Histological analysis of fundic gland polyps secondary to PPI therapy

Fukuda, Masahide; Ishigaki, Hirohito; Sugimoto, Mitsushige; Mukaisho, Ken‐ichi; Matsubara, Akiko; Ishida, Hideyuki; Moritani, Suzuko; Itoh, Yasushi; Sugihara, Hiroyuki; Andoh, Akira; Ogasawara, Kunio; Murakami, Kazunari; Kushima, Ryoji

doi:10.1111/his.13902

Cited by 31 publications

(31 citation statements)

References 35 publications

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“…The maximum diameter of fundic gland cysts within the fundic gland polyps was larger in patients on PPI treatment than in those not receiving the drugs. 22 A retrospective study revealed three types of PPIassociated gastric polyps in chronic users, (1) fundic gland type,…”

Section: Ppi-related Histophatological Gastric Mucosal Changesmentioning

confidence: 99%

Proton Pump Inhibitor-Related Gastric Mucosal Changes

Kim

2021

Gut and Liver

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Proton pump inhibitors (PPIs) are used worldwide to treat of acid-related disorders such as peptic ulcer and gastroesophageal reflux disease and to prevent gastroduodenal injuries due to nonsteroidal anti-inflammatory drugs. PPIs are the most potent inhibitors of gastric acid secretion currently available, and they are one of the most commonly prescribed classes of drugs because of their high efficacy and low toxicity. However, long-term PPI use causes histopathological changes such as parietal cell protrusion into the gland lumen, cystic dilation of gastric fundic glands, and foveolar epithelial hyperplasia. These changes can manifest on endoscopic examination as fundic gland polyps, hyperplastic polyps, multiple white and flat elevated lesions, cobblestonelike mucosa, or black spots. Clinicians must be aware of PPIinduced endoscopic features in patients with chronic longterm PPI use. Conversely, identifying patients with long-term PPI use based on their endoscopic findings is important. Recently, potassium-competitive acid blockers (P-CABs), a new class of acid suppressants that inhibit gastric acid secretion more strongly than PPIs, have recently been introduced clinically. Further long-term prospective studies on these gastric mucosal lesions in patients with either PPI or P-CAB use are required to investigate their association with histopathological changes and to establish the clinical significance of these findings.

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Section: Ppi-related Histophatological Gastric Mucosal Changesmentioning

confidence: 99%

Proton Pump Inhibitor-Related Gastric Mucosal Changes

Kim

2021

Gut and Liver

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“…Pathologically, hyperplasia of parietal cells and parietal cell protrusion into the lumen are typical findings [3]. Although hypoacidity and hypergastrinemia increase the risk of gastric cancer in the corpus and fundus [4,5], the relationship between long-term PPI administration and tumor development remains unclear. Herein, we report the rare case of a 22 × 22 × 10 mm FGP in Helicobacter pylori (H. pylori)-uninfected gastric mucosa associated with long-term PPI administration that was mimicking gastric-type neoplasm and resected via endoscopy.…”

Section: Introductionmentioning

confidence: 99%

Large Fundic Gland Polyp Associated with Long-Term Proton Pump Inhibitor Administration Mimicking Gastric-Type Neoplasm

Ochiai

Kikuchi

Ito

et al. 2021

Case Rep Gastroenterol

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A 57-year-old man with a 10-year history of proton pump inhibitor (PPI) use presented with multiple fundic gland polyps (FGPs) including one >20 mm, whitish, semi-pedunculated polyp. Black spots and cobblestone-like mucosa were also observed in the stomach upon endoscopy; therefore, the lesion was considered to result from long-term PPI administration. Endoscopically, we diagnosed this polyp as a neoplastic lesion with gastric phenotype rather than a non-neoplastic lesion. Biopsy revealed an atypical glandular lesion that was indeterminate for neoplasia; therefore, we performed en bloc resection via endoscopic submucosal dissection (ESD) of the 22 × 22 × 10 mm-sized polyp. Histologically, the polyp was composed of hyperplastic foveolar epithelia in the upper half of the mucosa and hyperplastic fundic glands in the lower half of the mucosa, with luminal dilatation and parietal cell protrusion. The pathological diagnosis for this ESD specimen was FGP associated with PPI administration. We herein describe this rare case of a large FGP in <i>Helicobacter pylori</i>-uninfected gastric mucosa associated with long-term PPI administration, which was mimicking gastric-type neoplasm and resected by endoscopy.

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“…Anyhow, PPI induced FGPs disappear when stopping treatment [ 127 , 128 ], for instance after anti-reflux surgery [ 129 ]. FGPs due to PPI treatment were reported to have higher percentage of proliferating cells assessed by Ki67 than other sporadic FGPs [ 130 ]. Similarly, three FGPs that were developed after 8 years of PPI therapy showed low grade dysplasia and in one adenocarcinoma [ 131 ].…”

Section: Gastric Polypsmentioning

confidence: 99%

Gastritis, Gastric Polyps and Gastric Cancer

Fossmark

2021

IJMS

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Gastric cancer is still an important disease causing many deaths worldwide, although there has been a marked reduction in prevalence during the last few decades. The decline in gastric cancer prevalence is due to a reduction in Helicobacter pylori infection which has occurred for at least 50 years. The most probable mechanism for the carcinogenic effect of H. pylori is hypergastrinemia since H. pylori infected individuals do not have increased risk of gastric cancer before the development of oxyntic atrophy. When atrophy has developed, the carcinogenic process continues independent of H. pylori. Autoimmune gastritis also induces oxyntic atrophy leading to marked hypergastrinemia and development of ECL cell neoplasia as well as adenocarcinoma. Similarly, long-term treatment with efficient inhibitors of acid secretion like the proton pump inhibitors (PPIs) predisposes to ECL cell neoplasia of a different degree of malignancy. Contrasting the colon where most cancers develop from polyps, most polyps in the stomach have a low malignant potential. Nevertheless, gastric polyps may also give rise to cancer and have some risk factors and mechanisms in common with gastric cancer. In this overview the most common gastric polyps, i.e., hyperplastic polyps, adenomatous polyps and fundic gland polyps will be discussed with respect to etiology and particularly use of PPIs and relation to gastric carcinogenesis.

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Histological analysis of fundic gland polyps secondary to PPI therapy

Cited by 31 publications

References 35 publications

Proton Pump Inhibitor-Related Gastric Mucosal Changes

Proton Pump Inhibitor-Related Gastric Mucosal Changes

Large Fundic Gland Polyp Associated with Long-Term Proton Pump Inhibitor Administration Mimicking Gastric-Type Neoplasm

Gastritis, Gastric Polyps and Gastric Cancer

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