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Gastric Hyperplastic Polyps


A routine EGD for GERD, found to have one gastric polyp 8mm – turned out to be a hyperplastic polyp in at 45M? No H. pylori, no atrophy. Follow up?

Short answer: No surveillance is necessary in this patient, especially because the patient is NOT infected with H. pylori and there was no gastric atrophy. To have some “piece of mind” I would resect that polyp on the index endoscopy.

Extended discussion: Hyperplastic gastric polyps larger than 10 mm should be removed as they are associated with malignancy, i.e. harboring a cancer.

On the other side, any sized hyperplastic gastric polyp, but only in the presence of H. pylori infection, is associated with higher incidence of gastric cancer. However, in addition to H. pylori infection, other “stomach risk factors” such as atrophy, intestinal metaplasia, distribution of the gastritis (body versus antrum versus pan-gastritis) should be thrown into the equation when deciding on surveillance gastroscopy. Of course, geographical location and family history are also important factors that determine the decision to endoscopically surveille or not.

I am adding the seminal prospective study from 2001 on Helicobacter pylori infection and development of gastric cancer done by Naomi Uemura et al. This study gives us some insight on some factors to consider when considering surveillance gastroscopy.

The key finding of this study was that gastric cancer developed in persons infected with H. pylori but not in uninfected persons.

Additionally, those with histologic findings of severe gastric atrophy, corpus-predominant gastritis, or intestinal metaplasia were at highest risk.

Importantly, persons with H. pylori infection and non-ulcer dyspepsia, gastric ulcers, or gastric hyperplastic polyps were also at risk, but those with duodenal ulcers are not.

Summary and results of study:

In this study the authors prospectively studied 1526 Japanese patients who had duodenal ulcers, gastric ulcers, gastric hyperplasia, or non-ulcer dyspepsia at the time of enrollment; 1246 had H. pylori infection and 280 did not. The mean follow-up was 7.8 years (range, 1.0 to 10.6). Patients underwent endoscopy with biopsy at enrollment and then between one and three years after enrollment. H. pylori infection was assessed by histologic examination, serologic testing, and rapid urease tests and was defined by a positive result on any of these tests.

A total of 36 gastric cancers were found, with 23 intestinal-type and 13 diffuse- type cancers. Among the patients with H. pylori infection, those with severe gastric atrophy, corpus- predominant gastritis, and intestinal metaplasia were at significantly higher risk for gastric cancer. Gastric cancers were detected in 21 (4.7 percent) of the 445 patients with non-ulcer dyspepsia, 10 (3.4 percent) of the 297 with gastric ulcers, 5 (2.2 percent) of the 229 with gastric hyperplastic polyps, and none of the 275 with duodenal ulcers.

(N Engl J Med 2001; 345:784-9)

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