COMMONLY ASSOCIATED CONDITIONS


  • Associated with certain familial syndromes
    • FAP: fundic gland polyps (1)
    • Peutz-Jeghers syndrome, juvenile polyposis, Cronkhite-Canada syndrome, Cowden disease: hamartomas (1)
  • Carcinoid polyps
    • Type 1: achlorhydria, hypergastrinemia, and pernicious anemia (4)
    • Type 2: Zollinger-Ellison syndrome, MEN-1 syndrome (4)

DIAGNOSIS


HISTORY


  • Asymptomatic (>90%)
  • Larger polyps or patients with multiple polyps can present with the following:
    • Anemia due to blood loss
    • Epigastric pain
    • Nausea
    • Gastric outlet obstruction
    • Vomiting; hematemesis
    • Dyspepsia

PHYSICAL EXAM


No specific findings on physical examination. Longstanding polyps may show evidence of anemia (pallor) on exam if associated with chronic blood loss.  

DIFFERENTIAL DIAGNOSIS


Gastric malignancy  

DIAGNOSTIC TESTS & INTERPRETATION


Most polyps are found incidentally during endoscopy.  
Initial Tests (lab, imaging)
  • Upper GI endoscopy (esophagogastroduodenoscopy, EGD) is the gold standard for diagnosis.
  • Check for associated morbidity.
    • CBC: anemia
    • H. pylori blood antibody test, urea breath test, or stool antigen test
  • CT scan (generally unnecessary)
    • May be able to identify larger polyps but not able to differentiate type and is not a first-line diagnostic test

Diagnostic Procedures/Other
  • Biopsy or polypectomy is necessary for histologic evaluation (3)[A].
  • When hyperplastic or adenomatous polyps are suspected, biopsy surrounding nonpolypoid mucosa to exclude dysplasia (4)[A].
  • Endoscopic US (EUS) can assess polyp depth.
  • GISTs; c-kit mutation detected by immunohistochemical staining against KIT (4)

Test Interpretation
The most common gastric polyps are fundic gland, hyperplastic, and adenomatous polyps (1).  

TREATMENT


ADDITIONAL THERAPIES


  • Biopsy polyps for histologic evaluation (1,3,7)[A]
  • Post histologic evaluation:
    • Fundic gland polyps
      • Frequently regress spontaneously
      • Consider histologic evaluation to assess for malignant features (7)[A].
      • Histologic assessment of all polyps >0.5 cm
      • Consider discontinuing PPIs for large polyps
      • Evidence of dysplasia should raise suspicion for FAP. Polyps in this setting carry a 40% risk of dysplasia (8)[A].
    • Hyperplastic polyp
      • Remove single polyps <2 cm if dysplastic on biopsy (7)[A].
      • Remove all polyps >2 cm (4)[A].
      • Repeat EGD in 1 year if multiple hyperplastic polyps (7)[A].
      • Eliminate offending mucosal agents.
      • Initiate eradication therapy if positive for H. pylori (4,7)[A].
    • Adenomatous polyp
      • Polypectomy for all adenomatous polyps. Sample rest of gastric mucosa. Repeat EGD in 1 year (7)[A].
    • Carcinoid polyp
      • Type I: Remove all polyps >1 cm (4,8)[A].
      • Type II: regresses once gastrinoma is removed (8)[A]
    • GIST
      • CT scan to assess for metastasis (8)[A]
      • EUS to assess for dimensions
      • Surgical resection if isolated to stomach (8)[A]
      • If metastasized, initiate treatment with a tyrosine kinase inhibitor (imatinib) (4,5)[A].
    • Inflammatory fibroid polyp
      • Local excision (1,8)[A]
    • Hamartomas
      • Assess for polyposis syndromes.
      • If associated with syndrome
      • Biopsy >5 polyps (8)[A]
      • Remove polyps >1 cm (7)[A].
      • Follow-up EGD every 2 to 3 years (8)[A]

ONGOING CARE


FOLLOW-UP RECOMMENDATIONS


  • Fundic gland polyp
    • Sporadic type: No follow-up necessary (7)[A]
    • FAP: Repeat EGD every 2 years (7)[A].
  • Hyperplastic polyp
    • If multiple, repeat EGD in 1 year (7)[A].
  • Adenoma
    • Repeat EGD in 1 year (4,7)[A].
  • FAP
    • EGD every 2 years after age 18 (7)[A]
  • Peutz-Jeghers
    • EGD every 2 years after age 18 years (7)[A]
  • Juvenile polyposis
    • EGD every 3 years after age 18 years (7)[A]

REFERENCES


11 Carmack  SW, Genta  RM, Graham  DY, et al. Management of gastric polyps: a pathology-based guide for gastroenterologists. Nat Rev Gastroenterol Hepatol.  2009;6(6):331-341.22 Hirota  WK, Zuckerman  MJ, Adler  DG, et al. ASGE guidelines: the role of endoscopy in the surveillance of premalignant conditions of the upper GI tract. Gastrointest Endosc.  2006;63(4):570-580.33 Sonnenberg  A, Genta  RM. Prevalence of benign gastric polyps in a large pathology database. Dig Liver Dis.  2015;47(2):164-169.44 Sharaf  RN, Shergill  AK, Odze  RD, et al. Endoscopic mucosal tissue sampling. Gastrointest Endosc.  2013;78(2):216-224.55 Shaib  YH, Rugge  M, Graham  DY, et al. Management of gastric polyps: an endoscopy-based approach. Clin Gastroenterol Hepatol.  2013;11(11):1374-1384.66 Park do  Y, Lauwers  GY. Gastric polyps: classification and management. Arch Pathol Lab Med.  2008;132(4):633-640.77 Ahn  JY, Sonda  H, Choi  KD, et al. Neoplasms arising in large gastric hyperplastic polyps: endoscopic and pathologic features. Gastrointest Endosc.  2014;80(6):1005.e2-1013.e2.88 Gonzalez-Obeso  E, Fujita  H, Deshpande  V, et al. Gastric hyperplastic polyps: a heterogeneous clinicopathologic group including a distinct subset best categorized as mucosal prolapse polyp. Am J Surg Pathol.  2011;35(5):670-677.

ADDITIONAL READING


  • Amaravadi  RK, Hamilton  KE, Ma  X, et al. Multiple gastrointestinal polyps in patients treated with BRAF inhibitors. Clin Cancer Res.  2015;21(23):5215-5221.
  • Goddard  AF, Badreldin  R, Pritchard  DM, et al. The management of gastric polyps. Gut.  2010;59(9):1270-1276.
  • Ha  M, Chung  JW, Hahm  KB, et al. A case of Cowden syndrome diagnosed from multiple gastric polyposis. World J Gastroenterol.  2012;18(8):861-864.
  • Jang  HW, Jeong  HY, Kim  SH, et al. Adenocarcinoma occurring in a gastric hyperplastic polyp treated with endoscopic submucosal dissection. J Gastric Cancer.  2013;13(2):117-120.
  • Morais  DJ, Yamanaka  A, Zeitune  JM, et al. Gastric polyps: a retrospective analysis of 26,000 digestive endoscopies. Arq Gastroenterol.  2007;44(1):14-17.

CODES


ICD10


  • K31.7 Polyp of stomach and duodenum
  • D13.1 Benign neoplasm of stomach

ICD9


211.1 Benign neoplasm of stomach  

SNOMED


  • Gastric polyp (disorder)
  • Hyperplastic adenomatous polyp of stomach
  • Solitary fundic gland polyp (disorder)
  • Inflammatory fibroid polyps of stomach (disorder)

CLINICAL PEARLS


  • Most gastric polyps are asymptomatic, incidental findings on EGD.
  • Most gastric polyps are epithelial in origin and rarely show malignant changes.
  • Biopsy gastric polyps. Diagnosis and management depend on the histology.
  • Any polyp with dysplastic changes should be completely excised and followed with repeat EGD after 1 year.
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