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Gastric polyps are growths that project from the mucosal or submucosal tissue of the stomach, often discovered incidentally during upper endoscopy. While most gastric polyps are benign, some, particularly adenomatous polyps, carry a risk of dysplasia and progression to invasive gastric cancer. The types of polyps include hyperplastic, fundic gland, and adenomatous, each with varying degrees of malignant potential. The prevalence of gastric polyps is around 2%, with higher detection rates in patients undergoing endoscopy for gastrointestinal symptoms. Proper identification, biopsy, and histologic evaluation of polyps are crucial to assess their risk and guide management strategies. Participants in this course gain a comprehensive understanding of the evaluation and management of gastric polyps, focusing on the importance of biopsy and histological examination. Clinicians learn to differentiate between various types of polyps and assess their potential for malignancy. The course emphasizes adherence to gastroenterological guidelines, ensuring appropriate follow-up and treatment. Collaborating with an interprofessional team, including gastroenterologists, pathologists, and surgeons, enhances patient outcomes by integrating expertise from different specialties. This teamwork ensures that polyps are accurately diagnosed, treated effectively, and monitored for recurrence or progression, reducing the risk of gastric cancer. Objectives: Identify the different types of gastric polyps and their respective histologic features. Differentiate between benign and potentially malignant gastric polyps based on endoscopic and histologic findings. Apply guidelines from gastroenterological societies in the management and surveillance of patients with gastric polyps. Coordinate care with an interprofessional team to optimize the management and follow-up of patients with gastric polyps, including gastroenterologists, surgeons, and primary care providers. Access free multiple choice questions on this topic.

Gastric polyps are projections of mucosal or submucosal tissue into the stomach lumen, representing many tissue types with a spectrum of malignant potential. The prevalence of gastric polyps in the general population is estimated to be 2%, but reports vary. Most gastric polyps are found incidentally during esophagogastroduodenoscopy (EGD), and it is reported that polypoid lesions are reported during approximately 6% of EGD procedures. Most upper endoscopies are performed for gastroesophageal reflux, dyspepsia, anemia, and abdominal pain. Common types of gastric polyps are fundic gland polyps, featuring dilated and irregularly budded fundic glands, hyperplastic polyps, characterized by pronounced foveolar hyperplasia, and adenomatous polyps that demonstrate low-grade glandular dysplasia.[1] Additional gastric lesions encountered on EGD include neuroendocrine tumors, hamartomatous lesions such as those found in Peutz-Jegher, Cowden, and juvenile polyposis syndromes, ectopic pancreatic tissue, lymphoid proliferation, and mesenchymal growths such as gastrointestinal stromal tumors, leiomyoma and fibroid polyps. Diagnosing a polyp based on visualization is often difficult, and biopsy with histologic evaluation is usually necessary.[2][3][4][5][6] Most polyps are asymptomatic, but larger polyps may cause abdominal pain, bleeding, or obstruction.[7] Hyperplastic polyps, which often proliferate in response to atrophic gastritis, may give rise to iron deficiency anemia and are correlated with pernicious anemia. There is an association between dyspepsia and fundic gland polyps, and possibly a connection between fundic gland polyps and prolonged use of a proton pump inhibitor.[8]

Gastric polyps represent a spectrum of etiologies and are classified histologically by the tissue layer from which they originate. Examples include hyperplastic, fundic gland, adenomas, and less common lesions such as neuroendocrine tumors, gastrointestinal stromal tumors, leiomyomas, ectopic pancreatic tissue, polyps associated with familial adenomatous polyposis (FAP), juvenile polyposis, Peutz-Jegher, Cowden syndromes. Fundic gland polyps are epithelial polyps that are sporadic or associated with the use of proton pump inhibitors (PPI) or hereditary syndromes such as FAP. Sporadic fundic gland polyps are found most frequently within the body and fundus and are generally sessile, smooth, and hyperemic, measuring 1 mm to 8 mm. A prospective cohort demonstrated the risk for fundic gland polyps increased with years of PPI use, showing a relative risk increase of 17 over 10 years.[9] A retrospective analysis of 186 persons with gastric polyps found that greater than 5 years of  PPI use increased the incidence of fundic gland polyps.[10] A case of a 37-year-old woman taking daily PPI and presenting with hematemesis secondary to multiple fundic gland polyps is described. Once the PPI was discontinued, she experienced a significant regression of the polyps.[11] Fundic gland polyps associated with FAP are numerous, and up to 40% may be dysplastic.[12] Even nondysplastic fundic gland polyps in persons with FAP have the APC gene mutation. Sporadic fundic gland polyps with dysplasia have also been found to have mutations in the APC gene but rarely progress to high-grade dysplasia or adenocarcinoma. In a study comparing 147 persons with FAP-related polyps versus sporadic fundic gland polyps followed for 54 months, the results concluded, based on deoxyribonucleic acid analysis, that fundic gland polyps do not exhibit the chromosomal changes inherent to the adenoma-carcinoma progression seen with many gastrointestinal malignancies.[13][14]

Fundic gland polyps associated with FAP are numerous, and up to 40% may be dysplastic.[12] Even nondysplastic fundic gland polyps in persons with FAP have the APC gene mutation. Sporadic fundic gland polyps with dysplasia have also been found to have mutations in the APC gene but rarely progress to high-grade dysplasia or adenocarcinoma. In a study comparing 147 persons with FAP-related polyps versus sporadic fundic gland polyps followed for 54 months, the results concluded, based on deoxyribonucleic acid analysis, that fundic gland polyps do not exhibit the chromosomal changes inherent to the adenoma-carcinoma progression seen with many gastrointestinal malignancies.[13][14] Hyperplastic polyps, the second most common type of gastric polyp, can be sessile or pedunculated, are generally less than 2 cm, are most frequently found in the antrum, and are usually incidental findings. The extent of malignant transformation is not well characterized. Distal ulcerations on a polyp may become a site of malignancy. In a retrospective cohort of 195 patients who underwent endoscopic resection of a hyperplastic polyp, low-grade dysplasia was found in 5, high-grade dysplasia in 4, and adenocarcinoma in 1. Multivariate analysis demonstrated that a size greater than 25 mm, intestinal metaplasia, and dysplasia in adjacent mucosa were associated with an increased risk of malignant transformation.[15][16] Gastric adenomatous polyps are precursors to adenocarcinoma, and are most common in the antrum, but can be found anywhere in the stomach. Antral adenomas are usually sessile, but those in the body and fundus are more pedunculated.[17] Large villous polyps are most often associated with malignancy. Risks for developing gastric adenoma include age and chronic inflammation, which can cause intestinal metaplasia and increase the potential for malignant transformation. The finding of gastric adenomas in a young person can be indicative of an underlying genetic condition such as FAP and merits further investigation.[3][18][19]

Gastric adenomatous polyps are precursors to adenocarcinoma, and are most common in the antrum, but can be found anywhere in the stomach. Antral adenomas are usually sessile, but those in the body and fundus are more pedunculated.[17] Large villous polyps are most often associated with malignancy. Risks for developing gastric adenoma include age and chronic inflammation, which can cause intestinal metaplasia and increase the potential for malignant transformation. The finding of gastric adenomas in a young person can be indicative of an underlying genetic condition such as FAP and merits further investigation.[3][18][19] Neuroendocrine polyps, usually located in the corpus and fundus, represent hyperplasia of enterochromaffin-like cells in response to hypergastrinemia. There are 4 types of neuroendocrine polyps. Types I and II feature many polyps arranged in clusters within the body and fundus. Type I is most common and is secondary to an autoimmune process, whereas type II, often occurring in the setting of multiple endocrine neoplasia I and Zollinger-Ellison, is rare. Type III, the second most common, is sporadic and solitary, found throughout the stomach, and is often associated with metastases when greater than 2 cm. Type IV is rare, may be located anywhere in the stomach, is poorly differentiated, often ulcerated, and is prognostically unfavorable.[6][20][21] The rarer lesions encountered in the stomach are difficult to differentiate endoscopically from the more common polyps. Mesenchymal polyps can be mucosal or submucosal but are usually within deeper layers. Cowden syndrome, associated with breast, thyroid, and endometrial cancers, produces polyps that are usually benign, but there are rare reports of malignant transformation.[22] Gastrointestinal stromal tumors (GIST), originating in the muscularis propria, are rare but often malignant. Inflammatory polyps, described as polyploid, small, and well-circumscribed, make up less than 0.1% of all gastric polyps. They are usually found in the antrum or prepyloric region and, if symptomatic, are associated with epigastric pain and early satiety.[23][24] Ectopic pancreatic tissue, appearing as a submucosal mass, is often asymptomatic but may also cause nonspecific symptoms and present with central umbilication.[25]

The rarer lesions encountered in the stomach are difficult to differentiate endoscopically from the more common polyps. Mesenchymal polyps can be mucosal or submucosal but are usually within deeper layers. Cowden syndrome, associated with breast, thyroid, and endometrial cancers, produces polyps that are usually benign, but there are rare reports of malignant transformation.[22] Gastrointestinal stromal tumors (GIST), originating in the muscularis propria, are rare but often malignant. Inflammatory polyps, described as polyploid, small, and well-circumscribed, make up less than 0.1% of all gastric polyps. They are usually found in the antrum or prepyloric region and, if symptomatic, are associated with epigastric pain and early satiety.[23][24] Ectopic pancreatic tissue, appearing as a submucosal mass, is often asymptomatic but may also cause nonspecific symptoms and present with central umbilication.[25] Leiomyoma, a smooth muscle tumor miscategorized as GIST in the past, varies in size from 0.5 cm to 20 cm and can grow within tissue layers or as an exophytic mass, but tends to extend intraluminally, as compared with GIST, which often grows extraluminally. Leiomyomas are asymptomatic, found incidentally, and appear endoscopically as submucosal lesions.[26] Gastric granular cell tumors, a rare yellow subepithelial mass or nodule, arise from the submucosa, are found incidentally in the proximal stomach, are usually benign but have malignant potential, and are more prevalent in the esophagus. They are also concurrently found in the esophagus if encountered in the stomach. Gastric granular cell tumors can range from several mm to 7 cm and may appear similar to lipomas.[27]

Leiomyoma, a smooth muscle tumor miscategorized as GIST in the past, varies in size from 0.5 cm to 20 cm and can grow within tissue layers or as an exophytic mass, but tends to extend intraluminally, as compared with GIST, which often grows extraluminally. Leiomyomas are asymptomatic, found incidentally, and appear endoscopically as submucosal lesions.[26] Gastric granular cell tumors, a rare yellow subepithelial mass or nodule, arise from the submucosa, are found incidentally in the proximal stomach, are usually benign but have malignant potential, and are more prevalent in the esophagus. They are also concurrently found in the esophagus if encountered in the stomach. Gastric granular cell tumors can range from several mm to 7 cm and may appear similar to lipomas.[27] Gastric polyps may represent a mix of tissue types, and the polyp and surrounding mucosa must be closely examined and subject to histologic analysis. A Chinese study of 125 patients with mostly sessile, single adenomas, primarily in the corpus and antrum, provided results demonstrating that 23% of the polyps had a hyperplastic and/or fundic gland tissue component. In addition, synchronous adenocarcinoma was found in 13% of sampled polyps, low-grade intraepithelial neoplasm in 18%, and chronic atrophic gastritis with intestinal metaplasia in over 50%. Autoimmune gastritis accounted for 11% of those with gastritis. In addition, Helicobacter pylori was found in 21% of the polyps. Of the polyps studied, independent risk factors for malignancy were size greater than 1 cm, uneven surface, and erosion.[28]

Gastric polyps are found during 6% of EGDs. Sporadic fundic gland polyps represent 37% to 77% of all gastric polyps and are most common in middle-aged women.[29][30][31] Hyperplastic polyps are the second most common, reported between 17% and 42% of cases, and gastric adenomas 0.5 % to 1%. Malignancy is found in 1% to 2% of polyploid gastric lesions.[30][32] Diet and lifestyle practices are thought to contribute to the wide variations reported between studies.[33][34] The prevalence of H pylori has decreased with a concomitant decline in peptic ulcer disease and hyperplastic polyps. Gastroesophageal reflux is the most common pathology noted at endoscopy, with an associated increase in esophageal cancer, cancer of the cardia, and an increase in eosinophilic esophagitis. Gastric adenoma, historically seen more frequently in countries with a high gastric cancer rate, such as China, may be found in up to 10% of gastric polyps in Asian countries and is increasing in Western countries.[31] The epidemiology of gastric polyps in individuals with FAP is distinct from the general population. A retrospective review of the distribution of gastric polyps in patients with FAP found 68% fundic gland polyps, 20% hyperplastic polyps, and 15% adenomas, 10% of which contained high-grade dysplasia. High-grade dysplasia was identified in every polyp type, and 2 people with high-grade dysplasia progressed to gastric cancer, but 8 individuals under surveillance for over 5 years did not progress.[35] Fundic gland polyps were found in 88% of those with FAP in a screened population. In one study of this group, results showed that dysplasia was found in 42% of fundic gland polyps. In a pediatric FAP cohort, fundic gland polyps with low-grade dysplasia were identified in 42% of screening endoscopies. Gastric adenomas are found in 10% of those with FAP in the United States and Western Europe and 36% to 50% in Asia. There are case reports of individuals with FAP developing gastric cancer as young as 16 years old, and there has been an overall increase in gastric adenocarcinoma in this population with a reporter incidence of 1.3%.[17]

The epidemiology of gastric polyps in individuals with FAP is distinct from the general population. A retrospective review of the distribution of gastric polyps in patients with FAP found 68% fundic gland polyps, 20% hyperplastic polyps, and 15% adenomas, 10% of which contained high-grade dysplasia. High-grade dysplasia was identified in every polyp type, and 2 people with high-grade dysplasia progressed to gastric cancer, but 8 individuals under surveillance for over 5 years did not progress.[35] Fundic gland polyps were found in 88% of those with FAP in a screened population. In one study of this group, results showed that dysplasia was found in 42% of fundic gland polyps. In a pediatric FAP cohort, fundic gland polyps with low-grade dysplasia were identified in 42% of screening endoscopies. Gastric adenomas are found in 10% of those with FAP in the United States and Western Europe and 36% to 50% in Asia. There are case reports of individuals with FAP developing gastric cancer as young as 16 years old, and there has been an overall increase in gastric adenocarcinoma in this population with a reporter incidence of 1.3%.[17] Mesenchymal polyps are rare, with a reported incidence of less than 0.1%. The most common type of neuroendocrine polyp, type I, occurs most frequently in middle-aged women, whereas type IV is found mostly in older men. Cowden polyps carry a slight predilection to women between 16 and 65. Inflammatory fibroid polyps are found in all ages but most frequently in those aged between 50 and 60. However, they are slightly more prevalent in women, with an overall documented prevalence of 0.09%.[30][36] Granular cell tumors are equally dispersed between men and women, usually between the fourth and sixth decades. GIST are usually found incidentally and represent 1% to 3% of all malignant gastrointestinal tumors. There are 5000 new cases of gastrointestinal stromal tumors reported in the United States per year.[31]

Gastric polypoid lesions reflect a range of pathophysiology. The development of hyperplastic polyps is thought to be due to chronic inflammation associated with H pylori infection and atrophic gastritis. H pylori increases serum gastrin levels, which can lead to atrophic gastritis. Enterochromaffin-like cell proliferation and hypergastrinemia promote the formation of hyperplastic polyps as cells release growth-inducing hormones and peptides. Autoimmune gastritis gives rise to oxyntic gland atrophy which results in secondary hypergastrinemia. Hyperplastic polyps regress within a year after eradicating H pylori infection, assuming no reinfection occurs. H pylori may also give rise to gastric intestinal metaplasia, which confers up to a 10-fold increase in gastric cancer risk compared with the general population. Smoking and high salt intake may be contributing factors to metaplasia.[15][37][38] Hyperplastic polyps are associated with concurrent malignancy elsewhere within the gastric mucosa, possibly arising in response to inflammation and hyperactive mucosal healing response. Inflammation gives rise to metaplasia and polyp development. Etiologies associated with hyperplastic polyps include portal hypertension and pernicious anemia. Those with chronic liver disease develop hyperplastic polyps more frequently and in greater numbers than those with gastroesophageal reflux, and smokers are also at greater risk for the development of hyperplastic polyps.[3][39] Hyperplastic polyps recede following antacid therapy and treatment for H pylori.[15][40] Malignant transformation of hyperplastic polyps ranges between 0.6% to 8%. The exact mechanism of metaplasia and dysplasia is uncertain, although excess gastrin may be a contributor. Genetic mutations have been proposed to explain malignant transformation, and P53, KRAS, APC, and Ki-67 mutations have been correlated with pathologic findings. A hyperplasia-dysplasia-carcinoma sequence may occur but is not shown with metaplasia. Factors associated with higher risk of malignancy include increased age, number and size of polyps, lobulation, pedunculation, and H pylori. Recurrence of hyperplastic polyps is not thought to be a risk factor for malignant transformation.[3][41]

Malignant transformation of hyperplastic polyps ranges between 0.6% to 8%. The exact mechanism of metaplasia and dysplasia is uncertain, although excess gastrin may be a contributor. Genetic mutations have been proposed to explain malignant transformation, and P53, KRAS, APC, and Ki-67 mutations have been correlated with pathologic findings. A hyperplasia-dysplasia-carcinoma sequence may occur but is not shown with metaplasia. Factors associated with higher risk of malignancy include increased age, number and size of polyps, lobulation, pedunculation, and H pylori. Recurrence of hyperplastic polyps is not thought to be a risk factor for malignant transformation.[3][41] Fundic gland polyps arise in the setting of proton pump inhibitor use and those with FAP. Most sporadic fundic gland polyps have activating mutations in the β-catenin gene, are involved with cell growth signaling, and have a reported less than 1% risk of malignancy. FAP-associated polyps feature the inactivation of the APC  tumor suppressor gene and often contain low-grade dysplasia. Both mutations result in abnormal accumulation of the β-catenin protein in affected cells.[42] Dysplastic fundic gland polyps in persons with FAP are often greater than 1 cm. Even when dysplastic, the polyps rarely progress to adenocarcinoma, and those that do are generally greater than 3 cm in the setting of multiple polyps.[17] Persons with FAP also develop adenomas, found largely in the antrum.[13] Polypoid masses in persons with FAP can be a mixture of adenomas, dysplastic fundic gland polyps, and adenocarcinomas.[43] Gastric adenocarcinoma and proximal polyposis of the stomach, an autosomal dominant condition involving a mutation of the APC promoter 1B, features proximal stomach polyps and an absence of polyps in the duodenum or colon.[38]

Persons with FAP also develop adenomas, found largely in the antrum.[13] Polypoid masses in persons with FAP can be a mixture of adenomas, dysplastic fundic gland polyps, and adenocarcinomas.[43] Gastric adenocarcinoma and proximal polyposis of the stomach, an autosomal dominant condition involving a mutation of the APC promoter 1B, features proximal stomach polyps and an absence of polyps in the duodenum or colon.[38] Atrophic gastritis and intestinal metaplasia are also associated with gastric adenomas and neuroendocrine tumors. Chronic gastritis, particularly autoimmune gastritis, affects parietal cells, causing reduced gastric acid secretion and vitamin B12 deficiency. The resulting hypergastrinemia promotes gastric mucosa proliferation and stimulates neuroendocrine cell growth, giving rise to tumors.[44] Atrophy within the stomach body is a hallmark of autoimmune gastritis, and tumors arising in the setting of gastric body atrophy require evaluation for neuroendocrine etiology.[45] Type I gastric neuroendocrine tumors form from enterochromaffin-like cell hyperplasia in the setting of atrophic or autoimmune gastritis. The autoimmune destruction of parietal cells reduces gastric acid production, leading to increased gastrin secretion by antral G cells. The tumors appear as multiple small nodules and can progress to malignancy. Type II polyps arise in the setting of multiple endocrine neoplasia type I, Zollinger-Ellison syndrome, or another gastrin-secreting tumor. Type IV is thought to be caused by a deficiency of acid secretion by parietal cells and is often advanced at the time of diagnosis.[46]

Atrophic gastritis and intestinal metaplasia are also associated with gastric adenomas and neuroendocrine tumors. Chronic gastritis, particularly autoimmune gastritis, affects parietal cells, causing reduced gastric acid secretion and vitamin B12 deficiency. The resulting hypergastrinemia promotes gastric mucosa proliferation and stimulates neuroendocrine cell growth, giving rise to tumors.[44] Atrophy within the stomach body is a hallmark of autoimmune gastritis, and tumors arising in the setting of gastric body atrophy require evaluation for neuroendocrine etiology.[45] Type I gastric neuroendocrine tumors form from enterochromaffin-like cell hyperplasia in the setting of atrophic or autoimmune gastritis. The autoimmune destruction of parietal cells reduces gastric acid production, leading to increased gastrin secretion by antral G cells. The tumors appear as multiple small nodules and can progress to malignancy. Type II polyps arise in the setting of multiple endocrine neoplasia type I, Zollinger-Ellison syndrome, or another gastrin-secreting tumor. Type IV is thought to be caused by a deficiency of acid secretion by parietal cells and is often advanced at the time of diagnosis.[46] Many genetic conditions can manifest in gastric polypoid masses. Peutz-Jegher, an autosomal dominant condition caused by a mutation of STK11, a tumor suppressor gene, involves mucosal epithelial hyperplasia and proliferation of the muscularis mucosa smooth muscle, and affected persons carry an increased risk of cancer in the gastrointestinal tract, pancreas, breast, ovaries, testes, and lungs.[47] Cowden Syndrome, caused by a mutation in the PTEN tumor suppressor gene that results in cellular proliferation and angiogenesis, produces hamartomas in the skin, mucous membranes, and gastrointestinal tract, as well as malignancies of the breast, thyroid, and endometrium, and may give rise to autism and developmental disorders.[48] Cronkhite-Canada, characterized by malabsorption and protein-losing enteropathy, is a non-hereditary condition marked by multiple polyps in the gastrointestinal tract, especially within the stomach and colon, and cutaneous manifestations.[49] Juvenile polyposis also features protein-losing enteropathy and hamartomatous polyps throughout the gastrointestinal tract that may cause obstruction, abdominal pain, and bleeding.[50] The gastric polyps associated with these syndromes are difficult to distinguish from hyperplastic polyps, and biopsies are needed from the small bowel and colon to make a definitive diagnosis. Patients with these syndromes require careful cancer surveillance.[51][52]

Many genetic conditions can manifest in gastric polypoid masses. Peutz-Jegher, an autosomal dominant condition caused by a mutation of STK11, a tumor suppressor gene, involves mucosal epithelial hyperplasia and proliferation of the muscularis mucosa smooth muscle, and affected persons carry an increased risk of cancer in the gastrointestinal tract, pancreas, breast, ovaries, testes, and lungs.[47] Cowden Syndrome, caused by a mutation in the PTEN tumor suppressor gene that results in cellular proliferation and angiogenesis, produces hamartomas in the skin, mucous membranes, and gastrointestinal tract, as well as malignancies of the breast, thyroid, and endometrium, and may give rise to autism and developmental disorders.[48] Cronkhite-Canada, characterized by malabsorption and protein-losing enteropathy, is a non-hereditary condition marked by multiple polyps in the gastrointestinal tract, especially within the stomach and colon, and cutaneous manifestations.[49] Juvenile polyposis also features protein-losing enteropathy and hamartomatous polyps throughout the gastrointestinal tract that may cause obstruction, abdominal pain, and bleeding.[50] The gastric polyps associated with these syndromes are difficult to distinguish from hyperplastic polyps, and biopsies are needed from the small bowel and colon to make a definitive diagnosis. Patients with these syndromes require careful cancer surveillance.[51][52] Inflammatory fibroid polyps are submucosal, benign lesions that may arise in any part of the gastrointestinal tract but are most common in the stomach. They are marked by vascular fibrous tissue that is infiltrated by inflammatory cells.[53] Inflammatory fibroid polyps have an activating mutation in the platelet-derived growth factor receptor alpha gene.[24][54] GIST derives from the interstitial cells of Cajal, the pacemaker cells of the gastrointestinal tract, located between the inner circular and outer longitudinal layers of the muscularis propria. Most GIST have proto-oncogenes c-KIT or PDGFR mutations, while others may have a mutation of the succinate dehydrogenase gene.[55][56]

Histologic assessment is necessary for a diagnostic evaluation of any gastric tissue. Assessing gastric polyps and the surrounding tissue for dysplasia or malignancy on endoscopic assessment is difficult without histologic evaluation.[57][58] Hyperplastic polyps are characterized histologically by cellular proliferation within gastric pit lining, surface foveolar cell proliferation, elongation, branching, and dilation, conveying a corkscrew appearance. Hyperplastic polyps may contain pyloric glands, chief cells, and parietal cells and appear similar to hamartomas. The polyp surface may contain bleeding erosions, and the background stroma may be inflamed and edematous, containing small bundles of disorganized smooth muscle. Foveolar hyperplasia may be seen as a precursor to a hyperplastic polyp in which gastric pits elongate but do not dilate, and stroma may be normal or slightly inflamed.[41][59] Pyloric adenomas are differentiated from gastric hyperplastic polyps by ground glass cytoplasm without apical mucin and feature-packed, pyloric gland-like tubules with a single layer of cuboidal or low columnar epithelial cells, often in the body of the stomach within a background of autoimmune gastritis and intestinal metaplasia.[60] There can be difficulty in distinguishing gastric hamartomatous polyps arising from heritable or acquired syndromes from hyperplastic polyps. Peutz-Jegher polyps demonstrate proliferation of the muscularis mucosa covered by hypertrophic mucosa and have glandular epithelium with dilated cystic glands supported by smooth muscle that is continuous with the muscularis mucosa. Juvenile polyposis polyps have excess lamina propria, dilated cystic glands, distended mucus-filled glands, inflammatory cells, and edema.[61][62]

There can be difficulty in distinguishing gastric hamartomatous polyps arising from heritable or acquired syndromes from hyperplastic polyps. Peutz-Jegher polyps demonstrate proliferation of the muscularis mucosa covered by hypertrophic mucosa and have glandular epithelium with dilated cystic glands supported by smooth muscle that is continuous with the muscularis mucosa. Juvenile polyposis polyps have excess lamina propria, dilated cystic glands, distended mucus-filled glands, inflammatory cells, and edema.[61][62] Fundic gland polyps feature hyperplasia and distortion of oxyntic glands, hyperproliferative pits, and cystic dilation of glands. Polyps associated with PPI use have more significant cystic dilation due to the proliferation of foveolar cells, protrusion of parietal cells, and monocyte infiltration, and these polyps demonstrate a greater amount of ki-67 positivity and fewer β-catenin mutations.[63] The foveolar cells secrete mucinous product within the deeper layers of the fundic gland secondary to the PPI-induced hypergastrin, and the enlarged parietal cells obstruct the isthmus glands, contributing to the enlargement of fundic gland cysts and overall polyp size. While there is dysplasia in both sporadic and syndromic fundic gland polyps, the polyps don't exhibit the nuclear aberrancies common to lesions that cause cancer.[64] FAP-associated polyps exhibit microcysts lined by fundic epithelium with limited parietal cell hyperplasia and scarce foveolar hyperplasia.[12] Gastric adenomas feature the proliferation of dysplastic epithelium, often in a background of intestinal metaplasia and mucosal irritation or atrophy. They may be classified as intestinal-type, gastric-type, or indeterminate. The intestinal type contains goblet cells, and the gastric type is lined with gastric mucin cells.[65]

Gastric adenomas feature the proliferation of dysplastic epithelium, often in a background of intestinal metaplasia and mucosal irritation or atrophy. They may be classified as intestinal-type, gastric-type, or indeterminate. The intestinal type contains goblet cells, and the gastric type is lined with gastric mucin cells.[65] Gastric neuroendocrine tumors contain cells with round or ovoid nuclei and eosinophilic cytoplasm arranged in trabecular, insular, or sheet-type patterns. Distinguishing the 4 types of neuroendocrine tumors by histology is difficult, as analysis depends on local tissue sampling and stains for chromogranin A and synaptophysin, mitotic index grading, and evaluation of the ki-67 proliferation index.[66] Neuroendocrine tumor types I-III, derived from the histamine-producing enterochromaffin-like cells, are positive for vesicular monoamine transporter 2. Type I and II display a trabecular or nodular histological pattern and a Ki-67 index less than 2%, whereas type III features a more invasive solid trabecular pattern, demonstrates lymphovascular invasion, and often has local or distant metastases that stain for chromogranin A or synaptophysin by immunohistochemistry.[67] GIST is the most prevalent mesenchymal gastric polyp. Most GIST demonstrate spindle cell morphology, but 10% to 15% have epithelioid cell morphology. GIST stain positive for the c-kit protein on immunohistochemistry, the receptor tyrosine kinase protein encoded by protooncogene c-kit, but 5% of GIST are only weakly positive, and all of these have epitheliod morphology. Nearly all GIST are negative for desmin, a filament protein and a marker for smooth muscle cells, and for S100, a calcium-binding protein that serves as a Schwann cell marker. Leiomyoma, by contrast, represents about 10% of mesenchymal gastric polyps and is desmin positive and c-kit negative. Schwannomas, which comprise 5% of gastrointestinal mesenchymal tumors, are spindle cell growths that are positive for S100 and negative for c-kit and desmin.[68] Inflammatory fibroid polyps feature an arrangement of reticular fibers and spindle-shaped nuclei, with spindle and stellate stromal cells arranged around vessels in an onion skin format. These polyps contain collagen fibers with eosinophilic infiltration and scant additional inflammatory cells, and they stain positive for CD34 and negative for c-kit.[24][53]

Most gastric polyps are asymptomatic; over 90% are found incidentally on endoscopy. In a subset of cases, gastric polyps may be associated with gastrointestinal bleeding, anemia, abdominal pain, and, occasionally, obstruction. Patients found to have polyps may report acid reflux, dyspepsia, chest pain, early satiety, and fatigue. There are case reports of large inflammatory fibroid polyps causing obstruction, hemorrhage, and shock.[24] Patients with neuroendocrine polyps may exhibit nausea, vomiting, weight loss, and diarrhea.[69] Individuals found to have fundic gland polyps may have a history of chronic proton pump inhibitor use or a personal or family history of FAP. Hyperplastic polyps are vascular, may bleed from surface erosions, and are often associated with atrophic or immune gastritis, H pylori, and pernicious anemia. Those with hyperplastic polyps may also have reflux, may rarely present with gastric outlet obstruction, and occasionally chest pain. Hyperplastic polyps are on the differential diagnosis for anemia, especially when other entities are ruled out. There is also an association between atrophic gastritis and gastric adenomas.[6][69][70] Gastric polyps as part of genetic syndromes may be associated with physical findings such as the lip hyperpigmentation seen with Peutz-Jegher syndrome or facial trichilemmomas and acral keratoses along with malignancies of the breast, thyroid, and genitourinary tract found in those with Cowden syndrome.[6] Persons with juvenile polyposis may experience abdominal pain and obstruction, gastrointestinal bleeding, diarrhea, and, in the neonatal period, signs and symptoms related to anomalies of the central nervous and cardiovascular systems.[71]

Polyps may be encountered during esophagogastroduodenoscopies that are frequently performed for symptoms such as abdominal pain, gastroesophageal reflux, or dyspepsia as part of an evaluation for anemia or as screening or surveillance due to family or personal history of gastrointestinal malignancy. Seeing larger gastric polyps on noninvasive imaging such as computed tomography or magnetic resonance imaging is possible.[38] Please refer to the American Society for Gastrointestinal Endoscopy [ASGE] for guidelines on general endoscopy, as well as recommendations for the endoscopic management of upper gastrointestinal obstruction, dyspepsia, premalignant conditions of the stomach, and the role of endoscopy in surveillance of FAP. The British Society of Gastroenterology recommends image-enhanced endoscopy and biopsies in areas of atrophy and intestinal metaplasia for those at increased risk of gastric adenocarcinoma including persons with H pylori or chronic gastritis, and those with a personal or family history of gastric cancer. The Sydney System Biopsy Protocol, recommended for those with a high risk of gastric cancer, standardizes biopsies from the antrum, incisura, and lesser and greater curvatures to improve diagnostic accuracy and risk stratification during tissue sampling.[72][73][74] The American Gastroenterological Association clinical practice guidelines on the management of gastric intestinal metaplasia identify H Pylori as a primary risk factor for intestinal-type non-cardia gastric cancer, which follows a progression from atrophic gastritis to intestinal metaplasia to gastric adenocarcinoma. No population-wide screening exists in countries with low incidence of gastric cancer, such as the United States, but there are guidelines for screening and surveillance for specific populations depending on risk factors. H pylori is associated with up to 89% of non-cardia gastric cancers globally, and its eradication correlates with a 32% pooled relative risk reduction for related gastric cancer.[75]

The American Gastroenterological Association clinical practice guidelines on the management of gastric intestinal metaplasia identify H Pylori as a primary risk factor for intestinal-type non-cardia gastric cancer, which follows a progression from atrophic gastritis to intestinal metaplasia to gastric adenocarcinoma. No population-wide screening exists in countries with low incidence of gastric cancer, such as the United States, but there are guidelines for screening and surveillance for specific populations depending on risk factors. H pylori is associated with up to 89% of non-cardia gastric cancers globally, and its eradication correlates with a 32% pooled relative risk reduction for related gastric cancer.[75] While most specialists recommend resection of all larger polyps, some researchers have worked on differentiating polyps that require resection from those that might be observed. LaFeuille et al describe an endoscopic method to identify malignancy within a polyp using dual focus and acetic acid dye, the application of which yields a quicker acetowhitening disappearance in malignant components of polyps compared with hyperplastic portions. The authors cite a case of a hyperplastic polyp with intramucosal adenocarcinoma identified with this method and propose using this technique to avoid indiscriminate resection of all large hyperplastic polyps.[16] Diagnosing a polyp based solely on endoscopic appearance is difficult, and it is important to biopsy polyps and the background tissue, especially with suspected hyperplastic polyps, to assess for gastritis and other pathology. Tissue should be tested using immunohistochemistry for further clarification, and deeper lesions may require evaluation with endoscopic ultrasound. Because many polyps are histologically similar, it is important to communicate background information to the pathologist, such as the density and gross appearance of the polyps.[17]

Diagnosing a polyp based solely on endoscopic appearance is difficult, and it is important to biopsy polyps and the background tissue, especially with suspected hyperplastic polyps, to assess for gastritis and other pathology. Tissue should be tested using immunohistochemistry for further clarification, and deeper lesions may require evaluation with endoscopic ultrasound. Because many polyps are histologically similar, it is important to communicate background information to the pathologist, such as the density and gross appearance of the polyps.[17] Subepithelial polyps should undergo evaluation by endoscopic ultrasound with biopsies. This category includes lesions such as GIST, granular cell tumors, leiomyomas, and inflammatory fibroid polyps. A GIST may also be found on computed tomography imaging to assess for metastases and local invasion.[76] If dysplasia or malignancy is found or multiple polyps are encountered, a colonoscopy is recommended to assess for FAP. Multiple fundic gland polyps within the body of the stomach, with or without dysplasia, coupled with adenomatous lesions and an absence of duodenal or colonic polyps, suggest gastric adenocarcinoma and proximal polyposis.[77]

There are general guidelines for treating gastric polyps and specific recommendations according to histologic subtype. There is a potential for sampling error during biopsy, so consideration should always be given to polypectomy. There are many techniques available to biopsy or remove polyps, including hot and cold forceps, hot and cold snare, endoscopic mucosal resection, and endoscopic submucosal dissection.[78] The American College of Gastroenterology recommends endoscopic ultrasound as part of the diagnosis of supepithelial lesions.[38] When evaluating a hyperplastic polyp, the surrounding tissue must be sampled for metaplasia, dysplasia, and adenocarcinoma due to the risk of synchronous cancer and H pylori.[15] If testing reveals H pylori infection, antibiotic therapy should be initiated.[4] Without eradicating H pylori, the recurrence rate of hyperplastic polyps is high. The American Society of Gastrointestinal Endoscopy recommends biopsy or polypectomy for all polyps, noting that dysplasia and focal cancer are found in 5% to 19% of hyperplastic polyps; size greater than 1 cm and pedunculation are risk factors for dysplasia. Recommendations include the removal of gastric fundic polyps larger than 1 cm, hyperplastic polyps larger than 0.5 cm, and sampling surrounding tissue.[4][79] Guidelines for precursors of gastric adenocarcinoma, as proposed by Saltzman, in the setting of atrophic gastritis or intestinal metaplasia, include high-definition and image-enhanced endoscopy with biopsies and documentation of grade, location, and extent of gastritis or metaplasia. The antrum/incisura is considered low risk, and the proximal body is high risk. Recommendations include screening individuals younger than 50 with risk factors such as smoking, male sex, anemia, and a first-degree relative with gastric cancer. In those with nonvisible low-grade dysplasia, follow-up endoscopy with enhanced imaging and biopsies in 1 year is recommended. Urgent enhanced imaging and biopsies are indicated in those with nonvisible high-grade dysplasia, with a subsequent 6-month follow-up. Endoscopy is performed one year following endoscopic removal of adenomas.[80]

Guidelines for precursors of gastric adenocarcinoma, as proposed by Saltzman, in the setting of atrophic gastritis or intestinal metaplasia, include high-definition and image-enhanced endoscopy with biopsies and documentation of grade, location, and extent of gastritis or metaplasia. The antrum/incisura is considered low risk, and the proximal body is high risk. Recommendations include screening individuals younger than 50 with risk factors such as smoking, male sex, anemia, and a first-degree relative with gastric cancer. In those with nonvisible low-grade dysplasia, follow-up endoscopy with enhanced imaging and biopsies in 1 year is recommended. Urgent enhanced imaging and biopsies are indicated in those with nonvisible high-grade dysplasia, with a subsequent 6-month follow-up. Endoscopy is performed one year following endoscopic removal of adenomas.[80] The American Society of Gastrointestinal Endoscopy advocates removing all gastric adenomas via submucosal resection, citing a recurrence rate of 2.6%.[38][80] Gastric cancer is diagnosed in 1.3% of persons who have had an adenoma removed, and the recommended follow-up to adenoma resection is a repeat endoscopy in 1 year, followed by surveillance every 3 to 5 years.[38][81] Pernicious anemia, a causative etiology of type A gastritis, has a 1% to 3% association with adenocarcinoma. Some study results have demonstrated a 2- to 3-fold increased risk of gastric cancer in those with pernicious anemia. Recommendations include endoscopy upon diagnosis with pernicious anemia and surveillance every 3 years in those with extensive metaplasia and gastritis, with a family history of gastric adenocarcinoma, or persistent H pylori.[38]

The American Society of Gastrointestinal Endoscopy advocates removing all gastric adenomas via submucosal resection, citing a recurrence rate of 2.6%.[38][80] Gastric cancer is diagnosed in 1.3% of persons who have had an adenoma removed, and the recommended follow-up to adenoma resection is a repeat endoscopy in 1 year, followed by surveillance every 3 to 5 years.[38][81] Pernicious anemia, a causative etiology of type A gastritis, has a 1% to 3% association with adenocarcinoma. Some study results have demonstrated a 2- to 3-fold increased risk of gastric cancer in those with pernicious anemia. Recommendations include endoscopy upon diagnosis with pernicious anemia and surveillance every 3 years in those with extensive metaplasia and gastritis, with a family history of gastric adenocarcinoma, or persistent H pylori.[38] Surveillance of patients with FAP is associated with earlier detection and improved survival. Studies from the United Kingdom recommend yearly endoscopy for those with low-grade dysplasia and resection for high-grade dysplasia due to the risk of concurrent adenocarcinoma. This practice is recommended in the United States for those with a family history of adenocarcinoma or Asian heritage. Up to 25% of patients with high-grade dysplasia progress to adenocarcinoma in a year.[38] The recommended treatment for areas of polyp mounds includes 3- to 6-month surveillance with endoscopy, biopsies, and debulking. Endoscopic ultrasound of polyp mounds with biopsy may be indicated as studies have found that mucosal sampling may be insufficient to diagnose malignancy within dense areas. All antral polyps should be removed, and dysplastic polyps or adenomas that fail endoscopic management require surgical excision.[17] A prospective study on persons with FAP undergoing surveillance at Cleveland Clinic for high-risk adenomas, hyperplastic polyps, and fundic gland polyps studied a total of 150 gastric polyps and, from them, developed criteria to distinguish high-risk from lower-risk polyps with no dysplasia or low-grade dysplasia.[82]

Surveillance of patients with FAP is associated with earlier detection and improved survival. Studies from the United Kingdom recommend yearly endoscopy for those with low-grade dysplasia and resection for high-grade dysplasia due to the risk of concurrent adenocarcinoma. This practice is recommended in the United States for those with a family history of adenocarcinoma or Asian heritage. Up to 25% of patients with high-grade dysplasia progress to adenocarcinoma in a year.[38] The recommended treatment for areas of polyp mounds includes 3- to 6-month surveillance with endoscopy, biopsies, and debulking. Endoscopic ultrasound of polyp mounds with biopsy may be indicated as studies have found that mucosal sampling may be insufficient to diagnose malignancy within dense areas. All antral polyps should be removed, and dysplastic polyps or adenomas that fail endoscopic management require surgical excision.[17] A prospective study on persons with FAP undergoing surveillance at Cleveland Clinic for high-risk adenomas, hyperplastic polyps, and fundic gland polyps studied a total of 150 gastric polyps and, from them, developed criteria to distinguish high-risk from lower-risk polyps with no dysplasia or low-grade dysplasia.[82] Gastric inflammatory fibroid polyps comprise about 0.1% of gastric polyps and are usually treated with snare polypectomy. Larger inflammatory polyps require endoscopic ultrasound to clarify anatomy, followed by endoscopic mucosal resection.[83] Inflammatory polyps have no malignant potential but can cause gastric outlet obstruction, as in the case of a large, partially obstructing inflammatory fibroid polyp in a 64-year-old man excised with endoscopic submucosal resection.[84][85] The protocol for a GIST depends on the stage; the GIST may be excised if there are no metastases or local invasions. An invasive tumor can be genotyped to determine treatment options. A tumor positive for a c-kit mutation can be treated with imatinib; a small asymptomatic GIST can undergo surveillance. The American College of Gastroenterology (2023) recommends resecting any GIST greater than 2 cm using endoscopic mucosal resection or endoscopic submucosal dissection.[79]

The protocol for a GIST depends on the stage; the GIST may be excised if there are no metastases or local invasions. An invasive tumor can be genotyped to determine treatment options. A tumor positive for a c-kit mutation can be treated with imatinib; a small asymptomatic GIST can undergo surveillance. The American College of Gastroenterology (2023) recommends resecting any GIST greater than 2 cm using endoscopic mucosal resection or endoscopic submucosal dissection.[79] Peutz-Jegher polyps have the potential to become gastric carcinoma by an average age of 30. Yearly screening is recommended for persons diagnosed with Peutz-Jegher in childhood. Polyps greater than 1 cm are resected, followed by annual surveillance, and surveillance for smaller polyps is conducted every 2 to 3 years. These polyps can also cause obstruction, bleeding, and intussusception. Recommendations include baseline surveillance in affected persons starting at age 10 and resuming at age 18 if no polyps are initially encountered. Those with juvenile polyposis have a 50% lifetime risk of gastric malignancy; screening begins at 18 years if there are no earlier symptoms and continues annually. Those with gastric adenocarcinoma and proximal polyposis require regular surveillance, and some may require prophylactic gastrectomy.[86] Per the American College of Gastroenterology, neuroendocrine tumors are either resected surgically or removed via endoscopic mucosal resection or endoscopic submucosal dissection, including biopsies of surrounding tissue. An endoscopic ultrasound can help guide the excision approach.[79] Gastric fluid is aspirated for pH testing, and a fasting serum gastrin is obtained. Surveillance is a reasonable option for lesions less than 1 cm.  Neuroendocrine tumors Types I and II can generally undergo endoscopic treatment. Neuroendocrine type III tumors should undergo surgical resection except for possibly tiny lesions lacking lymphatic involvement that can be treated with endoscopic mucosal resection. Type IV neuroendocrine tumors should be surgically excised, along with any variant of a neuroendocrine lesion exhibiting aggressive features such as a high mitotic rate, metastases, angioinvasion, and incursion into the muscular wall. An antrectomy can be performed to remove G-cell stimulation.[38]

Per the American College of Gastroenterology, neuroendocrine tumors are either resected surgically or removed via endoscopic mucosal resection or endoscopic submucosal dissection, including biopsies of surrounding tissue. An endoscopic ultrasound can help guide the excision approach.[79] Gastric fluid is aspirated for pH testing, and a fasting serum gastrin is obtained. Surveillance is a reasonable option for lesions less than 1 cm.  Neuroendocrine tumors Types I and II can generally undergo endoscopic treatment. Neuroendocrine type III tumors should undergo surgical resection except for possibly tiny lesions lacking lymphatic involvement that can be treated with endoscopic mucosal resection. Type IV neuroendocrine tumors should be surgically excised, along with any variant of a neuroendocrine lesion exhibiting aggressive features such as a high mitotic rate, metastases, angioinvasion, and incursion into the muscular wall. An antrectomy can be performed to remove G-cell stimulation.[38] In general, follow-up after biopsy is determined by the polyp histology. A repeat esophagogastroduodenoscopies is recommended at 1 year for a hyperplastic polyp without dysplasia. If H pylori is found in biopsies associated with the polyp, a repeat EGD is performed in 3 to 6 months to confirm infection eradication and assess for polyp regression. In the case of a fundic gland polyp, if there is a history of chronic proton pump inhibitor use, discontinuation when possible is recommended, and a 1-year follow-up EGD is performed when lesions greater than 5 mm to 10 mm are found on initial EGD. The recommended follow-up for adenoma resection is a repeat endoscopy in 1 year followed by surveillance every 3 to 5 years.[81] When multiple adenomas are found in patients younger than 40, a colonoscopy is recommended to rule out FAP. If dysplasia or early adenocarcinoma is detected in a gastric polyp, repeat EGD is performed at 1 year and again at 3 years.[4][18][38][69][87]

A comprehensive differential diagnosis of polypoid gastric masses includes: Hyperplastic polyp Fundic gland polyp Adenoma Familial adenomatous polyposis Carcinoid Xanthoma Gastrointestinal stromal tumors Leiomyoma Fibroid polyps Peutz-Jegher syndrome Cowden syndrome Cronkhite-Canada syndrome Juvenile polyposis syndrome Hemangioma Lymphangioma Lymphoma Neuroma Submucosal ectopic glands Gastric adenocarcinoma Gastric adenocarcinoma and proximal polyposis of the stomach Neuroendocrine tumors Ectopic pancreas Metastatic tumors [88][89] More than 80% of individuals with FAP have multiple fundic gland polyps and gastric adenomas are also common, as well as intestinal-type adenomas in the distal stomach. Considering FAP with these endoscopic findings is important.[89][90]

Gastric polyp distribution and etiology have changed within the past decade. A retrospective analysis published in 2024 studied the dictations of 23,668 endoscopies performed between 2003 and 2018, comparing 2 time periods, 2003 to 2010 and 2010 to 2018. Of the endoscopy dictations studied, 4.2% reported a polyp involving 989 persons, with a mean age of 63, with 65% of the polyps smaller than 5 mm. Histology of the polyps included hyperplastic, fundic gland, adenoma, non-epithelial lesions, normal mucosa, and chronic gastritis.[8] Biopsies were taken from 742 individuals, and concurrent sampling of surrounding mucosa from 350 of these, while 10 cases in which polyps were identified had biopsies only of the surrounding mucosa.[8] The percentage of epithelial polyps in that population was 1.7%, and 28% of those with a polyp tested positive for H pylori. There was an increase in patients with multiple polyps within the second period, a shift in polyp location from corpus to fundus, an increased number of fundic gland polyps, and a decrease in other histologic types within the second time interval.[8] A study focusing on polyp recurrence was conducted of 1018 hyperplastic gastric polyps greater than 1 cm removed from 869 patients. The patients were followed over 2, 5, and 10 years, and recurrence was identified in 7%, 13%, and 20% of persons over those periods. Factors associated with recurrence include larger size, multiple polyps, lobulated polyps, and polyps with exudate.[37]

A study focusing on polyp recurrence was conducted of 1018 hyperplastic gastric polyps greater than 1 cm removed from 869 patients. The patients were followed over 2, 5, and 10 years, and recurrence was identified in 7%, 13%, and 20% of persons over those periods. Factors associated with recurrence include larger size, multiple polyps, lobulated polyps, and polyps with exudate.[37] Wang et al studied fundic gland polyps in FAP. They found that 3 patients who progressed to gastric cancer demonstrated signet ring cell cancer within dysplastic foci of a fundic gland polyp. In addition, they documented progression from non-dysplasia to low-grade dysplasia to gastric cancer over 34 months. They concluded that polyp size greater than 10 mm increases the risk for gastric cancer in persons with FAP, with a 36% 5-year risk of developing dysplasia. As a result, they recommend rigorous sampling of fundic gland polyps in this cohort to optimize the early detection of dysplasia.[91] Results from a study of endoscopic features in 80 adults with FAP concluded that certain endoscopic features, in addition to demographics and genetics, were associated with gastric neoplasm. The study authors found those with sessile gastric polyps were older, more likely to have a family history of gastric cancer, displayed white mucosal patches in the proximal stomach with concurrent antral polyps, and most had the APC variant 5 at codon 1309.[92]

Gastric polyps are often benign and prognostically favorable but represent a spectrum of histology and malignant potential. Study results note an overall malignancy rate of less than 2%.[93] Characteristics of polyps that indicate a poorer prognosis include large size, advanced patient age, and the presence of multiple adenomas. The risk of dysplasia or malignancy increases in lesions larger than 20 cm in older patients and in genetic conditions such as FAP, which carries a higher risk for the development of adenocarcinoma.[4] The prognosis of neuroendocrine polyps depends on the subtype. Type I neuroendocrine polyps do not shorten lifespan or increase morbidity. However, those with type II neuroendocrine polyps are found to have lymph node metastases 10% to 30% of the time upon diagnosis, and survival is 60% to 75% at 5 years. Persons with type IV polyps are usually diagnosed at an advanced stage with extensive metastases and have a 50% 1-year survival rate.[94] The gastric polyps associated with Cowden Syndrome are usually benign, but these patients are at risk of cancer in other locations. Peutz-Jeghers gastric polyps are difficult to differentiate from hyperplastic polyps and have malignant potential. Those with juvenile polyposis carry a 50% lifetime risk of gastric cancer.[4] The prognosis for a gastrointestinal stromal tumor is determined by size, mitotic index, and site.[95] Inflammatory fibroid polyps and ectopic pancreas in the stomach are benign processes.[4]

Gastric cancer is the third most common cause of death from cancer worldwide. Gastric polyps can represent precancerous lesions, and timely treatment of gastric polyps may reduce the incidence of gastric cancer. Modifications that may reduce a patient’s gastric polyp risk include decreasing alcohol and dietary saturated fat, increasing fiber intake, and smoking cessation. Smoking may be an independent risk factor for hyperplastic polyps.[4] Hyperplastic polyps are also associated with H pylori infection, autoimmune gastritis, increased gastrin, and gastric atrophy—and may signify an increased risk for gastric carcinoma. While there is no preventative screening program for gastric cancer in Western nations due to the relatively low risk, those with increased risk factors should undergo surveillance for gastric cancer and pre-cancerous lesions.[33]

Results from multiple studies have demonstrated a trend towards an increasing number of fundic gland polyps, fewer hyperplastic polyps, and a tendency towards more numerous but smaller polyps. There is a postulation that the variance in polyp subtype may reflect increased use of proton pump inhibitors and a decline in H pylori infection. In addition, the ability to detect polyps improves with more sophisticated equipment and training.[8] A Korean study investigating missed adenomas found intestinal metaplasia may indicate a missed adenoma.[96] Study results have emphasized the importance of identifying nonfundic gland polyps, gastritis, and metaplasia, all risk factors for gastric adenocarcinoma. However, those who have numerous large or dysplastic fundic gland polyps, particularly at a younger age, need to be evaluated for FAP and are at increased risk for adenocarcinoma.[80] Subepithelial lesions and those masses of unclear origin should undergo evaluation using endoscopic ultrasound, which distinguishes layers within the stomach wall.[79]

Gastric polyps may be found during evaluation for anemia, fatigue, and dyspepsia and are often incidental findings during esophagogastroduodenoscopy for clinical entities such as peptic ulcer disease, Barrett esophagus, and gastritis. The American Society of Gastrointestinal Endoscopy guidelines (asge.org) can be applied to guide diagnosis and follow-up for gastric polyps.[38] Interprofessional communication between the gastroenterologist/endoscopist, the primary care clinician, and all healthcare team members is essential to ensure the appropriate information is conveyed to pathologists to facilitate accurate and timely diagnosis. Interprofessional collaboration is instrumental in providing information to patients and scheduling follow-ups.[4] Pathologists, geneticists, gastroenterologists, and surgeons may be involved in diagnosing, treating, and caring for patients with gastric polyps, and interprofessional teamwork is important in achieving optimal patient outcomes.