Changing Trends in Gastric Polyps

Velazquez-Dohorn, M.; López-Durand, C.F.; Gamboa‐Domínguez, Armando

doi:10.24875/ric.17002430

Cited by 19 publications

(16 citation statements)

References 12 publications

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“…Gastric hyperplastic polyp (HP), which is usually associated with H pylori infection in humans, develops in the context of chronic inflammation 62 . Fundic gland polyp (FGP), a major human tumor, is a hyperplasia that is not associated with either inflammation or H pylori infection, and is considered to be different from the inflammation-related process such as that seen in the stCldn18–/– mice 63 . Another disease, Peutz-Jeghers polyp (PJP), is an autosomal-dominant inherited disorder characterized by hamartoma in the digestive tract, including gastric tumors, and also has a different disease process from that seen in the stCldn18–/– mice 64 …”

Section: Resultsmentioning

confidence: 99%

Deficiency of Stomach-Type Claudin-18 in Mice Induces Gastric Tumor Formation Independent of H pylori Infection

Suzuki

Sentani

Tanaka

et al. 2019

Cellular and Molecular Gastroenterology and Hepatology

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Background & Aims Epithelial cells are joined by tight junctions (TJs) to form a cell sheet. In the stomach, epithelial cell sheet forms an essential barrier against gastric material, including gastric acid. Although the decreased expression of stomach-type claudin-18 ( stCldn18 ), a TJ protein, is generally observed in human gastritis and gastric cancer, its pathological roles are not fully understood. We previously reported that mice lacking stCldn18 ( stCldn18-/- ) exhibit gastric acid leakage through TJs, which induces active gastritis at a young age. Here, we examined the gastric pathologies in mice after long-term stCldn18 deficiency. Methods The gastric pathologies in stCldn18-/- mice were sequentially analyzed from youth to old age, and compared to those in humans. To examine the relationship between stCldn18 deficiency-induced gastric pathologies and Wnt-dependent tumorigenesis, we generated Wnt1 -overexpressing stCldn18-/- mice. Results StCldn18-/- mice developed chronic active gastritis at middle age, with expression of the chemoattractant CCL28. At old age, 20-30% of these mice developed gastric tumors with CXCL5 expression, indicative of EMT. In this process, spasmolytic polypeptide-expressing metaplasia (SPEM) cells appeared. Increased expressions of CD44-variants, TLR2, and CXCL5 indicated age-dependent changes in cell characteristics. Some features of the s tCldn18-/- mouse gastric tumorigenesis resembled H pylori -infection-related human carcinogenesis. The gastric tumorigenesis was accelerated in Wnt1 -overexpressing stCldn18-/- mice, indicating that Wnt is involved in the s tCldn18-/- mouse gastric tumorigenesis. Conclusions StCldn18 deficiency induced gastric tumorigenesis in mice without H pylori infection. Our findings revealed that several signaling networks, including the cytokine-, stemness-, and Wnt-signaling pathways, may be activated under the stCldn18 -deficiency-induced chronic active gastritis to accelerate the gastric tumorigenesis.

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Section: Resultsmentioning

confidence: 99%

Deficiency of Stomach-Type Claudin-18 in Mice Induces Gastric Tumor Formation Independent of H pylori Infection

Suzuki

Sentani

Tanaka

et al. 2019

Cellular and Molecular Gastroenterology and Hepatology

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“…GHPs used to be the most common polyps of benign epithelial gastric polyps 1 . However, the prevalence of GHPs has decreased to 14-40% of gastric polyps in recent decades [11][12][13] . In our study of 6418 cases of gastric polyp, 1115 cases (17.4%, 1115/6418) were GHPs.…”

Section: Discussionmentioning

confidence: 99%

Risk factors and clinical correlates of neoplastic transformation in gastric hyperplastic polyps in Chinese patients

Zhang

Chen

et al. 2020

Sci Rep

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remain unknown. This study aimed to analyze possible risk factors that are associated with the neoplastic transformation of gastric hyperplastic polyps. Results Demographics features. During January 2010 and June 2017, there were 6418 cases of gastric polyp diagnosed. 1115 of these (17.4%, 1115/6418) were histologically confirmed GHPs. 30 of these GHPs (2.69%, 30/1115) were diagnosed as containing dysplasia or adenocarcinoma. The mean age was 61.73 ± 9.024 years old (range 32-79). Absence of Helicobacter pylori was found in 63.6% (35/55). Within the 16 patients who showed evidence of neoplastic transformation there were 12 females and 4 males, the mean age was 63.44 ± 12.27 years (range 32-79). 9 (56.3%) of the patients who had GHPs with neoplastic transformation and 10 (25.6%) of the patients with pure GHPs had a history of anaemia. The patients who had a history of anaemia were more likely to have GHPs with evidence of neoplastic transformation (9/16 vs 10/39 in the GHP patients with or without neoplastic transformation, χ 2 = 4.701, P = 0.030) (Table 1). The initial indications for performing EGD were: 27 patients screening for early gastric cancer, 15 bloating, 4 abdominal pain, 7 heartburn or acid reflux and 2 anaemia. However, 20 patients (36.4%) actually had evidence of anaemia when tested. Only 3 patients took PPI, but all of them had normal fasting serum gastrin-17 concentrations.

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“…The most frequent types of gastric polyps are represented by hyperplastic polyps, which are related to H. pylori infection, as occurred with the patient in this report, and the polyps of the fundic gland that are associated with the use of the proton pump inhibitor. H. pylori eradication may induce regression of hyperplastic polyps related to the reduction or even disappearance of inflammation of the gastric mucosa caused by infection with H. pylori [32,33].…”

Section: Discussionmentioning

confidence: 99%

Birt-Hogg-Dubé syndrome with simultaneous hyperplastic polyposis of the gastrointestinal tract: case report and review of the literature

et al. 2020

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Background: Birt-Hogg-Dubé syndrome (BHDS) is a rare autosomal dominant genodermatosis characterized by benign growth of the hair follicles, the presence of pulmonary cysts, spontaneous pneumothorax, and bilateral renal tumors that are usually hybrid oncocytic or multifocal chromophobe renal cell carcinoma. The diagnosis is confirmed by the presence of a pathogenic variant in the tumor suppressor folliculin (FLCN) gene mapped at 17p11.2. Although the dermatological lesions typical of BHDS are benign and only cause aesthetic concerns, and the pulmonary manifestations are controllable, the greater tendency of patients with this syndrome to present benign or malignant renal tumors, often bilateral and multifocal, makes the diagnosis of this syndrome important for the prognosis of the patients. The objective was to report the case of a patient with BHDS, without pulmonary manifestations and with hyperplastic polyposis of the gastrointestinal tract, and to perform a literature review. Case presentation: A 60-year-old man complained of abdominal pain and diarrhoea for 2 months. Physical examination was normal except for the presence of normochromic papules in the frontal region of the face associated with hyperkeratotic and hyperchromic papules in the dorsal region. The excisional biopsies of the skin lesions indicated trichodiscomas. Esophagogastroduodenoscopy, enteroscopy, and colonoscopy showed the presence of hyperplastic polyps in the stomach, duodenum, jejunum, colon, and rectum. Computed tomography (CT) and magnetic resonance imaging (MRI) of the abdomen revealed multiple expansive solid lesions in both kidneys, with necrotic and calcified areas. Renal magnetic resonance angiography also showed a solid lesion in the right kidney measuring 5 cm in diameter and another solid lesion in the left kidney measuring 8 cm in diameter, both suggestive of renal angiomyolipoma. CT scans of the skull, chest, and temporal bones were normal. The genetic study revealed the presence of a variant of FLCN in the intron 13. Conclusions: To the best of our knowledge, this is the first reported case of BHDS with the simultaneous finding of gastrointestinal hyperplastic polyposis, which may represent a possible phenotypic expression of this syndrome that has not yet been described.

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Changing Trends in Gastric Polyps

Abstract: The 1400% change of FGP explains the increased prevalence of gastric polyps. Chronic treatment with proton pump inhibitors and Helicobacter pylori eradication are possible explanations.

Cited by 19 publications

References 12 publications

Deficiency of Stomach-Type Claudin-18 in Mice Induces Gastric Tumor Formation Independent of H pylori Infection

Deficiency of Stomach-Type Claudin-18 in Mice Induces Gastric Tumor Formation Independent of H pylori Infection

Risk factors and clinical correlates of neoplastic transformation in gastric hyperplastic polyps in Chinese patients

Birt-Hogg-Dubé syndrome with simultaneous hyperplastic polyposis of the gastrointestinal tract: case report and review of the literature

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