FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3041704625> ?p ?o ?g. }

• W3041704625 endingPage "452" @default.
• W3041704625 startingPage "431" @default.
• W3041704625 abstract "Key points•Gastric epithelial polyps comprise a wide spectrum of lesions with different cause, histology, malignant potential, and sometimes associations with tumor predisposition syndromes.•Most gastric polyps are sporadic with no malignant potential, but clinical correlation is necessary, and pathologists should be familiar with the morphologic characteristics of gastric polyps as an indication for a search for an underlying genetic syndrome, such as familial adenomatous polyposis, Peutz-Jeghers syndrome, or juvenile polyposis syndrome.•In the presence of a gastric polyp, preferably biopsies of background mucosa are taken of at least the antrum and corpus. Evaluation of the background nonpolypoid mucosa is essential in reaching a diagnosis that can characterize the condition in which the polyp developed and may have therapeutic consequences. •Gastric epithelial polyps comprise a wide spectrum of lesions with different cause, histology, malignant potential, and sometimes associations with tumor predisposition syndromes.•Most gastric polyps are sporadic with no malignant potential, but clinical correlation is necessary, and pathologists should be familiar with the morphologic characteristics of gastric polyps as an indication for a search for an underlying genetic syndrome, such as familial adenomatous polyposis, Peutz-Jeghers syndrome, or juvenile polyposis syndrome.•In the presence of a gastric polyp, preferably biopsies of background mucosa are taken of at least the antrum and corpus. Evaluation of the background nonpolypoid mucosa is essential in reaching a diagnosis that can characterize the condition in which the polyp developed and may have therapeutic consequences. Gastric polyps comprise a wide spectrum of lesions arising from different cell or epithelial compartments in the stomach and with different causes, histology, malignant potential, and association with different tumor predisposition syndromes. Gastric polyps can be defined as lesions projecting above the plane of the surrounding gastric mucosa.1Park D.Y. Lauwers G.Y. Gastric polyps: classification and management.Arch Pathol Lab Med. 2008; 132: 633-640PubMed Google Scholar In about 1% to 6% of gastroscopies, polyps are found in the stomach.2Castro R. Pimentel-Nunes P. Dinis-Ribeiro M. Evaluation and management of gastric epithelial polyps.Best Pract Res Clin Gastroenterol. 2017; 31: 381-387Crossref PubMed Scopus (18) Google Scholar,3Carmack S.W. Genta R.M. Graham D.Y. et al.Management of gastric polyps: a pathology-based guide for gastroenterologists.Nat Rev Gastroenterol Hepatol. 2009; 6: 331-341Crossref PubMed Scopus (104) Google Scholar Most polyps are of epithelial origin and asymptomatic.2Castro R. Pimentel-Nunes P. Dinis-Ribeiro M. Evaluation and management of gastric epithelial polyps.Best Pract Res Clin Gastroenterol. 2017; 31: 381-387Crossref PubMed Scopus (18) Google Scholar Less frequently found subepithelial lesions presenting as gastric polyps include neuroendocrine tumors, pancreatic heterotopia, mesenchymal polyps (eg, inflammatory fibroid polyp, gastrointestinal stromal tumor, leiomyoma, schwannoma, inflammatory myofibroblastic tumor) as well as lymphomas.4Carmack S.W. Genta R.M. Schuler C.M. et al.The current spectrum of gastric polyps: a 1-year national study of over 120,000 patients.Am J Gastroenterol. 2009; 104: 1524-1532Crossref PubMed Scopus (188) Google Scholar Large geographic differences have been observed in the occurrence of gastric polyps, mainly caused by differences in Helicobacter pylori (H pylori) infection rate.5Brosens L.A.A. Wood L.D. Offerhaus G.J. et al.Pathology and genetics of syndromic gastric polyps.Int J Surg Pathol. 2016; 24: 185-199Crossref PubMed Scopus (24) Google Scholar In areas with high rates of H pylori infection, hyperplastic polyps (HPs), with or without dysplasia, are most prevalent. In contrast, fundic gland polyps (FGPs) are the most frequently encountered type of polyps in areas with a low prevalence of H pylori infection as well as high use of proton-pump inhibitory therapy, for example, western countries.3Carmack S.W. Genta R.M. Graham D.Y. et al.Management of gastric polyps: a pathology-based guide for gastroenterologists.Nat Rev Gastroenterol Hepatol. 2009; 6: 331-341Crossref PubMed Scopus (104) Google Scholar,4Carmack S.W. Genta R.M. Schuler C.M. et al.The current spectrum of gastric polyps: a 1-year national study of over 120,000 patients.Am J Gastroenterol. 2009; 104: 1524-1532Crossref PubMed Scopus (188) Google Scholar Gastric polyps often arise in association with an inflammatory background or a polyposis syndrome. Careful attention to the background mucosa and awareness of syndromic gastric polyps are therefore important for correct interpretation and diagnosis of gastric polyps. Gastric polyps can be classified based on their cell or epithelial compartment of origin (Table 1). The stomach consists of the following anatomic regions: cardia, fundus, body, antrum, and pylorus. These areas have variable histologic appearances, which reflect differences in physiologic functions. Gastric pits or foveolae, lined by mucus-secreting foveolar cells, comprise the whole luminal surface of the stomach. Underneath these pits, the mucous neck cells as well as deep gastric glands are located, of which the cellular composition is region-dependent. The glands in the fundus and body consist of parietal cells, chief cells, and enterochromaffin-like cells. In the cardia, antrum, and pylorus, mainly mucus cells with clear cytoplasm line the deep glands with a small mixture of neuroendocrine cells. In the transitional zones, small numbers of parietal and chief cells are present. Familiarity with these histologic features will aid in gastric polyp recognition and diagnosis.Table 1Overview of gastric epithelial polyps classified by cell or epithelial compartment of originOriginNonneoplasticNeoplasticFoveolar layerHyperplastic polypFoveolar-type adenomaIntestinal-type adenomaCharacteristicsPolyp consisting of dilated, branched, and elongated glands in edematous stromaBackground of chronic gastritisPolyp with atypical foveolar cells (at least low-grade dysplasia)No background of inflammation, atrophy, or metaplasiaExpression of MUC5AC; usually no expression of MUC2Polyp with intestinal-type columnar epithelium containing absorptive cells, goblet cells, endocrine cells, and/or Paneth cells with at least low-grade dysplasiaBackground of intestinal metaplasia and/or inflammation or atrophy. Variable expression of MUC2; no or slight expression of MUC5AC and MUC6Of noteHistopathologically indistinguishable from hamartomatous polyp/hamartomatous polyposis syndromeReasonable risk of malignancy (background)Association with FAPLow risk of malignant transformationAssociation with FAP (although rare)Relatively high risk of malignant transformationGlandular layerFundic gland polypPyloric gland adenomaOxyntic gland adenomaCharacteristicsPolyp consisting of dilated glands with parietal and chief cells and some mucous cellsPolyp with atypical pyloric-type glands (at least low-grade dysplasia)No background of inflammation, atrophy, or metaplasiaExpression of MUC6; usually no expression of MUC2Polyp with atypical oxyntic glands, consisting of chief cells or combination of chief and parietal cells (at least low-grade dysplasia)In general, no background of inflammation, atrophy, or metaplasiaOf noteSporadic (association with PPI therapy) or in the context of FAPLow risk of malignant transformationAssociation with several polyposis/tumor predisposition syndromesRelatively high risk of malignant transformationLow risk of malignant transformation Open table in a new tab FGPs are the most common type of gastric polyp, comprising almost 80% of all gastric polyps, and seem to be more common in areas with low H pylori infection rates.3Carmack S.W. Genta R.M. Graham D.Y. et al.Management of gastric polyps: a pathology-based guide for gastroenterologists.Nat Rev Gastroenterol Hepatol. 2009; 6: 331-341Crossref PubMed Scopus (104) Google Scholar,4Carmack S.W. Genta R.M. Schuler C.M. et al.The current spectrum of gastric polyps: a 1-year national study of over 120,000 patients.Am J Gastroenterol. 2009; 104: 1524-1532Crossref PubMed Scopus (188) Google Scholar Sporadic FGPs are strongly related to the use of proton-pump inhibitors (PPIs). Long-term use leads especially to increased risk of developing FGPs. PPI therapy gives acid suppression, which elevates serum gastrin, a growth factor for oxyntic mucosa and a downstream target of Wnt signaling. Patients on PPI therapy have hyperplasia and protrusions of parietal cells in their gastric biopsy, which is thought to be an initial step in the development of an FGP. After this, there is development of small and subsequently larger fundic gland cysts. The glands dilate because of increased intraglandular pressure, probably because of the parietal cell hyperplasia that gives increased outflow resistance. In younger patients with multiple FGPs (>20), that is, fundic gland polyposis, or FGPs with dysplasia, an underlying familial adenomatous polyposis (FAP) syndrome (owing to a germline mutation in the Adenomatous Polyposis Coli [APC] gene) or MUTYH polyposis should be considered, and colonoscopy is advised, in particular if there are also duodenal adenomas. FGPs are typically less than 5 mm and have a smooth surface. Sporadic FGPs are usually solitary or few in number (Fig. 1). However, FGPs can be numerous in patients using PPIs and in patients with familial polyposis syndrome (Fig. 2).5Brosens L.A.A. Wood L.D. Offerhaus G.J. et al.Pathology and genetics of syndromic gastric polyps.Int J Surg Pathol. 2016; 24: 185-199Crossref PubMed Scopus (24) Google Scholar,6Vogt S. Jones N. Christian D. et al.Expanded extracolonic tumor spectrum in MUTYH-associated polyposis.Gastroenterology. 2009; 137: 1976-1985.e1-10Abstract Full Text Full Text PDF PubMed Scopus (216) Google ScholarFig. 2FAP-associated FGP: gross features. Numerous FGPs and foveolar adenomas throughout the stomach of a patient with FAP syndrome.View Large Image Figure ViewerDownload Hi-res image Download (PPT) FGPs are characterized by cystically dilated oxyntic glands mainly lined by parietal and chief cells and variable numbers of mucous neck cells (Fig. 3). The overlying foveolar surface is usually normal. Surface erosion can be present with resulting reactive changes of the foveolar epithelium, which may be misinterpreted as dysplasia. Sporadic single FGPs rarely show dysplasia; however, in some FGPs, dysplasia of the overlying foveolar epithelium is observed. Dysplasia in FGPs is of foveolar type, characterized by low columnar cells resembling foveolar cells with round to oval nuclei (Fig. 4). The cytoplasm contains a MUC5AC-positive mucin cap. The surrounding mucosa of FGPs is normal or shows signs of PPI use. There is no background of atrophy or intestinal metaplasia.Fig. 3FGP: microscopic features. (A) Low-power view of an FGP, consisting of cystically dilated glands lined by parietal and chief cells and variable numbers of mucous neck cells. (B) High-power view of the same polyp. The polyp is lined by nondysplastic foveolar epithelium at the surface.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig. 4FGP with high-grade dysplasia. (A) This FGP from a patient with FAP shows a focus of high-grade dysplasia of the overlying foveolar epithelium, characterized by columnar cells showing severe nuclear atypia with round to oval, vesicular nuclei with prominent nucleoli and loss of polarity as well as some architectural atypia with crowding and branching of glands. (B) The dysplastic cells show p53 overexpression.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig. 4FGP with high-grade dysplasia. (A) This FGP from a patient with FAP shows a focus of high-grade dysplasia of the overlying foveolar epithelium, characterized by columnar cells showing severe nuclear atypia with round to oval, vesicular nuclei with prominent nucleoli and loss of polarity as well as some architectural atypia with crowding and branching of glands. (B) The dysplastic cells show p53 overexpression.View Large Image Figure ViewerDownload Hi-res image Download (PPT) In general, FGPs are straightforward to diagnose both endoscopically and microscopically. Some FGPs can be difficult to differentiate from pyloric or oxyntic gland adenomas (OGAs), depending on the degree of cystic changes and pyloric or oxyntic differentiation, respectively. GNAS mutations are often present in pyloric gland adenomas (PGAs) and absent in FGPs, and this may be used to differentiate between PGA and FGP.7Hackeng W.M. Montgomery E.A. Giardiello F.M. et al.Morphology and genetics of pyloric gland adenomas in familial adenomatous polyposis.Histopathology. 2017; 70: 549-557Crossref PubMed Scopus (15) Google Scholar Very large FGPs can pose a differential diagnosis with HPs. The key difference between FGPs and HPs is that the cystically dilated glands in FGPs are lined by a mixture of cell types, including parietal and foveolar cells, whereas in HPs, the glands are lined by hyperplastic foveolar epithelium. FGPs with dysplasia can be difficult to distinguish from foveolar-type adenomas with low-grade dysplasia, but this is of little clinical significance because both lesions carry a low risk of neoplastic progression.8Wood L.D. Salaria S.N. Cruise M.W. et al.Upper GI tract lesions in familial adenomatous polyposis (FAP).Am J Surg Pathol. 2014; 38: 389-393Crossref PubMed Scopus (73) Google Scholar FGPs are generally regarded as nonneoplastic lesions, either hamartomatous or hyperplastic/functional in nature, because they are retention cysts caused by corpus gland secretion impairment. However, the frequent finding of mutations in the Wnt pathway (APC and CTNNB1 genes) indicates that FGPs are neoplastic growths as well. Most (60%–90%) sporadic FGPs without dysplasia have somatic CTNNB1 mutations.9Abraham S.C. Park S.J. Mugartegui L. et al.Sporadic fundic gland polyps with epithelial dysplasia: evidence for preferential targeting for mutations in the adenomatous polyposis coli gene.Am J Pathol. 2002; 161: 1735-1742Abstract Full Text Full Text PDF PubMed Scopus (80) Google Scholar,10Sekine S. Shibata T. Yamauchi Y. et al.Beta-catenin mutations in sporadic fundic gland polyps.Virchows Arch. 2002; 440: 381-386Crossref PubMed Scopus (53) Google Scholar Dysplastic sporadic FGPs may have a somatic APC mutation without CTNNB1 (β-catenin) mutation.9Abraham S.C. Park S.J. Mugartegui L. et al.Sporadic fundic gland polyps with epithelial dysplasia: evidence for preferential targeting for mutations in the adenomatous polyposis coli gene.Am J Pathol. 2002; 161: 1735-1742Abstract Full Text Full Text PDF PubMed Scopus (80) Google Scholar In contrast, FGPs in FAP show somatic second-hit inactivation of the APC gene that precedes dysplasia, but lacks CTNNB1 mutations.11Abraham S.C. Nobukawa B. Giardiello F.M. et al.Fundic gland polyps in familial adenomatous polyposis.Am J Pathol. 2000; 157: 747-754Abstract Full Text Full Text PDF PubMed Scopus (172) Google Scholar The type of second-hit APC mutation may play a role in the chance of progression to high-grade dysplasia in FAP-associated FGPs.12Sekine S. Shimoda T. Nimura S. et al.High-grade dysplasia associated with fundic gland polyposis in a familial adenomatous polyposis patient, with special reference to APC mutation profiles.Mod Pathol. 2004; 17: 1421-1426Crossref PubMed Scopus (22) Google Scholar Dysplasia in sporadic FGPs is extremely rare and has an indolent nature.13Straub S.F. Drage M.G. Gonzalez R.S. Comparison of dysplastic fundic gland polyps in patients with and without familial adenomatous polyposis.Histopathology. 2018; 72: 1172-1179Crossref PubMed Scopus (11) Google Scholar, 14Levy M.D. Bhattacharya B. Sporadic fundic gland polyps with low-grade dysplasia: a large case series evaluating pathologic and immunohistochemical findings and clinical behavior.Am J Clin Pathol. 2015; 144: 592-600Crossref PubMed Scopus (16) Google Scholar, 15Abraham S.C. Fundic gland polyps: common and occasionally problematic lesions.Gastroenterol Hepatol (N Y). 2010; 6: 48-51PubMed Google Scholar, 16Burt R.W. Gastric fundic gland polyps.Gastroenterology. 2003; 125: 1462-1469Abstract Full Text Full Text PDF PubMed Scopus (95) Google Scholar, 17Torbenson M. Lee J.-H. Cruz-Correa M. et al.Sporadic fundic gland polyposis: a clinical, histological, and molecular analysis.Mod Pathol. 2002; 15: 718-723Crossref PubMed Scopus (63) Google Scholar In general, sporadic FGPs do not progress to cancer and tend to regress when PPI therapy is stopped. Presence of FGPs is inversely correlated with H pylori infection, active gastritis, and gastric neoplasia.18Genta R.M. Schuler C.M. Robiou C.I. et al.No association between gastric fundic gland polyps and gastrointestinal neoplasia in a study of over 100,000 patients.Clin Gastroenterol Hepatol. 2009; 7: 849-854Abstract Full Text Full Text PDF PubMed Scopus (98) Google Scholar FAP is an autosomal-dominant polyposis syndrome caused by a germline mutation in the APC gene. It is characterized by hundreds to thousands of adenomatous polyps (≥100) throughout the colorectum and inevitable development of colorectal cancer if left untreated by colectomy. In addition, FAP patients develop several benign and malignant extracolonic lesions. In the stomach, most patients with FAP have multiple FGPs (polyposis). Low-grade dysplasia is often seen in FGPs in FAP, but the risk of malignant progression is low.5Brosens L.A.A. Wood L.D. Offerhaus G.J. et al.Pathology and genetics of syndromic gastric polyps.Int J Surg Pathol. 2016; 24: 185-199Crossref PubMed Scopus (24) Google Scholar,19Brosens L.A.A. Offerhaus G.J.A. Giardiello F.M. Hereditary colorectal cancer: genetics and screening.Surg Clin North Am. 2015; 95: 1067-1080Abstract Full Text Full Text PDF PubMed Scopus (31) Google Scholar Based on older literature, western FAP patients are considered not to carry an increased risk of gastric cancer compared with the general population,20Offerhaus G.J. Giardiello F.M. Krush A.J. et al.The risk of upper gastrointestinal cancer in familial adenomatous polyposis.Gastroenterology. 1992; 102: 1980-1982Abstract Full Text PDF PubMed Google Scholar whereas a 3 to 4 times increased risk of gastric cancer was reported in FAP patients from South Korea and Japan.21Park J.-G. Park K.J. Ahn Y.-O. et al.Risk of gastric cancer among Korean familial adenomatous polyposis patients.Dis Colon Rectum. 1992; 35: 996-998Crossref PubMed Scopus (72) Google Scholar,22Iwama T. Mishima Y. Utsunomiya J. The impact of familial adenomatous polyposis on the tumorigenesis and mortality at the several organs. Its rational treatment.Ann Surg. 1993; 217: 101-108Crossref PubMed Scopus (213) Google Scholar The increased risk of gastric cancer in Asian populations likely results from higher prevalence of H pylori infection and associated atrophic gastritis and intestinal metaplasia in these populations. However, several recent reports of FAP patients with gastric cancer suggest an increased incidence of gastric cancer in western patients.23Walton S.-J. Frayling I.M. Clark S.K. et al.Gastric tumours in FAP.Fam Cancer. 2017; 16: 363-369Crossref PubMed Scopus (25) Google Scholar,24Mankaney G. Leone P. Cruise M. et al.Gastric cancer in FAP: a concerning rise in incidence.Fam Cancer. 2017; 16: 371-376Crossref PubMed Scopus (40) Google Scholar Interestingly, these gastric cancers are almost exclusively located in the proximal stomach and are associated with extensive carpeting fundic gland polyposis, and a large size (>20 mm) of polyps and dysplasia.25Leone P.J. Mankaney G. Sarvapelli S. et al.Endoscopic and histologic features associated with gastric cancer in familial adenomatous polyposis.Gastrointest Endosc. 2019; 89: 961-968Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar One study reported an association between gastric cancer and desmoid tumors in FAP patients, suggesting a genotype-phenotype correlation for gastric cancer.23Walton S.-J. Frayling I.M. Clark S.K. et al.Gastric tumours in FAP.Fam Cancer. 2017; 16: 363-369Crossref PubMed Scopus (25) Google Scholar In addition, gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) is characterized by carpeting proximal fundic gland polyposis of the stomach with antral sparing, increased risk of gastric cancer, and no or a small number of duodenal and colorectal adenomas. Because it is caused by a point mutation in exon 1B of APC, it is now considered a variant of FAP with a unique gastric phenotype, further supporting that gastric cancer risk may depend on the genotype.26Worthley D.L. Phillips K.D. Wayte N. et al.Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome.Gut. 2012; 61: 774-779Crossref PubMed Scopus (137) Google Scholar, 27Li J. Woods S.L. Healey S. et al.Point mutations in exon 1B of APC reveal gastric adenocarcinoma and proximal polyposis of the stomach as a familial adenomatous polyposis variant.Am J Hum Genet. 2016; 98: 830-842Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar, 28van der Post R.S. Carneiro F. Emerging concepts in gastric neoplasia: heritable gastric cancers and polyposis disorders.Surg Pathol Clin. 2017; 10: 931-945Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar GAPPS patients with gastric cancer more often have gastric adenomas, FGPs, and PGAs with high-grade dysplasia.25Leone P.J. Mankaney G. Sarvapelli S. et al.Endoscopic and histologic features associated with gastric cancer in familial adenomatous polyposis.Gastrointest Endosc. 2019; 89: 961-968Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar Thus, although low-grade gastric foveolar-type dysplasia is not very alarming in FAP patients, extensive proximal gastric polyposis and possibly also the presence of PGAs (see later discussion) may be markers of an increased risk of proximal gastric cancer in FAP. In addition, it remains important to detect FAP patients with H pylori infection, gastric atrophy, and intestinal-type adenomas because these patients seem to be at increased risk for distal intestinal-type adenocarcinomas.29Leggett B. FAP: another indication to treat H pylori.Gut. 2002; 51: 463-464Crossref PubMed Scopus (7) Google ScholarPathologic Key Features•Cystically dilated oxyntic glands lined by parietal and chief cells•Lined by nondysplastic foveolar epithelium•Rarely foveolar-type dysplasia (mainly in FAP)Differential Diagnosis•Pyloric or oxyntic gland adenomas•Large FGPs can be difficult to distinguish from HPs•FGPs with dysplasia versus foveolar-type adenomasPitfall!Multiple FGPs (fundic gland polyposis) are associated with FAP and GAPPS. •Cystically dilated oxyntic glands lined by parietal and chief cells•Lined by nondysplastic foveolar epithelium•Rarely foveolar-type dysplasia (mainly in FAP) •Pyloric or oxyntic gland adenomas•Large FGPs can be difficult to distinguish from HPs•FGPs with dysplasia versus foveolar-type adenomas !Multiple FGPs (fundic gland polyposis) are associated with FAP and GAPPS. Gastric HPs are among the most common epithelial polyps of the stomach; incidences vary among populations and range between 15% and 75% of all gastric polyps.30Abraham S.C. Singh V.K. Yardley J.H. et al.Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy.Am J Surg Pathol. 2001; 25: 500-507Crossref PubMed Scopus (129) Google Scholar HPs are localized, nonneoplastic mucosal expansions consisting of elongated, tortuous, and cystically dilated foveolae supported by an edematous lamina propria with distended vessels. In contrast to colonic HPs, which are neoplastic polyps, gastric HPs are reactive lesions resulting from reparative and regenerative responses to mucosal injury. First, there is an ongoing healing and reparative response in the form of foveolar hyperplasia after mucosal injury and erosion. This hyperplastic reaction can end or persist and progress with the formation of an HP. Mostly the initial inflammation is caused by H pylori or autoimmune gastritis, although any agent causing chronic gastritis or mucosal erosion may lead to the formation of an HP. In addition, mucosal prolapse can result in HPs.31Gonzalez-Obeso E. Fujita H. Deshpande V. et al.Gastric hyperplastic polyps: a heterogeneous clinicopathologic group including a distinct subset best categorized as mucosal prolapse polyp.Am J Surg Pathol. 2011; 35: 670-677Crossref PubMed Scopus (17) Google Scholar HPs can be multiple, which is the case in 20% of patients.30Abraham S.C. Singh V.K. Yardley J.H. et al.Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy.Am J Surg Pathol. 2001; 25: 500-507Crossref PubMed Scopus (129) Google Scholar Gastric “inflammatory polyp” is a commonly used misnomer for an HP and should not be used in the stomach to avoid confusion with an inflammatory fibroid polyp. Hamartoma defines an overgrowth of normal tissue elements in their own native location. Hamartomatous gastric polyps are rare in the stomach and are, from a histopathological point of view, indistinguishable from HPs because they share the same morphology. Hamartomatous gastric polyps occur in the context of Peutz-Jeghers syndrome (PJS), juvenile polyposis syndrome (JPS), and Cowden (PTEN hamartoma tumor) syndrome.32Lam-Himlin D. Park J.Y. Cornish T.C. et al.Morphologic characterization of syndromic gastric polyps.Am J Surg Pathol. 2010; 34: 1656-1662PubMed Google Scholar HPs are mostly small, generally less than 2 cm, although sizes of up to 12 cm are reported. The polyps are usually solitary, smooth or lobulated, and can be sessile or pedunculated. There is often surface erosion. HPs cannot reliably be distinguished from small adenomas endoscopically. HPs are most common in the antrum (60%), but may arise throughout the stomach, including the cardia and gastroesophageal area.30Abraham S.C. Singh V.K. Yardley J.H. et al.Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy.Am J Surg Pathol. 2001; 25: 500-507Crossref PubMed Scopus (129) Google Scholar,33Abraham S.C. Singh V.K. Yardley J.H. et al.Hyperplastic polyps of the esophagus and esophagogastric junction: histologic and clinicopathologic findings.Am J Surg Pathol. 2001; 25: 1180-1187Crossref PubMed Scopus (43) Google Scholar HPs have a polypoid form and show elongated, branching, and cystically dilated foveolar glands (Fig. 5). The foveolar cells have a hyperplastic appearance with abundant mucinous cytoplasm. The glands may contain prominent globoid cells. There is crowding of foveolar cells, and glands may be tortuous or have a corkscrew appearance. The lamina propria can be edematous and moderately to heavily infiltrated by immune cells. In other cases, the lamina propria is more fibrotic with or without chronic inflammatory infiltrate. The surface of the polyp can be eroded and have a regenerative appearance with nuclear enlargement and depletion of cytoplasmic mucin.30Abraham S.C. Singh V.K. Yardley J.H. et al.Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy.Am J Surg Pathol. 2001; 25: 500-507Crossref PubMed Scopus (129) Google Scholar Small lesions may be best addressed as polypoid foveolar hyperplasia.31Gonzalez-Obeso E. Fujita H. Deshpande V. et al.Gastric hyperplastic polyps: a heterogeneous clinicopathologic group including a distinct subset best categorized as mucosal prolapse polyp.Am J Surg Pathol. 2011; 35: 670-677Crossref PubMed Scopus (17) Google ScholarFig. 5HP. (A) Low-power view of an HP, showing elongated, branching, and cystically dilated foveolar glands with abundant mucinous cytoplasm. The lamina propria is edematous and infiltrated by immune cells. (B) High-power view of the same polyp.View Large Image Figure ViewerDownload Hi-res image Download (PPT) HPs have an overlapping morphology with polyps arising in juvenile polyposis, Peutz-Jeghers (PJ) polyposis, and Cowden/PTEN hamartoma tumor syndrome (see Overview).32Lam-Himlin D. Park J.Y. Cornish T.C. et al.Morphologic characterization of syndromic gastric polyps.Am J Surg Pathol. 2010; 34: 1656-1662PubMed Google Scholar Many of the hamartomatous syndrome polyps lack specific histology, and to distinguish them from each other and from sporadic HPs based on only histology is unreliable. Therefore, one should think of the possibility of an underlying hamartomatous polyposis syndrome in the case of multiple gastric hyperplastic-type polyps but at the same time be cautious to establish a diagnosis of a polyposis syndrome based on gastric polyp pathologic condition alone.5Brosens L.A.A. Wood L.D. Offerhaus G.J. et al.Pathology and genetics of syndromic gastric polyps.Int J Surg Pathol. 2016; 24: 185-199Crossref PubMed S" @default.
• W3041704625 created "2020-07-16" @default.
• W3041704625 creator A5024569067 @default.
• W3041704625 creator A5025655629 @default.
• W3041704625 creator A5037416658 @default.
• W3041704625 date "2020-09-01" @default.
• W3041704625 modified "2023-10-09" @default.
• W3041704625 title "Gastric Epithelial Polyps" @default.
• W3041704625 cites W1506145248 @default.
• W3041704625 cites W1568900873 @default.
• W3041704625 cites W1678223592 @default.
• W3041704625 cites W1878924852 @default.
• W3041704625 cites W1967099788 @default.
• W3041704625 cites W1973141426 @default.
• W3041704625 cites W1974918697 @default.
• W3041704625 cites W1981410941 @default.
• W3041704625 cites W1981964922 @default.
• W3041704625 cites W1986518336 @default.
• W3041704625 cites W1992451009 @default.
• W3041704625 cites W1994076335 @default.
• W3041704625 cites W2000747571 @default.
• W3041704625 cites W2001831239 @default.
• W3041704625 cites W2002219266 @default.
• W3041704625 cites W2003063054 @default.
• W3041704625 cites W2016248025 @default.
• W3041704625 cites W2023709736 @default.
• W3041704625 cites W2036238354 @default.
• W3041704625 cites W2043634528 @default.
• W3041704625 cites W2045953814 @default.
• W3041704625 cites W2052670096 @default.
• W3041704625 cites W2058780680 @default.
• W3041704625 cites W2060266620 @default.
• W3041704625 cites W2064957416 @default.
• W3041704625 cites W2064992233 @default.
• W3041704625 cites W2069008582 @default.
• W3041704625 cites W2074352606 @default.
• W3041704625 cites W2081138569 @default.
• W3041704625 cites W2083126777 @default.
• W3041704625 cites W2083320982 @default.
• W3041704625 cites W2103635373 @default.
• W3041704625 cites W2105256330 @default.
• W3041704625 cites W2106893670 @default.
• W3041704625 cites W2109337378 @default.
• W3041704625 cites W2110750762 @default.
• W3041704625 cites W2120838811 @default.
• W3041704625 cites W2130501804 @default.
• W3041704625 cites W2140881019 @default.
• W3041704625 cites W2149775719 @default.
• W3041704625 cites W2150509079 @default.
• W3041704625 cites W2162077547 @default.
• W3041704625 cites W2188684296 @default.
• W3041704625 cites W2188696541 @default.
• W3041704625 cites W2211308751 @default.
• W3041704625 cites W2254544358 @default.
• W3041704625 cites W2323792012 @default.
• W3041704625 cites W2336910514 @default.
• W3041704625 cites W2523260315 @default.
• W3041704625 cites W2533575211 @default.
• W3041704625 cites W2565335586 @default.
• W3041704625 cites W2586267660 @default.
• W3041704625 cites W2586772563 @default.
• W3041704625 cites W2592263754 @default.
• W3041704625 cites W2625792577 @default.
• W3041704625 cites W2766904454 @default.
• W3041704625 cites W2768328317 @default.
• W3041704625 cites W2777420813 @default.
• W3041704625 cites W2791441244 @default.
• W3041704625 cites W2793875443 @default.
• W3041704625 cites W2800625068 @default.
• W3041704625 cites W2908361055 @default.
• W3041704625 cites W4243434735 @default.
• W3041704625 doi "https://doi.org/10.1016/j.path.2020.05.004" @default.
• W3041704625 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32773193" @default.
• W3041704625 hasPublicationYear "2020" @default.
• W3041704625 type Work @default.
• W3041704625 sameAs 3041704625 @default.
• W3041704625 citedByCount "8" @default.
• W3041704625 countsByYear W30417046252021 @default.
• W3041704625 countsByYear W30417046252022 @default.
• W3041704625 countsByYear W30417046252023 @default.
• W3041704625 crossrefType "journal-article" @default.
• W3041704625 hasAuthorship W3041704625A5024569067 @default.
• W3041704625 hasAuthorship W3041704625A5025655629 @default.
• W3041704625 hasAuthorship W3041704625A5037416658 @default.
• W3041704625 hasBestOaLocation W30417046251 @default.
• W3041704625 hasConcept C111368507 @default.
• W3041704625 hasConcept C121608353 @default.
• W3041704625 hasConcept C126322002 @default.
• W3041704625 hasConcept C127313418 @default.
• W3041704625 hasConcept C142724271 @default.
• W3041704625 hasConcept C203635412 @default.
• W3041704625 hasConcept C2779422922 @default.
• W3041704625 hasConcept C2910151845 @default.
• W3041704625 hasConcept C71924100 @default.
• W3041704625 hasConceptScore W3041704625C111368507 @default.
• W3041704625 hasConceptScore W3041704625C121608353 @default.
• W3041704625 hasConceptScore W3041704625C126322002 @default.
• W3041704625 hasConceptScore W3041704625C127313418 @default.

• next