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Literature review current through: Mar 2014. | This topic last updated: Jan 06, 2014.

INTRODUCTION — Gastric polyps are usually found incidentally on upper gastrointestinal endoscopy performed for an unrelated indication and only in rare cases do they cause symptoms. Nevertheless, the diagnosis and appropriate management of gastric polyps are important, as some polyps have malignant potential.

This topic will review the epidemiology, clinical manifestations, histopathology, and management of gastric polyps. Our recommendations are largely consistent with the American Society for Gastrointestinal Endoscopy (ASGE) guidelines [1,2]. The clinical manifestations, diagnosis and management of gastric gastrointestinal stromal tumors (GISTs), leiomyomas, lipomas, and other subepithelial lesions that may have a polypoid appearance on upper endoscopy are discussed in detail, separately. (See "Endoscopic ultrasound for the characterization of subepithelial lesions of the upper gastrointestinal tract" and "Epidemiology, classification, clinical presentation, prognostic features, and diagnostic work-up of gastrointestinal mesenchymal neoplasms including GIST" and "Local treatment for gastrointestinal stromal tumors, leiomyomas, and leiomyosarcomas of the gastrointestinal tract".)

EPIDEMIOLOGY — Gastric polyps are found in approximately 6 percent of upper gastrointestinal endoscopic procedures in the United States [3]. However, lower rates have been reported in other countries [4,5]. Hyperplastic polyps and adenomas are relatively more prevalent as compared with fundic gland polyps in regions where Helicobacter pylori infection is common [4-6]. In contrast, in western countries, where the prevalence of H. pylori infection is lower and proton pump inhibitor (PPI) use is common, the most commonly encountered polyps are fundic gland polyps (picture 1A-B) [3,6].

INITIAL EVALUATION — The initial approach to gastric polyps should include an evaluation of both polyp histology and the surrounding mucosa.

Evaluation of polyp histology – In patients with small solitary polyps, either biopsy samples should be obtained or polypectomy performed so that the polyp can be examined microscopically for histologic characterization [7-11]. Polypectomy should be performed for all known neoplastic polyps and for all polyps ≥1 cm in diameter, as biopsies alone cannot exclude foci of high-grade dysplasia or early gastric cancer [9]. In patients with multiple polyps, the largest polyp should be excised and representative biopsies obtained from the remaining polyps [1,2]. In patients with sessile polyps, endoscopic mucosal resection may be needed to provide an accurate histological assessment and achieve complete resection. Further management should be based on histology [12]. (See "Overview of endoscopic resection of gastrointestinal tumors" and 'Types of gastric polyps and specific management' below.)

Assessment of surrounding mucosa – Once polyps are biopsied or resected, the normal appearing antral and corpus mucosa should be sampled to rule out dysplasia occurring in the background of metaplastic atrophic gastritis and to diagnose H. pylori [2]. We obtain 7 to 12 biopsies: four quadrant biopsies from antrum (2 to 3 cm proximal to pylorus), two from the angularis, four from the mid corpus (two lesser curvature, two greater curvature), and two from the cardia. Gastritis should be classified using a validated histologic staging system such as the Operative Link on Gastritis Assessment (OLGA) staging system, a gastric mucosal staging system designed to provide an estimate of the risk of developing gastric cancer based on the degree of antral and corpus atrophy [13,14]. (See "Classification and diagnosis of gastritis and gastropathy" and "Metaplastic (chronic) atrophic gastritis" and "Risk factors for gastric cancer" and "Indications and diagnostic tests for Helicobacter pylori infection" and 'Clinical and pathologic features' below.)

TYPES OF GASTRIC POLYPS AND SPECIFIC MANAGEMENT — The management of gastric polyps and surveillance are specific to the underlying presentation, pathology, and malignant potential.

Hyperplastic polyps — Hyperplastic polyps account for approximately 75 percent of gastric polyps in geographic areas where H. pylori is common.

Etiology — Hyperplastic polyps result from hyper-regenerative epithelium in response to an underlying chronic inflammatory stimulus. They are therefore observed in the setting of chronic inflammatory conditions (eg, chronic atrophic gastritis), H. pylori, pernicious anemia, adjacent to ulcers and erosions, and at sites of gastroenterostomies [15].

Clinical and pathologic features — Men and women are equally affected. Hyperplastic polyps typically appear in mid to late adult life.

Clinical manifestations – Hyperplastic polyps are usually asymptomatic and are discovered incidentally on upper endoscopy. Over time, polyps may remain stable, increase in size, or regress following H. pylori eradication [16,17]. Rare polyps that cause symptoms are most likely to present with gastrointestinal (GI) bleeding due to erosion of the surface epithelium. Bleeding is usually occult but occasionally overt [18,19]. In rare cases, intermittent obstruction may occur when pedunculated polyps in the antrum prolapse into or through the pylorus (picture 2).

Endoscopic features and pathology – On upper endoscopy, hyperplastic polyps are smooth, dome-shaped, or stalked with an average size ranging from 0.5 to 1.5 cm. Hyperplastic polyps are often multiple and may develop in the antrum, body, fundus or cardia (image 1) [4,20]. Microscopically, they are composed of elongated, dilated, and/or cystic, architecturally distorted, foveolar epithelium within an edematous, congested, and often actively and chronically inflamed lamina propria (picture 3) [21,22]. Other features that may be seen include epithelial regenerative changes, dystrophic goblet cells, intestinal metaplasia, pyloric metaplasia (in corpus and fundic lesions), surface erosion, and ulceration.

Malignant potential – Malignancy develops in hyperplastic polyps through a dysplasia/carcinoma sequence [3,23,24]. Between 1 and 20 percent of hyperplastic polyps have been reported to harbor foci of dysplasia [23-28]. The risk of malignancy in hyperplastic polyps is increased in polyps >1 cm and pedunculated in shape, but invasive cancer (into the muscularis propria or serosa) is rare [23].

Management — Hyperplastic polyps measuring >0.5 cm should be resected completely [1,2]. In addition, the normal appearing antral and corpus mucosa should be sampled to assess for the presence of dysplasia and H. pylori. All patients with H. pylori should be treated with eradication therapy [17]. (See 'Initial evaluation' above and "Treatment regimens for Helicobacter pylori".)

In patients with dysplasia or carcinoma beyond the confines of the polyp, a subtotal gastrectomy or endoscopic mucosal resection should be performed. (See "Early gastric cancer: Epidemiology, clinical manifestations, diagnosis, and staging".)

Surveillance – In patients with hyperplastic polyps without dysplasia or carcinoma, follow-up should be based on the cancer risk due to concurrent chronic atrophic gastritis and risk factors for gastric cancer.

In patients at high risk for gastric cancer (eg, Operative Link on Gastritis Assessment [OLGA] stage 3 or 4 with moderate diffuse or severe atrophy in the corpus or antrum usually accompanied by extensive intestinal metaplasia, migrants from areas with high gastric cancer incidence, family history of gastric cancer), we perform surveillance endoscopy at regular intervals (one to two years).

In patients at low risk for gastric cancer (eg, OLGA stage 1 or 2), we perform at least one follow-up endoscopy three to six months after therapy to confirm that H. pylori has been eradicated and that there are no new or residual polyps that warrant resection. (See "Early gastric cancer: Epidemiology, clinical manifestations, diagnosis, and staging" and "Metaplastic (chronic) atrophic gastritis" and "Risk factors for gastric cancer".)

Fundic gland polyps — In western countries, where H. pylori infection has a low prevalence and proton pump inhibitor (PPI) use is common, fundic gland polyps are the most commonly encountered polyps.

Etiology — Most fundic gland polyps are sporadic. Fundic gland polyps may also occur in association with polyposis syndromes, familial adenomatous polyposis (FAP), MUTYH-associated polyposis (MAP), and gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) [29-31]. Fundic gland polyps occur in 20 to 100 percent of patients with FAP and 11 percent of patients with MAP [31,32]. (See "Clinical manifestations and diagnosis of familial adenomatous polyposis".)

Hypergastrinemia associated with a gastrinoma, Zollinger-Ellison syndrome, or long-term therapy with PPIs has been shown to be associated with fundic gland polyps [6,33-37]. In an observational study that included 599 patients undergoing endoscopy, long-term (≥5 years) PPI use was associated with a fourfold increased risk of fundic gland polyps, while short-term (<1 year) PPI therapy was not associated with increased risk [6]. Regression of fundic gland polyps following withdrawal of PPIs provides further support for this association [38].

The incidence of H. pylori infection is very low in patients with fundic gland polyps and infection may be protective [3]. In contrast with gastric adenomas and hyperplastic polyps which may regress with eradication of H. pylori, regression of fundic gland polyps has been reported following an H. pylori infection [34,39].

Clinical and pathologic features — Sporadic fundic gland polyps occur in females more often than in males and usually occur in middle age. Up to 40 percent of patients have multiple polyps. In FAP, men and women are affected equally; polyps develop at an earlier age (mean age 40 years), as compared with sporadic fundic gland polyps, and are multiple in more than 90 percent of cases.

Clinical manifestations – Fundic gland polyps are usually asymptomatic and discovered incidentally at endoscopy. Only in rare cases can they reach a size large enough to cause obstruction or symptoms of abdominal pain or vomiting.

Endoscopic features and pathology – Fundic gland polyps are typically small (0.1 to 0.8 cm), hyperemic, sessile, and have a smooth surface contour (picture 1A-B). They occur exclusively in the gastric corpus. On narrow band imaging, fundic gland polyps have a honeycomb appearance with dense vasculature, a nonspecific pattern that also can be seen in hyperplastic polyps.

On pathology, fundic gland polyps are composed of normal gastric corpus-type epithelium, arranged in a disorderly and/or microcystic configuration (picture 4 and picture 5) [5,9,33]. Microcysts are characteristic, and may be lined by any of the normal cell types found in the gastric corpus. The glandular compartment typically reveals distorted architecture with irregular gland buds, tortuous glands, or irregular stellate glandular configurations. Inflammation is usually minimal. Mild hyperplasia of the muscularis mucosa may occur in a pericystic configuration. These lesions probably arise from proliferation and differentiation of aberrantly located proliferative cells in the stem cell compartment of the corpus epithelium.

Malignant potential – Somatic APC gene mutations have been detected in over 70 percent of syndromic fundic gland polyps without dysplasia, but in less than 10 percent of sporadic lesions [40]. Sporadic fundic gland polyps and those associated with PPI use have virtually no malignant potential, but may rarely show dysplasia [6,35,37,41]. Between 30 to 50 percent of fundic gland polyps in patients with FAP show dysplasia, which is typically low grade [42-44]. However, fundic gland polyps, in contrast with adenomas in patients with FAP, rarely progress to cancer [45]. (See "Clinical manifestations and diagnosis of familial adenomatous polyposis", section on 'Extracolonic manifestations' and 'Gastric adenomas' below.)

Management — Fundic gland polyps are frequently multiple and biopsies of one or more representative polyps is sufficient. The remaining polyps should be carefully inspected on endoscopy and any lesion that appears significantly different should be biopsied and, if possible, resected. Fundic gland polyps ≥1 cm in diameter, polyps that are ulcerated or located in the antrum should be resected to confirm the diagnosis and rule out dysplasia or neoplasia.

The possibility of a familial polyposis syndrome should be considered in patients with ≥20 polyps, fundic gland polyps in the antrum, young onset fundic polyps (prior to age 40 years), or concurrent duodenal adenomas, and a colonoscopy should be performed.

In patients with sporadic fundic gland polyps attributed to PPI use, we discontinue PPIs in patients with ≥20 polyps or polyps >1 cm. Hypergastrinemia in these patients suggests either the presence of a gastrinoma (Zollinger-Ellison syndrome) or more commonly PPI-induced hyperchlorhydria, which if present is further reason to stop or reduce the PPI dosage. If acid suppression is needed for the management of gastroesophageal reflux disease (GERD) and patients fail a trial of an H2 receptor blocker, we consider using a different PPI at the lowest effective dose.

Surveillance – Regular surveillance by upper endoscopy is not routinely recommended for sporadic fundic gland polyps without dysplasia as progression to gastric cancer is rare. In patients with an established diagnosis of a familial polyposis syndrome (eg, FAP), surveillance with upper endoscopy is recommended for polyps in the upper GI tract [42,46-48]. (See "Familial adenomatous polyposis and MUTYH associated polyposis: Screening and management of patients and families", section on 'Surveillance for upper intestinal tumors'.)

Gastric adenomas — Gastric adenomas, or raised intraepithelial neoplasia, are the most common gastric neoplastic polyp [49-51]. Gastric adenomas account for 6 to 10 percent of gastric polyps [4,20].

Etiology — Gastric adenomas typically occur in a background of chronic atrophic gastritis. Gastric adenomas are much less common than fundic gland polyps in patients with FAP; they are typically isolated and located in the antrum and are associated with a relatively low but real risk of progression to cancer. (See "Clinical manifestations and diagnosis of familial adenomatous polyposis", section on 'Extracolonic manifestations'.)

Clinical and pathologic features — Sporadic gastric adenomas occur equally in men and women and are most commonly seen in the sixth or seventh decade.

Clinical manifestations – Most gastric adenomas are asymptomatic. Polyps that cause symptoms are most likely to present with GI bleeding (usually occult but occasionally overt) or rarely obstruction.

Endoscopic features and pathology – Adenomas may be flat or polypoid, and are usually <2 cm in size (picture 6). Adenomas are usually solitary. Most are found in the antrum, but some occur in the corpus and cardia. The narrow band imaging features of gastric adenomas have not been well defined.

Microscopically, these lesions are similar to typical colonic adenomas (picture 7). They may be tubular, tubulovillous, or villous (papillary), are sessile or stalked, and occasionally reach large sizes (up to 15 cm). They may have an intestinal or gastric phenotype or some may be mixed.

Gastric adenomas are neoplastic and consist of dysplastic columnar cells with striated borders, often intermixed with dysplastic goblet cells, Paneth cells, parietal cells, or endocrine cells. The dysplastic cells show elongated, pencil-shaped nuclei with hyperchromasia, clumped chromatin, and pseudostratification. These lesions are often associated with underlying chronic gastritis with intestinal metaplasia. Some show a gastric phenotype composed of dysplastic mucinous foveolar cells.

Malignant potential – It is estimated that 8 to 59 percent of adenomas are associated with synchronous gastric carcinomas [52]. The presence of invasive carcinoma in an adenoma correlates with increasing size, villous contour, and the degree of dysplasia [23,53]. The risk of malignancy is lower in flat adenomas [54]. High-grade dysplasia has been identified in close proximity to a high proportion (40 to 100 percent) of early gastric cancers [55].

Dysplasia is a precursor of invasive adenocarcinoma. Patients with high-grade dysplasia have a higher risk of progression as compared with patients with low-grade dysplasia [56,57]. A nationwide cohort study in the Netherlands evaluated the progression of dysplasia to frank gastric cancer in 165 patients with high-grade dysplasia and 270 patients with low-grade dysplasia. Gastric cancer was diagnosed within 1, 5, and 10 years from the initial diagnosis in 25, 30, and 33 percent of patients with high-grade dysplasia and 2, 3, and 4 percent with low-grade dysplasia, respectively [56].

The risk of gastric cancer in patients with FAP is discussed in detail, separately. (See "Clinical manifestations and diagnosis of familial adenomatous polyposis", section on 'Extracolonic manifestations'.)

Management — Given the increased risk of gastric cancer, all gastric adenomas should be resected. This can usually be accomplished endoscopically, but on occasion surgery may be required for lesions that contain invasive carcinoma or in patients with multiple adenomas.

Because of the association of gastric dysplasia with synchronous gastric carcinomas, the remainder of the stomach must be examined carefully [13,14]. In addition, as adenomatous polyps are associated with atrophic gastritis, the normal appearing antral and corpus mucosa should be sampled to assess the stage of gastritis and, thus, cancer risk. All patients should be tested for active H. pylori infection and, if present, the infection should be treated. (See "Treatment regimens for Helicobacter pylori" and "Early gastric cancer: Epidemiology, clinical manifestations, diagnosis, and staging" and 'Initial evaluation' above.)

Surveillance – We perform an upper endoscopy for surveillance one year after initial resection of adenomatous gastric polyps to assess recurrence at the prior excision site, new or previously missed polyps, confirm eradication of H. pylori, and/or detect an early carcinoma [1].

In individuals at high risk for gastric cancer (eg, migrants from areas with high gastric cancer incidence, family history of gastric cancer, OLGA stage 3 or 4 with moderate diffuse or severe atrophy in the corpus or antrum usually accompanied by extensive intestinal metaplasia, patients with FAP), surveillance is continued indefinitely. (See "Risk factors for gastric cancer" and "Familial adenomatous polyposis and MUTYH associated polyposis: Screening and management of patients and families", section on 'Screening for extraintestinal malignancies'.)

Gastric neuroendocrine tumors (carcinoids) — Gastric neuroendocrine tumors are derived from enterochromaffin-like (ECL) cells.

Etiology — Gastric neuroendocrine tumors are subdivided into types 1 to 3 as they have different etiologies, biologic behavior, and prognoses [58-61]. Type 1 tumors represent 70 to 80 percent of all gastric neuroendocrine tumors. They are associated with prolonged hypergastrinemia typically resulting from autoimmune (corpus-restricted) atrophic gastritis. Type 2 gastric neuroendocrine tumors account for 5 to 8 percent of gastric neuroendocrine tumors and result from prolonged hypergastrinemia from a gastrin-secreting tumor. Type 3 neuroendocrine tumors are sporadic and account for 20 percent of gastric neuroendocrine tumors. (See "Clinical characteristics of carcinoid tumors".)

Clinical and pathologic features

Clinical manifestations – Type 1 gastric neuroendocrine tumors are found more commonly in older adults, particularly women, with atrophic gastritis and often are associated with pernicious anemia. Type 2 gastric neuroendocrine tumors are frequently detected as part of the work-up for MEN-1 syndrome or for Zollinger–Ellison syndrome in patients who present with peptic ulcer disease, abdominal pain, diarrhea, or bleeding. Type 3 tumors can be associated with atypical carcinoid syndrome. (See "Etiology and clinical manifestations of vitamin B12 and folate deficiency", section on 'Pernicious anemia' and "Multiple endocrine neoplasia type 1: Clinical manifestations and diagnosis" and "Clinical features of the carcinoid syndrome", section on 'Gastric carcinoid variant syndrome'.)

Endoscopic features and pathology – Gastric neuroendocrine tumors associated with hypergastrinemia (types 1 and 2) are usually multiple, broad based, firm yellowish lesions in the fundus and body of the stomach and rarely measure >2 cm (picture 8). In patients with MEN-1 syndrome, the gastric mucosa is normal or mildly inflamed, but not atrophic. The fundic mucosa of patients with Zollinger–Ellison syndrome often is hypertrophic, with long densely packed oxyntic glands and no significant inflammation. Type 3 tumors occur in the antrum and are usually single. (See "Clinical characteristics of carcinoid tumors".)

The pathologic diagnosis is usually established by recognizing the characteristic cytologic and architectural pattern of the cells, combined with immunohistochemical reactivity for chromogranin and/or synaptophysin [62]. Electron microscopy may be useful to confirm the presence of neurosecretory granules in the cytoplasm of tumor cells. There are four histologic architectural patterns in gastric neuroendocrine tumors, but it is common to find a mixture of these patterns in any particular lesion: solid or insular; trabecular; glandular; and undifferentiated, or diffuse (picture 9) [63-65]. Most gastric neuroendocrine tumors have a very prominent, solid nest or insular pattern, particularly those that arise from enterochromaffin-like cells. Cytologically, tumors show a homogeneous, regular population of round to oval-shaped cells with round to oval nuclei containing a characteristic stippled or speckled chromatin pattern. Gastric neuroendocrine tumors that develop in association with the Zollinger-Ellison syndrome or pernicious anemia may be associated with hyperplastic or dysplastic endocrine growths in the adjacent gastric mucosa [66].

Malignant potential – Type 1 and 2 gastric neuroendocrine tumors usually have an indolent course. Type 3 is the most aggressive; local or hepatic metastases are present in up to 65 percent of patients who undergo resection [59,61]. (See "Clinical characteristics of carcinoid tumors".)

Management — For type 1 and 2 gastric carcinoids smaller than 1 to 2 cm, endoscopic resection is the treatment of choice. In patients with multiple progressive tumors, antrectomy should be considered to remove the gastrin stimulus [67]. Sporadic (type 3) gastric carcinoids are treated by partial or total gastrectomy with local lymph node resection. The management of gastric neuroendocrine tumors is discussed in detail, separately. (See "Treatment and surveillance of non-metastatic carcinoid tumors", section on 'Stomach'.)

Surveillance – Consistent with the National Comprehensive Cancer Network (NCCN) recommendations following treatment of type 1 and 2 gastric neuroendocrine tumors ≤2 cm, we recommend history and physical examination with upper endoscopy every 6 to 12 months for three years and annually thereafter; imaging studies only as clinically indicated. The post-treatment surveillance for gastric neuroendocrine tumors is discussed in detail, separately. (See "Treatment and surveillance of non-metastatic carcinoid tumors", section on 'Posttreatment follow-up'.)

Inflammatory fibroid polyps — Inflammatory fibroid polyps are extremely rare lesions that represent less than 0.1 percent of all gastric polyps. Inflammatory fibroid polyps are mesenchymal tumors that arise in the submucosa and mucosa of the GI tract. Immunohistochemical staining suggests that these polyps have a dendritic cell origin [68].

Etiology — Although familial clustering of inflammatory fibroid polyps has been reported, the etiology of inflammatory fibroid polyps is largely unknown [69].

Clinical and pathologic features

Clinical manifestations – Most inflammatory fibroid polyps are asymptomatic, but larger polyps have been reported to cause abdominal pain, early satiety, anemia, and gastric outlet obstruction (picture 10).

Endoscopic features and pathology – On endoscopy, inflammatory fibroid polyps are usually firm, solitary, sessile or pedunculated, and often ulcerated. On endoscopic ultrasound, they have the appearance of a hypoechoic homogeneous lesion with an indistinct margin, located within the second or third layer with an intact fourth layer.

On histology, these polyps are characterized by submucosal proliferations of spindle cells with vessels surrounded by a characteristic circumferential deposition of fibroblasts giving it an onion skin appearance, and an inflammatory infiltrate with a predominance of eosinophils.

Malignant potential – Inflammatory fibroid polyps have been considered reactive and non-neoplastic. However, in one study of 23 inflammatory fibroid polyps, 70 percent were found to have gain-of-function mutations in the platelet-derived growth factor receptor alpha polypeptide gene, similar to those found in CD117-negative GI stromal tumors, suggesting the possibility of a neoplastic process [70].

Management — Following resection, inflammatory fibroid polyps typically do not recur, and surveillance is not recommended.

SUMMARY AND RECOMMENDATIONS

Most gastric polyps are asymptomatic and are discovered incidentally. Hyperplastic polyps are the most prevalent polyps in regions where H. pylori infection is common. In contrast, in western countries, where H. pylori infection has a lower prevalence and proton pump inhibitor (PPI) use is common, fundic gland polyps are more prevalent. (See 'Epidemiology' above.)

In patients with small solitary polyps, we recommend that polyps be biopsied and resected, if possible, for histologic characterization (Grade 1A). Polypectomy should be performed for all known neoplastic polyps and for all polyps ≥1 cm in diameter, as biopsies alone cannot exclude foci of high-grade dysplasia or early gastric cancer. In patients with multiple polyps, the largest polyp should be excised and representative biopsies obtained from the remaining polyps.

The normal appearing antral and corpus mucosa should be sampled to rule out dysplasia occurring in the background of metaplastic atrophic gastritis and infection with H. pylori. We suggest H. pylori eradication therapy in those who test positive. (Grade 2C). (See 'Initial evaluation' above.)

Fundic gland polyps may occur sporadically, in association with polyposis syndromes, or in response to chronic PPI therapy. They have very low to no malignant potential when associated with PPI use or occurring sporadically. Fundic gland polyps associated with polyposis syndromes have been associated with dysplasia but progression to malignancy is rare. Fundic gland polyps ≥1 cm in diameter, polyps with ulceration, or located in the antrum should be resected. In patients with multiple (≥20) or large (≥1 cm) sporadic fundic gland polyps, withdrawal of the PPI should be considered. (See 'Fundic gland polyps' above.)

Hyperplastic polyps occur in association with H. pylori-related atrophic gastritis, pernicious anemia, and adjacent to ulcers and erosions. They are generally benign, but have some malignant potential. Hyperplastic polyps >0.5 cm should be resected completely. Surveillance with upper endoscopy should be performed based on the cancer risk due to concurrent chronic atrophic gastritis and other risk factors for gastric cancer. (See 'Hyperplastic polyps' above.)

Gastric adenomas typically form in atrophic gastric mucosa and may also be seen in association with familial polyposis syndromes. Most gastric adenomas are asymptomatic. Polyps that cause symptoms are most likely to present with gastrointestinal bleeding or rarely obstruction. As gastric adenomas are a precursor lesion of gastric adenocarcinoma, we recommend resection of all gastric adenomas endoscopically or surgically if necessary (Grade 1A). We perform an upper endoscopy for surveillance one year after initial resection of adenomatous gastric polyps. In individuals at high risk for gastric cancer, surveillance is continued indefinitely. (See 'Gastric adenomas' above.)

Gastric neuroendocrine tumors may be associated with hypergastrinemia (type 1 and 2) or may occur sporadically (type 3). In contrast with patients with type 3 gastric neuroendocrine tumors who may have metastases at the time of resection, patients with type 1 and 2 gastric neuroendocrine tumors usually have an indolent course. For type 1 and 2 gastric neuroendocrine tumors smaller than 1 to 2 cm, endoscopic resection is the treatment of choice. Type 3 tumors are treated by partial or total gastrectomy with local lymph node resection. (See 'Gastric neuroendocrine tumors (carcinoids)' above and "Treatment and surveillance of non-metastatic carcinoid tumors".)

Inflammatory fibroid polyps are extremely rare lesions that represent less than 0.1 percent of all gastric polyps. Following resection, inflammatory fibroid polyps typically do not recur, and surveillance is not recommended. (See 'Inflammatory fibroid polyps' above.)

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REFERENCES

  1. Hirota WK, Zuckerman MJ, Adler DG, et al. ASGE guideline: the role of endoscopy in the surveillance of premalignant conditions of the upper GI tract. Gastrointest Endosc 2006; 63:570.
  2. ASGE Standards of Practice Committee, Sharaf RN, Shergill AK, et al. Endoscopic mucosal tissue sampling. Gastrointest Endosc 2013; 78:216.
  3. Carmack SW, Genta RM, Schuler CM, Saboorian MH. The current spectrum of gastric polyps: a 1-year national study of over 120,000 patients. Am J Gastroenterol 2009; 104:1524.
  4. Archimandritis A, Spiliadis C, Tzivras M, et al. Gastric epithelial polyps: a retrospective endoscopic study of 12974 symptomatic patients. Ital J Gastroenterol 1996; 28:387.
  5. Morais DJ, Yamanaka A, Zeitune JM, Andreollo NA. Gastric polyps: a retrospective analysis of 26,000 digestive endoscopies. Arq Gastroenterol 2007; 44:14.
  6. Jalving M, Koornstra JJ, Wesseling J, et al. Increased risk of fundic gland polyps during long-term proton pump inhibitor therapy. Aliment Pharmacol Ther 2006; 24:1341.
  7. Ginsberg GG, Al-Kawas FH, Fleischer DE, et al. Gastric polyps: relationship of size and histology to cancer risk. Am J Gastroenterol 1996; 91:714.
  8. Papa A, Cammarota G, Tursi A, et al. Management of gastric polyps: the need of polypectomy also for small polyps. Am J Gastroenterol 1997; 92:721.
  9. Muehldorfer SM, Stolte M, Martus P, et al. Diagnostic accuracy of forceps biopsy versus polypectomy for gastric polyps: a prospective multicentre study. Gut 2002; 50:465.
  10. Yoon WJ, Lee DH, Jung YJ, et al. Histologic characteristics of gastric polyps in Korea: emphasis on discrepancy between endoscopic forceps biopsy and endoscopic mucosal resection specimen. World J Gastroenterol 2006; 12:4029.
  11. Akahoshi K, Yoshinaga S, Fujimaru T, et al. Endoscopic resection with hypertonic saline-solution-epinephrine injection plus band ligation for large pedunculated or semipedunculated gastric polyp. Gastrointest Endosc 2006; 63:312.
  12. Carmack SW, Genta RM, Graham DY, Lauwers GY. Management of gastric polyps: a pathology-based guide for gastroenterologists. Nat Rev Gastroenterol Hepatol 2009; 6:331.
  13. Rugge M, Meggio A, Pennelli G, et al. Gastritis staging in clinical practice: the OLGA staging system. Gut 2007; 56:631.
  14. Rugge M, Correa P, Di Mario F, et al. OLGA staging for gastritis: a tutorial. Dig Liver Dis 2008; 40:650.
  15. Dirschmid K, Platz-Baudin C, Stolte M. Why is the hyperplastic polyp a marker for the precancerous condition of the gastric mucosa? Virchows Arch 2006; 448:80.
  16. Ljubicić N, Banić M, Kujundzić M, et al. The effect of eradicating Helicobacter pylori infection on the course of adenomatous and hyperplastic gastric polyps. Eur J Gastroenterol Hepatol 1999; 11:727.
  17. Ohkusa T, Takashimizu I, Fujiki K, et al. Disappearance of hyperplastic polyps in the stomach after eradication of Helicobacter pylori. A randomized, clinical trial. Ann Intern Med 1998; 129:712.
  18. Al-Haddad M, Ward EM, Bouras EP, Raimondo M. Hyperplastic polyps of the gastric antrum in patients with gastrointestinal blood loss. Dig Dis Sci 2007; 52:105.
  19. Kumar A, Quick CR, Carr-Locke DL. Prolapsing gastric polyp, an unusual cause of gastric outlet obstruction: a review of the pathology and management of gastric polyps. Endoscopy 1996; 28:452.
  20. Stolte M, Sticht T, Eidt S, et al. Frequency, location, and age and sex distribution of various types of gastric polyp. Endoscopy 1994; 26:659.
  21. Snover DC. Benign epithelial polyps of the stomach. Pathol Annu 1985; 20 Pt 1:303.
  22. Hattori T. Morphological range of hyperplastic polyps and carcinomas arising in hyperplastic polyps of the stomach. J Clin Pathol 1985; 38:622.
  23. Antonioli DA. Precursors of gastric carcinoma: a critical review with a brief description of early (curable) gastric cancer. Hum Pathol 1994; 25:994.
  24. Dijkhuizen SM, Entius MM, Clement MJ, et al. Multiple hyperplastic polyps in the stomach: evidence for clonality and neoplastic potential. Gastroenterology 1997; 112:561.
  25. Daibo M, Itabashi M, Hirota T. Malignant transformation of gastric hyperplastic polyps. Am J Gastroenterol 1987; 82:1016.
  26. Orlowska J, Jarosz D, Pachlewski J, Butruk E. Malignant transformation of benign epithelial gastric polyps. Am J Gastroenterol 1995; 90:2152.
  27. Gotoh Y, Fujimoto K, Sakata Y, et al. Poorly differentiated adenocarcinoma in a gastric hyperplastic polyp. South Med J 1996; 89:453.
  28. Zea-Iriarte WL, Sekine I, Itsuno M, et al. Carcinoma in gastric hyperplastic polyps. A phenotypic study. Dig Dis Sci 1996; 41:377.
  29. Lynch HT, Smyrk T, McGinn T, et al. Attenuated familial adenomatous polyposis (AFAP). A phenotypically and genotypically distinctive variant of FAP. Cancer 1995; 76:2427.
  30. Worthley DL, Phillips KD, Wayte N, et al. Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome. Gut 2012; 61:774.
  31. Vogt S, Jones N, Christian D, et al. Expanded extracolonic tumor spectrum in MUTYH-associated polyposis. Gastroenterology 2009; 137:1976.
  32. Domizio P, Talbot IC, Spigelman AD, et al. Upper gastrointestinal pathology in familial adenomatous polyposis: results from a prospective study of 102 patients. J Clin Pathol 1990; 43:738.
  33. Stolte M, Bethke B, Seifert E, et al. Observation of gastric glandular cysts in the corpus mucosa of the stomach under omeprazole treatment. Z Gastroenterol 1995; 33:146.
  34. Kazantsev GB, Schwesinger WH, Heim-Hall J. Spontaneous resolution of multiple fundic gland polyps after cessation of treatment with lansoprazole and Nissen fundoplication: a case report. Gastrointest Endosc 2002; 55:600.
  35. el-Zimaity HM, Jackson FW, Graham DY. Fundic gland polyps developing during omeprazole therapy. Am J Gastroenterol 1997; 92:1858.
  36. Modlin IM, Gilligan CJ, Lawton GP, et al. Gastric carcinoids. The Yale Experience. Arch Surg 1995; 130:250.
  37. Choudhry U, Boyce HW Jr, Coppola D. Proton pump inhibitor-associated gastric polyps: a retrospective analysis of their frequency, and endoscopic, histologic, and ultrastructural characteristics. Am J Clin Pathol 1998; 110:615.
  38. Kim JS, Chae HS, Kim HK, et al. [Spontaneous resolution of multiple fundic gland polyps after cessation of treatment with omeprazole]. Korean J Gastroenterol 2008; 51:305.
  39. Watanabe N, Seno H, Nakajima T, et al. Regression of fundic gland polyps following acquisition of Helicobacter pylori. Gut 2002; 51:742.
  40. Abraham SC, Nobukawa B, Giardiello FM, et al. Fundic gland polyps in familial adenomatous polyposis: neoplasms with frequent somatic adenomatous polyposis coli gene alterations. Am J Pathol 2000; 157:747.
  41. Genta RM, Schuler CM, Robiou CI, Lash RH. No association between gastric fundic gland polyps and gastrointestinal neoplasia in a study of over 100,000 patients. Clin Gastroenterol Hepatol 2009; 7:849.
  42. Bertoni G, Sassatelli R, Nigrisoli E, et al. Dysplastic changes in gastric fundic gland polyps of patients with familial adenomatous polyposis. Ital J Gastroenterol Hepatol 1999; 31:192.
  43. Declich P, Ambrosiani L, Bellone S, et al. Fundic gland polyps: a not so innocuous entity worth a careful evaluation. Am J Gastroenterol 1998; 93:2641.
  44. Wu TT, Kornacki S, Rashid A, et al. Dysplasia and dysregulation of proliferation in foveolar and surface epithelia of fundic gland polyps from patients with familial adenomatous polyposis. Am J Surg Pathol 1998; 22:293.
  45. Bianchi LK, Burke CA, Bennett AE, et al. Fundic gland polyp dysplasia is common in familial adenomatous polyposis. Clin Gastroenterol Hepatol 2008; 6:180.
  46. Offerhaus GJ, Giardiello FM, Krush AJ, et al. The risk of upper gastrointestinal cancer in familial adenomatous polyposis. Gastroenterology 1992; 102:1980.
  47. Marcello PW, Asbun HJ, Veidenheimer MC, et al. Gastroduodenal polyps in familial adenomatous polyposis. Surg Endosc 1996; 10:418.
  48. Sawada T, Muto T. Role of upper gastrointestinal surveillance in patients with familial adenomatous polyposis. Gastrointest Endosc Clin N Am 1997; 7:99.
  49. Rugge M, Correa P, Dixon MF, et al. Gastric dysplasia: the Padova international classification. Am J Surg Pathol 2000; 24:167.
  50. Hamilton SR, Aaltonen LA. Pathology and Genetics of Tumours of the Digestive System, IARC Press, Lyon 2000.
  51. Rugge M, Nitti D, Farinati F, et al. Non-invasive neoplasia of the stomach. Eur J Gastroenterol Hepatol 2005; 17:1191.
  52. Tomasulo J. Gastric polyps. Histologic types and their relationship to gastric carcinoma. Cancer 1971; 27:1346.
  53. Kolodziejczyk P, Yao T, Oya M, et al. Long-term follow-up study of patients with gastric adenomas with malignant transformation. An immunohistochemical and histochemical analysis. Cancer 1994; 74:2896.
  54. Nakamura K, Sakaguchi H, Enjoji M. Depressed adenoma of the stomach. Cancer 1988; 62:2197.
  55. Oehlert W, Keller P, Henke M, Strauch M. Gastric mucosal dysplasia: what is its clinical significance? Front Gastrointest Res 1979; 4:173.
  56. de Vries AC, van Grieken NC, Looman CW, et al. Gastric cancer risk in patients with premalignant gastric lesions: a nationwide cohort study in the Netherlands. Gastroenterology 2008; 134:945.
  57. Lansdown M, Quirke P, Dixon MF, et al. High grade dysplasia of the gastric mucosa: a marker for gastric carcinoma. Gut 1990; 31:977.
  58. Rindi G, Luinetti O, Cornaggia M, et al. Three subtypes of gastric argyrophil carcinoid and the gastric neuroendocrine carcinoma: a clinicopathologic study. Gastroenterology 1993; 104:994.
  59. Bordi C. Endocrine tumours of the stomach. Pathol Res Pract 1995; 191:373.
  60. Debelenko LV, Emmert-Buck MR, Zhuang Z, et al. The multiple endocrine neoplasia type I gene locus is involved in the pathogenesis of type II gastric carcinoids. Gastroenterology 1997; 113:773.
  61. Gilligan CJ, Lawton GP, Tang LH, et al. Gastric carcinoid tumors: the biology and therapy of an enigmatic and controversial lesion. Am J Gastroenterol 1995; 90:338.
  62. Thomas RM, Baybick JH, Elsayed AM, Sobin LH. Gastric carcinoids. An immunohistochemical and clinicopathologic study of 104 patients. Cancer 1994; 73:2053.
  63. Elsborg L, Jørgensen F. Sucralfate versus cimetidine in reflux oesophagitis. A double-blind clinical study. Scand J Gastroenterol 1991; 26:146.
  64. Solcia E, Bordi C, Creutzfeldt W, et al. Histopathological classification of nonantral gastric endocrine growths in man. Digestion 1988; 41:185.
  65. Solcia E, Fiocca R, Villani L, et al. Hyperplastic, dysplastic, and neoplastic enterochromaffin-like-cell proliferations of the gastric mucosa. Classification and histogenesis. Am J Surg Pathol 1995; 19 Suppl 1:S1.
  66. WHO Classification of Tumours of the Digestive System, Bosman F, Carneiro F, Hruban R, et al (Eds), IARC Press, Lyon, France 2010.
  67. Borch K, Ahrén B, Ahlman H, et al. Gastric carcinoids: biologic behavior and prognosis after differentiated treatment in relation to type. Ann Surg 2005; 242:64.
  68. Pantanowitz L, Antonioli DA, Pinkus GS, et al. Inflammatory fibroid polyps of the gastrointestinal tract: evidence for a dendritic cell origin. Am J Surg Pathol 2004; 28:107.
  69. Allibone RO, Nanson JK, Anthony PP. Multiple and recurrent inflammatory fibroid polyps in a Devon family ('Devon polyposis syndrome'): an update. Gut 1992; 33:1004.
  70. Schildhaus HU, Cavlar T, Binot E, et al. Inflammatory fibroid polyps harbour mutations in the platelet-derived growth factor receptor alpha (PDGFRA) gene. J Pathol 2008; 216:176.
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