Gastric Polyps—To Worry or Not?

Abstract

A 15-year-old white boy underwent upper endoscopy for persistent dyspepsia for which he had been receiving a proton pump inhibitor (PPI) (lansoprazole) for several years. The esophagus and duodenum were visually and histologically normal. Small, sessile polyps were seen on the gastric body (Fig. 1A). Biopsies of the gastric mucosa were normal; the polyps showed dilatation and hyperplasia of oxyntic glands (Fig. 1B) consistent with fundic gland polyps secondary to PPI therapy.FIGURE 1: Endoscopic (A) and histological (B) findings of fundic gland hyperplasia caused by long-term use of a protein pump inhibitor.Gastric polyps may be found at endoscopy as a spontaneous benign condition, part of an adenomatous polyp syndrome (familial adenomatous polyposis [FAP]), part of a hamartomatous polyp syndrome (juvenile polyposis syndrome, Peutz-Jegher syndrome, and PTEN hamartoma syndrome), or a result of medication (PPIs). Although patient history is important for developing a differential diagnosis of gastric polyps, diagnosis is confirmed by histological findings. Fundic gland polyps (FGPs) are seen in 2% to 12% of patients with no PPI exposure, 26% to 36% of patients on long-term (>12 months) PPI therapy, and in up to 81% of adults and 51% of children with FAP (1–5). FGPs are characterized by cystically dilated and irregularly budded fundic glands, which are lined by normal parietal cells, chief cells, or mucous neck cells. FGPs in FAP (Fig. 2A) are distinguished by foveolar dysplasia and may develop adenomatous transformation (Fig. 2B). Incipient hamartomatous polyps can mimic FGP endoscopically. These polyps are characterized by an edematous lamina propria with inflammatory cells and cystically dilated glands lined by cuboidal to columnar epithelium with reactive changes; Peutz-Jegher polyps are differentiated by arborization of smooth muscle.FIGURE 2: Endoscopic (A) and histological (B) findings of gastric polyps in a patient with familial adenomatous polyposis.FGPs in FAP carry a risk of malignant transformation necessitating surveillance endoscopy. Consensus as to when to initiate surveillance does not exist; recommendations are included at the time of initial colonoscopy or around age 20 years. Interval of surveillance endoscopy for gastric FAP is every 1 to 3 years (5,6). Although there is no need to worry about malignancy related to PPI-induced FGPs, long-term use (>5 years) of PPIs has been associated with osteopenia and osteoporosis-related fractures. Conflicting data are found regarding the role of PPIs in predisposing to small bowel bacterial overgrowth. The patient was informed of the risks of long-term PPI use, received dietary counseling; the PPI was discontinued and an H2-receptor antagonist started. No further surveillance was performed as the polyps regress with cessation of PPIs.