Materiały źródłowe

• #1 Novel classification of gastric polyps: The good, the bad and the ugly

  https://wjgnet.com/1007-9327/full/v30/i31/3640.htm

  Gastric polyps (GPs) are luminal lesions that arise above the mucosal surface. This simple definition encompasses a wide range of lesions with varying histology and neoplastic potential. The detection of GPs is becoming increasingly common in clinical practice, with an estimated current incidence of 6% of upper gastrointestinal endoscopic procedures in the United States. This trend likely underestimates the actual occurrence, as the majority of GPs are asymptomatic, reflecting the widespread access to esophago-gastroduodenoscopy (OGD) in recent years. […] During an OGD, it is important to thoroughly examine the gastric mucosa and any polyps encountered using white light and narrow band imaging (NBI) to classify their morphology according to the Paris classification. Chromoendoscopy may be used in some occasions. Most GPs have a typical endoscopic appearance in the stomach and can be associated with diseases such as Helicobacter pylori (H. pylori) infection, autoimmune gastritis, or inherited polyposis syndrome. However, it is essential to conduct histological examination of GPs and the surrounding mucosa for an accurate assessment and diagnosis. While most polyps are non-neoplastic and do not necessitate treatment, some GPs pose a risk of malignancy or are already malignant at the time of endoscopic examination. Therefore, a deep understanding of the diagnosis, classification, and management of GPs is crucial for patient prognostication.

• #2 Gastric Polyps: A Review of Clinical, Endoscopic, and Histopathologic Features and Management Decisions

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3992058/

  The increasing use of endoscopy has led to more discernable abnormalities in the stomach, including polyps. […] Gastric polyps most frequently originate in the mucosa but encompass a broad spectrum of pathologic conditions that may even be submucosal or extrinsic. […] These polyps are caused by an activating mutation of the beta-catenin gene, which is involved in cell growth signaling pathways. […] Since 1993, there have been multiple reports of the role of PPIs in the development of gastric polyps. […] The pathogenesis of type I neuroendocrine tumors is as follows: the autoimmune destruction of parietal cells leads to reduced gastric acid production and loss of feedback inhibition of gastrin secretion in the antral G cells. […] The resulting high levels of gastrin stimulate ECL cells to proliferate, which appear as multiple small nodules in the body of the stomach.

• #3 Stomach Polyps: Symptoms, Causes, Types & Treatment

  https://my.clevelandclinic.org/health/diseases/17797-stomach-polyps

  Stomach polyps are tiny growths on the inside walls of your stomach. Different types have different causes. The most common types aren’t precancerous, but some less common types are. Your healthcare provider will remove them and send them to a lab for analysis. […] Stomach polyps are growths on the inside lining of your stomach. They’re also called gastric polyps. Polyps are a type of tumor that grows out of the mucous lining inside your hollow organs, like the ones in your gastrointestinal tract. Stomach polyps are usually benign, but some can become cancerous. […] Many of the most common types of stomach polyps have little to no cancerous potential. Some types are precancerous, so they usually aren’t yet cancerous when a healthcare provider finds them. Polyps take a long time to turn into cancer. Healthcare providers remove them to prevent this from happening.

• #4 Gastric Polyp – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560704/

  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. […] 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. 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. […] Gastric polypoid lesions reflect a range of pathophysiology.

• #5 Polyps of the Stomach | Abdominal Key

  https://abdominalkey.com/polyps-of-the-stomach/

  Gastric polyps are identified in as many as 6.3% of upper gastrointestinal (GI) endoscopic procedures. Polyps may develop as a result of epithelial or stromal cell hyperplasia, inflammation, ectopia, or neoplasia. […] More than 85% of hyperplastic polyps occur in a background of chronic gastritis, and this observation has led some to conclude that the lesions develop as a consequence of an exaggerated mucosal response to tissue injury and inflammation. It is thought that gastritis initiates the process of injury and that the mucosal healing response results in a stepwise progression through phases of foveolar hyperplasia and polypoid foveolar hyperplasia to the formation of a hyperplastic polyp. […] The tendency of hyperplastic polyps to occur more proximally in the stomach in the setting of autoimmune gastritis (which involves the corpus of the stomach) than in other types of gastritis supports the hypothesis that hyperplastic polyps develop as a consequence of chronic mucosal injury.

• #6 Gastric Polyps – Symptoms, Causes, Types, Treatment PACE Hospitals – Best Hospitals in Hitech City, Hyderabad, India | Near Madhapur, Kukatpally, KPHB, Kondapur, Gachibowli, Jubilee Hills, Banjara HillsPACE Hospitals Contact Number for ap

  https://www.pacehospital.com/gastric-polyps-symptoms-causes-types-diagnosis-and-treatment

  Hyperplastic polyps develop as a result of chronic gastric inflammation, often triggered by Helicobacter pylori (H. pylori) infection or chronic gastritis. […] These are precancerous lesions caused by dysplastic changes in the gastric epithelium, often found in patients with atrophic gastritis and intestinal metaplasia. […] The inflammatory fibroid polyps are rare, benign lesions of unknown exact cause, though often linked to chronic irritation and reactive hyperplasia of connective tissue. […] These develop due to chronic hypergastrinemia, which stimulates enterochromaffin-like (ECL) cell proliferation and small neuroendocrine tumor formation. […] Gastric polyps develop due to various factors, including chronic gastric inflammation, H. pylori infection, prolonged proton pump inhibitor (PPI) use, genetic syndromes like familial adenomatous polyposis (FAP), and dietary influences. […] Most gastric polyps are benign, but some, especially adenomatous polyps, have the potential to become cancerous. […] Regular monitoring is essential for identifying high-risk polyps.

• #7 Polyps of the Stomach – Clinical Tree

  https://clinicalpub.com/polyps-of-the-stomach/

  Gastric polyps are identified in up to 6.3% upper gastrointestinal (GI) endoscopic procedures. They may develop as a result of epithelial or stromal cell hyperplasia, inflammation, ectopia, or neoplasia. […] The prevalence of hyperplastic polyps is predominantly related to the rate of Helicobacter pylori infection and to the geographic locale. […] More than 85% of hyperplastic polyps occur in patients with chronic gastritis, and this has led to the hypothesis that these lesions develop as a consequence of an exaggerated mucosal response to tissue injury and inflammation. […] It is believed that inflammation initiates the process of injury and that the mucosal healing response results in a stepwise progression through phases of foveolar hyperplasia and polypoid foveolar hyperplasia to, eventually, the formation of a hyperplastic polyp.

• #8 Gastric hyperplastic polyps: a narrative review – Zouridis – Digestive Medicine Research

  https://dmr.amegroups.org/article/view/8601/html

  Multiple risk factors have been linked to GHP pathogenesis and development, including Helicobacter pylori (H. pylori) infection, atrophic and autoimmune gastritis. […] The primary etiology of GHP formation has thus far been linked to hypergastrinemia. Elevated gastrin levels have been tied to H. pylori infection, long term PPI use, reactive gastritis, chemical gastritis, autoimmune gastritis or background metaplasia. […] Elevated gastrin levels, either due to an inability to produce acid, such is the case with autoimmune gastritis, or as a secondary response to PPI therapy has well known tropic and pro-carcinogenic effects, resulting in oxyntic cell atrophy which leads to hyperplasia of acid producing cells and eventual polyp formation. […] H. pylori infection is probably the most well described risk factor for GHP development, by increasing serum gastrin levels as discussed previously.

• #9 Proton Pump Inhibitor-Related Gastric Mucosal Changes

  https://www.gutnliver.org/journal/view.html?doi=10.5009/gnl20036

  An important issue with long-term PPI usage is that these drugs raise the level of the peptide hormone gastrin; as a result of the homoeostatic response of antral G cells, to the reduced acidity of gastric juice. Gastrin exerts trophic effects on the entire gastrointestinal tract tissue, including on both parietal and enterochromaffin-like cells distributed throughout the oxyntic mucosa. It has been reported that long-term PPI use also induces histopathological changes such as protrusion of parietal cells into the gland lumen and cystic dilation of gastric fundic glands. PPI-induced endoscopic features such as formation of fundic gland polyps, hyperplastic polyps, multiple white and flat elevated lesions, cobblestone-like mucosa, and black spots have been reported in recent studies. […] Chronic PPI use is associated with changes in the morphology of gastric parietal cells, including an increase in cell size and number and is associated with enterochromaffin-like cell proliferation in the gastric mucosa. Histopathologically, parietal cell enlargement can easily be identified as a convex bulging and swelling of the apical membrane into the lumen of oxyntic glands. This so-called parietal cell protrusion (PCP) appears as a serrated contour of the internal glands. Gastric hydrochloric acid accumulates in parietal cells due to inhibition of its active release from the secretory canaliculi by PPIs, which results in PCP. Development of this aberrant cellular morphology shows a positive correlation with hypergastrinemia. PCP further leads to cystic dilation of fundic glands and cytoplasmic vacuolation. Cystic dilation of fundic glands may result from outflow-obstruction. This is attributable to glandular isthmus blockage due to protrusion of parietal cells and plugging by mucus secreted from proliferating foveolar cells, secondary to PPI-induced hypergastrinemia. The resulting cystic dilation has the potential to further enlarge and progress to fundic gland polyp formation. Previous studies have reported that fundic gland dilatation occurred between 8 months and 60 months after starting PPIs, while a recent meta-analysis concluded that long-term use of PPIs (1 year) was associated with an increased risk of formation of fundic gland polyps.

• #10 What are stomach polyps? | MD Anderson Cancer Center

  https://www.mdanderson.org/cancerwise/5-questions-about-stomach-polyps–answered.h00-159538956.html

  These small masses inside the lining of the stomach can lead to cancer, but more often theyre benign. […] Its not always clear what causes stomach polyps especially if theyre not causing symptoms. But, Paul Mansfield, M.D., says, there are factors that can increase your risk of developing them The most common factor for stomach polyps is inflammation, which can come from different sources. […] One of the main causes of stomach polyps in the U.S. is use of proton pump inhibitors. These medications are available over-the-counter to help suppress stomach acid to treat heartburn and other common gastric issues. […] Your stomach needs those acids to maintain balance and work properly. Without acid, some cells in the stomach work overtime to increase production of a hormone called gastrin, which in turn encourages cells to increase acid production in your stomach.

• #11 Gastric Polyp – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560704/

  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. […] 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.

• #12 Hyperplastic Polyps (Stomach) | SpringerLink

  http://link.springer.com/10.1007/978-3-319-40560-5_1636

  Hyperplastic polyps are localized, non-neoplastic mucosal expansions consisting of elongated, tortuous, and cystically dilated foveolae supported by an edematous lamina propria and distended vessels. Hyperplastic polyps arise probably as a result of reparative and regenerative responses to mucosal injury. First there is ongoing healing and a 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 a hyperplastic polyp. The common causative agents of mucosal injury are Helicobacter pylori and autoimmune gastritis leading to chronic gastritis, although any agent causing chronic gastritis may be a predisposing condition. H. pylori has been shown to increase the expression of cyclo-oxygenase-2 (COX-2), interleukin 1-beta, and hepatocyte growth factor in stromal cells, which…

• #13 Gastric hyperplastic polyps: a narrative review – Zouridis – Digestive Medicine Research

  https://dmr.amegroups.org/article/view/8601/html

  However, persistent H. pylori infection may also lead to increased cytokine production and chronic active gastritis with subsequent epithelial cell proliferation. […] Based on current data, an estimated proportion of 10.5% of atrophic gastritis patients may develop GHP. […] The underlying mechanism is, again, hypothesized to be hypergastrinemia. […] However, and despite the exact cause of autoimmune gastritis is unknown, this condition leads to complete atrophy of the oxyntic glands, resulting in significant secondary hypergastrinemia when compared to other causes of atrophic gastritis. […] PPI leading to hypergastrinemia and as such to increased risk for polyp formation has been heavily investigated. […] Zeng et al. described an increased incidence of gastric polyps in GERD patients with most of them being GHP.

• #14 Frontiers | Diffuse benign inflammatory gastric polyps: A rare case in a young female: Case report and review of the literature

  https://www.frontiersin.org/journals/surgery/articles/10.3389/fsurg.2022.1090622/full

  Gastric polyps are one of the most common clinical diseases arising from the mucosal surface of the stomach. […] The pathogenesis of inflammatory polyps is indistinct, with several research reports suggesting that its pathogenesis is linked to Helicobacter pylori and chronic inflammatory infections. […] Infection with H. pylori promoted an inflammatory response via interleukin-1 and hepatocyte growth factors, leading to gastric epithelial cell proliferation and thus inflammatory polyp formation.

• #15 Polyps of the Stomach – Clinical Tree

  https://clinicalpub.com/polyps-of-the-stomach/

  The tendency of hyperplastic polyps to occur more proximally in the stomach in patients with autoimmune gastritis compared with other types of gastritis supports the hypothesis that hyperplastic polyps develop as a consequence of chronic mucosal injury. […] The H. pylori CagA protein may have a more direct role because expression of CagA in the gastric mucosa of transgenic mice produces hyperplastic polyps. […] The principle differential diagnosis of a hyperplastic polyp with dysplasia is a large and eroded polyp with marked regeneration. […] Dysplasia and carcinoma tend to occur in patients older than 50 years of age as well. […] Some data suggest that TP53 mutations, chromosomal loss, and chromosomal amplification may be important in the development of dysplasia and carcinoma in gastric hyperplastic polyps.

• #16 Fundic gland polyp – Libre Pathology

  https://librepathology.org/wiki/Fundic_gland_polyp

  Fundic gland polyp is a relatively common pathology of the stomach. It is associated with familial adenomatous polyposis and proton pump inhibitor use. […] Associated with chronic proton pump inhibitors (PPI) use — approximately 4x risk. […] PPIs may cause fundic gland polyposis – extremely rare (two reported cases as of 2012). […] Fundic gland polyps are associated with familial adenomatous polyposis (FAP), gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS), and proton pump inhibitor (PPI) use. PPI use appears to be the most likely explanation in this case, in the context of the provided history; however, FAP and GAPPS should be considered clinically. […] Fundic gland polyps are reported in association with proton pump inhibitor use, familial adenomatous polyposis (FAP), and gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS). The possibility of FAP and GAPPS should be considered.

• #17 Fundic gland polyposis – Wikipedia

  https://en.wikipedia.org/wiki/Fundic_gland_polyposis

  The development of polyps depends on the underlying disorder. In sporadic cases of FGPs, more than 90% of patients have activating mutations in the -catenin gene, so that they may be considered „neoplastic” polyps. […] In familial adenomatous polyposis, the abnormality is a mutation in the APC gene, resulting in its inactivity. Attenuated FAP can occur from other mutations in the APC gene, and causes a phenotype wherein colonic polyps may be few in number. […] Both the -catenin gene and the APC gene are involved in the same cell growth signalling pathway, but the APC gene is known to have a significantly higher association with the development of colorectal tumors.

• #18 Fundic gland polyps: Should my patient stop taking PPIs? | Cleveland Clinic Journal of Medicine

  https://www.ccjm.org/content/90/3/157

  Fundic gland polyps (FGPs) associated with proton pump inhibitors (PPIs) are generally considered benign, and patients without high-risk features (ie, more than 20 FGPs or polyp size greater than 1 cm) can be advised to continue taking the PPI if there is a clear indication for its use. […] Long-term PPI use can promote development of FGPs in the stomach because the decrease in stomach acidity leads to increased production of gastrin. Gastrin has trophic effects that lead to parietal cell and enterochromaffin-like cell hyperplasia and the formation of fundic gland cysts and polyps. […] Sporadic or PPI-associated FGPs exhibit activating beta-catenin gene mutations and rarely show dysplasia. […] PPI-associated FGPs have not been linked to an increased risk of malignant transformation compared with the risk in the general population. […] Evidence demonstrates regression of FGPs if PPIs are stopped, even if they were large in size, and endoscopic follow-up to confirm regression is unnecessary.

• #19 Large Fundic Gland Polyps in the Stomach – Gastroenterology & Hepatology

  https://www.gastroenterologyandhepatology.net/archives/march-2016/large-fundic-gland-polyps-in-the-stomach/

  A colonoscopy and esophagogastroduodenoscopy (EGD) were performed for symptom workup. The EGD showed approximately 30 large pedunculated polyps in the gastric body and fundus. The most likely etiology was thought to be the prolonged use of proton pump inhibitor (PPI) therapy. […] Mutations in the beta-catenin gene may be the causative factor in the development of sporadic FGPs. […] PPIs have been the most commonly prescribed drugs since they were introduced in 1988. There has been controversy regarding the role of PPIs in the formation of FGPs. In 1992, Graham was the first to describe the risk of gastric polyp formation due to PPI use. […] No clear mechanism has been found to explain the possible pathogenesis of FGPs due to PPI use. Hypergastrinemia due to PPI use was thought to be a probable cause of gastric mucosal hypertrophy and polyp formation. […] However, the use of PPIs for more than 2 years may increase the risk of FGP formation. […] No surveillance is required for FGPs because they are not premalignant lesions. […] In conclusion, this case demonstrates a possible association between long-term PPI use and large FGPs.

• #20 How to manage gastric polyps

  https://www.ijgii.org/journal/view.html?doi=10.18528/gii150035

  They are more commonly seen in western countries because of the low prevalence of H. pylori and more liberal use of PPI. […] A long term use of PPI (more than 1 year) is associated with FGP. […] Regression of FGPs is seen after discontinuation of PPI. […] Alteration in beta-catenin mutation is seen in sporadic FGP while germ line APC mutation and subsequent somatic mutation are seen in syndromic FGP. […] The pathogenesis involves autoimmune destruction of parietal cells which leads to loss of feedback inhibition of gastrin and enterochromaffin cell proliferation appearing as small nodules in the body of the stomach.

• #21 Stomach Polyps: Causes, Treatment, and more

  https://www.healthline.com/health/stomach-polyps

  Polyps are bits of extra cells that can grow in many of your tissues. Gastric polyps, or stomach polyps, are growths that develop in the lining of your stomach. […] Like polyps, cancers develop due to an unusual growth of cells. With cancer, cells can grow too fast, eventually taking over and destroying healthy tissues or organs. An estimated 6 to 10 percent of stomach polyps have the potential to become cancerous. […] Adenomatous polyps can develop anywhere in the stomach and tend to carry the highest risk of cancer. A 2013 review suggests they account for about 6 to 10 percent of all gastric polyps. […] The risk of cancer with adenomatous polyps depends on the specific cells that make up the polyp, and usually the size of the polyp. […] Larger polyps tend to carry higher risks of developing into cancers. If your doctor finds a polyp that’s larger than 10 millimeters in diameter during an endoscopy, they may decide to remove it right away. […] These polyps have a high risk of developing into cancer and are usually removed. If they are not removed during the initial endoscopy, your doctor will likely repeat the procedures to remove the polyp within 6 to 12 months from your first scope.

• #22 What to Know About Stomach Polyps

  https://www.verywellhealth.com/stomach-polyps-8737316

  Stomach polyps, also called gastric polyps, are abnormal tissue growths that develop in your stomach lining. Over 85% of stomach polyps are benign (noncancerous), and many don’t cause any symptoms. However, some stomach polyps are a sign of gastric cancer. […] Most stomach polyps are benign and asymptomatic. However, some stomach polyps are malignant (cancerous) and can lead to serious health complications. […] Adenomatous polyps, or adenomas, make up 6% to 10% of stomach polyps found in the United States. Particularly if they are large, adenomatous polyps are associated with a significantly increased risk of neoplasia (out-of-control cell growth), malignancy, and invasive gastric cancer. […] Like GHPs, adenomatous polyps are often caused by atrophic gastritis, whether due to a bacterial infection called Helicobacter pylori (H. pylori) infection or an autoimmune disorder.

• #23

  https://journals.lww.com/ijpm/fulltext/2021/64001/histomorphological_analysis_of_gastric_polyps.11.aspx

  Epigenetic and genetic mutations are known in the multistep process of carcinogenesis. Chronic atrophic gastritis to intestinal metaplasia progressing to gastric intestinal type of adenocarcinoma on the background of H pylori infection has been documented to be one of the pathways for gastric carcinogenesis. […] Since gastric and colon tumors share common genetic pathways, the pathogenesis for some of the gastric carcinoma may be on the lines similar to colonic adenoma-carcinoma sequence. […] Gastric adenomas are a preneoplastic condition. In this study, there were nine (2%) adenomatous polyps. All of them were less than 1 cm in size having low-grade dysplasia. This finding is similar to the study done by Wang FW et al. during 20152016 from Taiwan. […] We should be aware of adenomatous foci in benign polyps, which may progress to gastric carcinoma. […] With rising incidence of gastric carcinoma, identification of gastric polyps on endoscopy with biopsy can prevent progression to carcinogenesis.

• #24 Gastric Polyp – MD Searchlight

  https://mdsearchlight.com/gut-health/gastric-polyp/

  With adenomas, another type of polyp, the risks of developing them rise with age and long-term inflammation or irritation of the tissue. This can result in a condition known as intestinal metaplasia, where the cells lining the digestive tract change form, which then increases the risk for the polyp to turn into cancer. This could happen because of acquired mutations that change the way the p53 and Ki-67 genes work. […] Gastric polyps are typically located in the fundus (upper part) of the stomach and are more common with increasing age. […] Gastric polyps can block food passage through the stomach. […] Certain changes in eating habits and lifestyle can help reduce the risk of developing these polyps. This may include reducing the consumption of alcohol, quitting smoking, eating less fatty foods, and incorporating more fiber into the diet. Essentially, these changes can help in reducing the risk of stomach cancer to some extent.

• #25 Stomach polyps – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/stomach-polyps/symptoms-causes/syc-20377992

  Stomach polyps form in response to damage to your stomach lining. The most common causes of stomach polyps are: […] Long-lasting stomach inflammation. Also known as gastritis, this condition can cause the formation of hyperplastic polyps and adenomas. Hyperplastic polyps are unlikely to become cancerous, although those larger than about 2/5 inch (1 centimeter) carry a greater risk. […] Adenomas are the least common type of stomach polyp but the type most likely to become cancerous. For that reason, they are generally removed. […] Familial adenomatous polyposis. This rare, inherited syndrome causes certain cells on the stomach’s inner lining to form a type of polyp called fundic gland polyp. When associated with this syndrome, fundic gland polyps are removed because they can become cancerous. Familial adenomatous polyposis also can cause adenomas.

• #26 Gastric hyperplastic polyps: a narrative review – Zouridis – Digestive Medicine Research

  https://dmr.amegroups.org/article/view/8601/html

  While GERD has been described as possible association with H. pylori, Livovsky et al., found that patients with chronic liver disease develop GHP more often and at higher numbers when compared to GERD patients, revealing a strong relationship between chronic liver disease (or its complications) and GHP development. […] Even though GHP are considered benign neoplasms of the gastric mucosa, they have been linked to malignant potential in multiple studies. […] The risk for malignant transformation has been evaluated in detail with estimations mainly between 0.66.6% while a few studies suggest higher rates, up to 8.6%. […] The exact mechanism of malignant transformation has yet to be understood but multiple studies evaluating the underlying histopathology and immunochemistry tried to reveal possible underlying pathogenetic mechanisms of hyperplasia to carcinoma sequence.

• #27 The Clinicopathological Features of Gastric Hyperplastic Polyps with Neoplastic Transformations: A Suggestion of Indication for Endoscopic Polypectomy

  https://www.gutnliver.org/journal/view.html?volume=3&number=4&spage=271&year=2009

  The mechanism of carcinogenesis in gastric hyperplastic polyps is still unknown. However, it has been suggested that malignant transformations of gastric hyperplastic polyps arise from the dysplastic epithelium rather than directly from the hyperplastic epithelium because cancerous lesions exist either in the dysplastic lesions or adjacent to the dysplastic lesions. In this study, adenomatous changes were observed around the cancerous component in all of the gastric hyperplastic polyps with malignant transformations. Therefore, our study supports the previous findings that cancer cells arise from dysplastic areas in hyperplastic polyps rather than directly from the non-dysplastic hyperplastic epithelium. […] In our study, neoplastic transformations were more frequently found in gastric hyperplastic polyps larger than 1 cm than in polyps smaller than 1 cm. Other studies also showed that most hyperplastic polyps harboring cancer were larger than 1 cm in size. Therefore, EP should be considered for gastric hyperplastic polyps larger than 1 cm to avoid the risk of missing lesions with neoplastic transformations, although attention should also be paid to hyperplastic polyps less than 1 cm.

• #28 :: JGC :: Journal of Gastric Cancer

  https://jgc-online.org/DOIx.php?id=10.5230/jgc.2013.13.2.117

  Gastric hyperplastic polyps are generally considered benign lesions, although rare cases of adenocarcinoma have been reported. […] Although, the underlying mechanism of carcinogenesis in gastric hyperplastic polyps is still uncertain, most malignant polyps are seen to originate from dysplastic epithelium rather than from hyperplastic epithelium. […] Hyperplastic polyps are the most common type of non-neoplastic gastric polyps. Although, the pathogenesis of hyperplastic polyps has not been established, it has been suggested that reparative and regenerative responses contribute significantly. […] Hyperplastic polyps thus have some malignant potential. […] Although, the exact mechanism of carcinogenesis in gastric hyperplastic polyps is still uncertain, malignant changes in polyps are thought to arise from dysplastic epithelium rather than from hyperplastic epithelium. […] A few previous studies of gastric hyperplastic polyps have theorized that malignant changes develop via a hyperplasia-dysplasia-carcinoma sequence. […] This case and our findings support the existing hypothesis of a sequential progression from a benign polyp to cancer.

• #29 Gastric hyperplastic polyps: a narrative review – Zouridis – Digestive Medicine Research

  https://dmr.amegroups.org/article/view/8601/html

  Irrespective of the underlying mechanism, multiple risk factors have been associated with neoplasia development in GHP. Older age, number of GHP detected, size, lobulation, pedunculated shape are proven to have positive correlation with dysplasia/neoplasia presence within GHP. […] H. pylori infection is also associated with increased risk for dysplasia/neoplasia development within GHP, while eradication of the organism may even prevent malignant transformation. […] Finally, given their association with H. pylori infection, autoimmune gastritis, increased gastrin levels and gastric atrophy, GHP presence has also been identified as marker indicating high risk for gastric carcinoma development even in other stomach locations.

• #30 Gastric Polyp – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560704/

  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. […] 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 -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 -catenin protein in affected cells.

• #31 Gastric Polyps | Saint Luke’s Health System

  https://www.saintlukeskc.org/health-library/gastric-polyps

  Adenomatous polyps have a high risk of turning into cancer. Because of this, your healthcare provider will likely want to remove them. […] The main complication of gastric polyps is stomach cancer. The following is a list of some of the main types of gastric polyps and their cancer risk. […] You may be able to lower your risk for new gastric polyps. For instance, your healthcare provider may tell you to stop using proton-pump inhibitor medicines if you have fundic polyps. You may be able to reduce your risk for hyperplastic polyps if you take an antibiotic for an H. pylori infection.

• #32 Stomach polyps | UM Health-Sparrow

  https://www.uofmhealthsparrow.org/departments-conditions/conditions/stomach-polyps

  Regular use of certain stomach medications. Fundic gland polyps are common among people who regularly take proton pump inhibitors to reduce stomach acid. These polyps are generally small and aren’t a cause for concern. […] A fundic gland polyp with a diameter larger than about 2/5 inch (1 centimeter) carries a small risk of cancer. Your health care provider might recommend stopping proton pump inhibitors or removing the polyp or both. […] Helicobacter pylori (H. pylori) bacteria are a common cause of the gastritis that contributes to hyperplastic polyps and adenomas. […] Treatment depends on the type of stomach polyps you have: […] Adenomas. These polyps can become cancerous and are usually removed during endoscopy. […] Polyps associated with familial adenomatous polyposis. These are removed because they can become cancerous. […] Treating an H. pylori infection can make hyperplastic polyps disappear and also might stop polyps from recurring.

• #33 Stomach polyps – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/stomach-polyps/symptoms-causes/syc-20377992

  Regular use of certain stomach medications. Fundic gland polyps are common among people who regularly take proton pump inhibitors to reduce stomach acid. These polyps are generally small and aren’t a cause for concern. […] A fundic gland polyp with a diameter larger than about 2/5 inch (1 centimeter) carries a small risk of cancer. Your health care provider might recommend stopping proton pump inhibitors or removing the polyp or both.

• #34 What are stomach polyps? | MD Anderson Cancer Center

  https://www.mdanderson.org/cancerwise/5-questions-about-stomach-polyps–answered.h00-159538956.html

  Infections of the bacterium H. pylori are not as common in the U.S. as they are in other parts of the world, but they can also increase your risk of developing polyps and some cancers. […] Genetics may play a role in stomach polyps, too. A genetic condition called familial adenomatous polyposis, or FAP, is usually associated with developing polyps in the colon but can also increase your risk of developing polyps in the stomach and small intestine. […] Hyperplasltic polyps can be caused by conditions like gastritis and H. pylori. These polyps can occur all over the stomach and can become cancerous if left untreated. […] Antibiotics targeting H. pylori can relieve hyperplastic polyps and may even eliminate cancerous polyps in some cases. Once the infection goes away, the cancer can go away, too, Mansfield says.

• #35 Stomach Polyps: Symptoms, Causes, Types & Treatment

  https://my.clevelandclinic.org/health/diseases/17797-stomach-polyps

  Stomach polyps that are related to hereditary syndromes are genetic disorders. But sporadic stomach polyps are caused by a combination of genetics and other factors. That is, different genetic mutations create different types of polyps, but other factors seem to be involved in triggering these mutations. […] Chronic gastritis, inflammation in your stomach lining, can be erosive or nonerosive. Erosive gastritis is more common and is usually caused by chemical erosion or a chronic infection, like H. pylori. Nonerosive gastritis can lead to atrophy of your stomach lining (atrophic gastritis), which causes different cellular changes. Both kinds are related to different tumors, particularly hyperplastic polyps, adenomas, inflammatory fibroids and neuroendocrine tumors. […] Proton pump inhibitors are commonly prescribed to reduce gastric acid for people with chronic indigestion and acid reflux. Using them often for a long time can interfere with the way your stomach lining works. When the medication stops certain cells from producing acid, other cells start to overproduce to try and make up for it. This is a common cause of benign fundic gland polyps and also, occasionally, gastric neuroendocrine tumors.

• #36 Proton Pump Inhibitor-Related Gastric Mucosal Changes

  https://www.gutnliver.org/journal/view.html?doi=10.5009/gnl20036

  PPI-induced hypergastrinemia possibly also causes foveolar epithelial hyperplasia, which generally presents as hyperplastic polyps. This may also present as multiple white and flat elevated lesions. Therefore, hyperplastic polyps and multiple white and flat elevated lesions are considered as endoscopic features of foveolar epithelial hyperplasia, caused by chronic PPI consumption.

• #37 Novel classification of gastric polyps: The good, the bad and the ugly

  https://www.wjgnet.com/1007-9327/full/v30/i31/3640.htm

  Our new classification of gastrointestinal polyps is based on categorizing them into three groups according to their likelihood of becoming malignant: „Good” [polyps that generally do not progress to cancer, such as fundic GPs (FGPs), inflammatory fibroid polyps (IFPs), and ectopic pancreas (EP)], „bad” [polyps that pose a risk of malignancy, such as large hyperplastic polyps, adenomas, type 1 and 2 neuroendocrine tumors, and hamartomatous polyps (HaPs)], and „ugly” [the most aggressive and invasive polyps, such as type 3 neuroendocrine tumors and early gastric cancer (EGC)]. We aim to provide descriptions of the endoscopic appearance, pathology, treatment, and follow-up for different gastrointestinal polyps, as well as a clinical management flowchart.

• #38 CoxHealth | Gastric Polyps

  https://www.coxhealth.com/condition/gastric-polyps/

  Having many gastric polyps can also cause problems. For instance, familial adenomatous polyposis causes polyps to grow all along your digestive tract. This leads to a very high risk for colon cancer. […] You may be able to lower your risk for new gastric polyps. For instance, your health care provider may have you stop using proton-pump inhibitor medicines if you have fundic polyps. You may be able to reduce your risk for hyperplastic polyps if you take an antibiotic for an H. pylori infection.

• #39 Histologic Classification of Gastric Polyps | SpringerLink

  https://link.springer.com/chapter/10.1007/978-3-642-66481-6_3

  In all papers dealing with polyps of the gastro-intestinal tract the term polyp is defined in the introductory remarks. […] This misinterpretation can be counteracted if the histologic structure and the pathogenesis are the basis for the nomenclature of gastric polyps. […] Gastric polyps have a different histogenesis compared with large bowel polyps so that one cannot expect mucosal polyps in the stomach to grow the same way as in the colon. […] Neglect of this fact has, in my opinion, not only led to confusion in terminology but also to clinical misinterpretation.

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