Management of Gastric Polyps

An Endoscopy-Based Approach

Yasser H. Shaib; Massimo Rugge; David Y. Graham; Robert M. Genta


Clin Gastroenterol Hepatol. 2013;11(11):1374-1384. 

In This Article

Hyperplastic Polyps

Hyperplastic polyps are inflammatory proliferations of the gastric foveolar cells (the mucin-producing epithelial cells that line the gastric surface and the gastric pits). When the inflammatory infiltrates are prominent, they may be referred to as inflammatory polyps. When hyperproliferation of foveolar cells is the most salient characteristic, gastric pits (also known as foveolae, from the Latin word for "small pit") become elongated, tortuous, and generate elevations of the mucosa; these lesions are known as polypoid foveolar hyperplasia. In patients with post-Billroth I and II gastric stumps the gastric mucosa adjacent to the anastomosis continuously is exposed to bile reflux and significant degrees of foveolar hyperplasia may occur. In some cases there also may be cystic dilatation of the foveolae, with a resulting polypoid lesion consisting of cysts, tortuous pits, and often an eroded surface epithelium. This is sometimes referred to as gastritis cystica polyposa. Because all these are expressions of the same basic lesion we suggest that confusion be avoided by referring to all variants as hyperplastic polyps.

The classic association of gastric hyperplastic polyps has been with mucosal atrophy, whether caused by H pylori infection or autoimmune gastritis.[23,24] However, in recent years we have seen an increase in the proportion of such polyps in the background of a normal or reactive gastric mucosa with no evidence of current or prior H pylori infection. In Western countries, hyperplastic polyps have slipped from being the most common type of gastric polyp encountered at endoscopy to less than 20% of them.[1] Hyperplastic polyps are equally common in men and women and typically occur in the sixth and seventh decades (median age, 66 y). Endoscopically, they are found most frequently in the antrum and often are multiple. They are usually smooth, dome-shaped, and measure between 0.5 and 1.5 cm in diameter (Figure 2), although they may be much larger. Large hyperplastic polyps often become lobulated and pedunculated,[25] and the surface epithelium typically is eroded (Figure 2), which may result in chronic blood loss and iron-deficiency anemia. Rarely, patients with large hyperplastic polyps present with gastric outlet obstruction because the polyp may obstruct or prolapse through the pylorus.[26,27] Hyperplastic polyps are believed to arise as a hyperproliferative response to tissue injury (erosions or ulcers) accompanied by increased cellular exfoliation.[28] The resulting foveolar hyperplasia, long recognized as a prominent feature in chemical gastropathy and, to a lesser extent in H pylori gastritis, may be the initial step in their genesis. This could explain why they increasingly are seen arising in a background of reactive gastropathy.[29]

Figure 2.

Hyperplastic polyp. (A) Endoscopic view of a hyperplastic polyp on a stalk in the antrum. Histologically, (B) hyperplastic polyps are characterized by marked foveolar hyperplasia, and (C) a mixoid stroma are characterized with dilated tortuous glands lined by normal or reactive foveolar epithelium. (D) Larger polyps have prominent erosions covered with fibrinopurulent material with underlying granulation tissue, (E) often with areas of edematous stroma and oddly shaped glands.

Histopathologic Features and Diagnostic Criteria

The typical features of hyperplastic polyps include elongated, grossly distorted, branching, and dilated hyperplastic foveolae lying in an edematous stroma rich in vasculature, and small haphazardly distributed smooth muscle bundles with varying degrees of chronic and active inflammation (Figure 2). Between 1% and 20% of hyperplastic polyps have been reported to harbor foci of dysplasia (Figure 3). This wide range is more likely a reflection of the different criteria used in the assessment of dysplasia than because of real geographic or biological variability. Mutations of the p53 gene, chromosomal aberrations, and microsatellite instability all have been detected in these polyps.[30,31,32] The overall prevalence of carcinoma in hyperplastic polyps is less than 2%, and it is more frequent in polyps larger than 2 cm.[33,34,35]

Figure 3.

(A) Hyperplastic polyp with focus of high-grade dysplasia. (B) Multiple sections from this 3-cm hyperplastic polyp revealed an area with dysplastic epithelial cells forming complex glandular structures. These represent high-grade dysplasia or possibly a focus of intramucosal carcinoma.

When foci of dysplasia or carcinoma are diagnosed within a hyperplastic polyp, clinicians often inquire whether the lesion was in fact an adenoma or a carcinoma erroneously identified as a hyperplastic polyp. This is almost never the case. Adenomas (as detailed later) consist entirely of dysplastic epithelium; in contrast, hyperplastic polyps with dysplastic foci are inflammatory lesions formed by long distorted branching, and dilated hyperplastic foveolae lying in a vascular edematous stroma. Finding foci of dysplastic (ie, neoplastic) epithelium within these lesions does not call for a reconsideration of their original pathogenesis or classification, although it does change their management.

The histopathologic diagnosis rests on the detection of the earlier-mentioned features in traditional H&E-stained slides. Because erosions, ulcerations, and inflammation, even extensive, are expected features of these polyps, pathologists are encouraged to avoid adding the word "inflammatory" to the diagnostic line. This invariably results in calls from puzzled clinicians who want to know whether hyperplastic and inflammatory gastric polyps are different or, as one put it, one and the same. They are one and the same.

When inflammatory polyps measure less than 1 cm, the routine examination of representative sections from each polyp is considered adequate. Larger polyps (>1 cm) may harbor dysplasia and even carcinoma. Therefore, they should be sectioned in 2- to 3-mm slices, and sections should be prepared from each slice. This practice will allow the detection of otherwise easily missed dysplastic or neoplastic lesions (Figure 3). Outside the research arena, no special stains or molecular studies are necessary. If no specimens from other parts of the stomach are included, an immunohistochemical stain for H pylori can be helpful.

Clinical Approach

In view of the potential cancer risk, all hyperplastic polyps larger than 1 cm should be excised completely. If dysplasia or intramucosal carcinoma is found, but the stalk is not affected, the lesion can be considered completely removed and most likely cured.[36] The excision of the polypoid lesion always should be accompanied by additional sampling of the unaffected mucosa to obtain reliable information about the topography and severity of the background gastritis and atrophy.

When hyperplastic polyps arise in a background of chronic atrophic gastritis (a precursor lesion for gastric adenocarcinoma) the severity and extent of the atrophic gastritis should be evaluated. Risk stratification for gastric cancer can be assessed histologically using the Operative Link for Gastritis Assessment (OLGA) or the Operative Link on Gastritis/Intestinal Metaplasia Assessment staging systems.[37,38] Both require histologic grading of adequate samples from the antrum and corpus; grades then are combined to provide a risk stratification category. One can use the 5-biopsy specimen protocol recommended by the updated Sydney system.[39] We prefer an extended 7-biopsy protocol consisting of 3 specimens from the antrum (which can be submitted in a single formalin container), 2 from the lesser curvature of the corpus, and 2 from the greater curvature of the corpus, with each set in a separate container.[40] The topographic separation of specimens from the antrum and corpus is crucial because pseudopyloric metaplasia (a feature of corpus atrophy) mimics the antral mucosa histologically. Although it has not been established whether the additional information obtained by this extended sampling protocol substantially improves risk assessment, we prefer it because it allows a more detailed evaluation of the extent and distribution of atrophy.

If present, H pylori should be eradicated and an endoscopic follow-up evaluation should be scheduled between 3 and 6 months after therapy to confirm successful eradication. Alternatively, a noninvasive test such as the urea breath test may be used.[41] In many instances any remaining small hyperplastic polyps will have regressed or disappeared.[42,43] Patients with OLGA stages III and IV (moderate diffuse atrophy or severe atrophy in either the corpus or antrum, usually accompanied by extensive intestinal metaplasia) should be considered for long-term endoscopic surveillance. The best intervals for such surveillance are unclear (eg, annual, bi-annual, or some other interval) as is the number of years for which it should be continued. No evidence-based guidelines exist; therefore, local recommendations should be followed when available.