Prevalence and risk factors for fundic gland polyps

Abstract

The incidence of fundic gland polyps (FGPs) is increasing rapidly and has surpassed hyperplastic polyps to become the most common epithelial gastric polyps in Western countries and China.1, 2 They are usually multiple, small (1-5 mm), transparent, and sessile; the background gastric mucosa is typically normal.3 FGPs are more prevalent among females and are often located in the gastric fundus and body. There are two types of FGPs: sporadic and syndromic (in association with familial adenomatosis polyposis). Although different in their genetic and molecular backgrounds, sporadic and syndromic FGPs are histologically and histochemically indistinguishable. Syndromic FGPs occur in the presence of inherited germline mutation in the adenomatous polyposis coli (APC) gene plus the acquisition of a somatic mutation, leading to complete inactivation of the APC tumor suppressor gene.4 Familial adenomatosis polyposis should be excluded by colonoscopy if FGPs are numerous, large (>1 cm), or dysplasic.3 For sporadic FGPs, up to 23% are associated with proton pump inhibitor (PPI) use.5, 6 A recent review with meta-analysis indicated that long-term use of PPIs (≥12 months) increased the risk of FGPs (pooled odds ratio [confidence interval]: 3.81 [2.78-5.24] for the fixed effects model and 2.88 [0.97-8.55] for the random effects model).7 The risk was even higher if the exposure duration was more than 48 months (pooled odds ratio: 4.02). There is no or inverse association with Helicobacter pylori infection.1, 3 FGPs rarely harbor dysplastic lesions. A study in the USA of 35 372 FGPs found that only 0.3% had low-grade dysplasia.5 Moreover, even syndromic FGPs rarely progress to cancer.8 Once epithelial gastric polyps are found at initial endoscopy, it is important to sample polyps and/or normal-appearing gastric mucosa to establish histological diagnosis and to define who needs surveillance. Biopsies from the background antrum and corpus mucosa could rule out atrophic gastritis, intestinal metaplasia, dysplasia, and H. pylori infection. All these information is important for the management of other epithelial gastric polyps, including hyperplastic polyp, adenoma, and type 1 or 2 gastric neuroendocrine tumors.3 Once sporadic FGPs are diagnosed, routine endoscopic surveillance is not recommended in the absence of dysplasia. There is still no consensus on the indication of endoscopy resection of sporadic FGPs. However, many experts suggest the removal of FGPs larger than 10 mm.3 Few studies have considered risk factors other than age, gender, PPIs, and H. pylori infection for sporadic FGPs. A recent one-center, endoscopy-based retrospective study in Taiwan indicated the incidence of FGPs increased from 0.6% in 2010 to 1.3% in 2015.9 The controls were age- and gender-matched subjects who received upper endoscopy during the similar period with the cases. The authors found the presence of liver cirrhosis, gastric ulcer, duodenal ulcer (adjusted odds ratio: 0.18, 0.28, and 0.35, respectively, all P < 0.001), but not reflux esophagitis, were inversely associated with FGP risk. FGPs are commonly seen in patients with relatively healthy gastric mucosa. This is an interesting finding that implies causative factors to gastric mucosa, including cirrhosis and peptic ulcers, which could reduce the formation of FGPs, probably through the facilitation of glandular outflow. However, more than 30% of H. pylori status was missing, and the information of PPI exposure was less than adequate in this study. Future studies are necessary to support this finding and the proposed mechanism behind it. The author declares no conflict of interest.