Large gastric hyperplastic polyps: to resect or not to resect, that is the question!

Gastric hyperplastic polyps (GHPs) constitute 18 % – 70 % of all gastric polyps. They are generally detected as innocuous incidental findings in 1.2 % – 8 % of patients undergoing esophagogastroduodenoscopy; however, dysplasia or malignancy may be found within these GHPs in 2.1 % – 8 % of patients [1] [2] [3] [4]. Risk factors for the development of GHPs include Helicobacter pylori infection, previous gastric surgery (partial gastrectomy), autoimmune gastritis, liver cirrhosis, and noncirrhotic chronic liver disease causing portal hypertension [1] [2] [3] [5]. The etiopathogenesis of GHPs is unclear. The accepted hypothesis states that GHPs develop as the result of a hyperplastic mucosal healing regenerative response secondary to an inflammatory process [3]. Malignant transformation in GHPs has been reported in lesions > 10 mm, and therefore, endoscopic resection is recommended in these patients [2] [4] [6] [7]. However, results of endoscopic resection of GHPs are suboptimal and recurrences are frequent [8].

...in the absence of reliable predictors for neoplasia and the high recurrence rates, a general recommendation of endoscopic resection for all large gastric hyperplastic polyps appears unjustifiable.

In this issue of Endoscopy, Forte et al. discuss the potential risk factors for recurrence and neoplastic change of large GHPs in a retrospective multicenter study [9]. The study highlights several important aspects. Polyp size > 25 mm and presence of intestinal metaplasia were identified as risk factors for neoplastic transformation in multivariate analysis. Polyp size > 10 mm has been demonstrated as an important risk factor for dysplasia in GHPs, with an approximate risk of 10 %. Ahn et al. reported that, with the exception of older age, size > 10 mm, and lobular pattern, other parameters such as location, intestinal metaplasia, and H. pylori infection did not demonstrate any correlation with neoplastic potential [5]. Forte et al. predict that this risk increases exponentially when the polyp size increases beyond 25 mm, and GHPs > 40 mm demonstrated a 58.3 % risk.

Presence of intestinal metaplasia was another risk factor identified by Forte et al. Although Helicobacter pylori gastritis, intestinal metaplasia, and/or atrophic gastritis have been reported as risk factors in some studies [3] [7], others have found no correlation between these factors and occurrence of neoplasia [5]. Attempts at endoscopic characterization of GHPs for malignant change have generally been unsuccessful. Polyp biopsies can miss dysplasia in up to 50 % of cases [6]. In this scenario, can image-enhanced endoscopy (IEE) help to detect neoplasia in large GHPs? Horiuchi et al. and Omori et al. reported that by combining polyp size > 20 mm and features of magnification endoscopy with narrow-band imaging demonstrating abnormal microvascular pattern and micrification of the fine mucosal structure, they could achieve nearly 100 % sensitivity and 58 % specificity for a diagnosis of dysplasia or cancer [10] [11]. Unfortunately, IEE as a parameter was not included or reported in the study by Forte et al.

Although endoscopic resection is currently the recommended treatment for large GHPs, recurrence rates have been uniformly dismal, at around 50 % [8]. An alarming fact demonstrated by Forte et al. is that recurrence rates were not just high, but they increased further following subsequent endoscopic resection attempts (78 % and 89 % after second and third resections, respectively, compared with 51 % after the first resection). In addition, recurrences were often larger and more exuberant than the original lesions. Neoplastic transformation was seen in six patients with recurrent GHPs when the original GHP had not demonstrated dysplasia. An additional disturbing finding was that recurrence rates were not affected by the endoscopic resection type (endoscopic mucosal resection or submucosal dissection, en bloc or piecemeal, or R0 or R1).

Therefore, in the absence of reliable predictors for neoplasia and the high recurrence rates, a general recommendation of endoscopic resection for all large GHPs appears unjustifiable. It is possible that surveillance alone could be offered to certain carefully selected patients if the perceived risk was low. However, is it possible to preselect these patients? Based on the observations of Forte et al., in the absence of intestinal metaplasia, could the threshold for endoscopic resection for large GHPs be raised from 10 mm to 25 mm? This question is highly relevant in the context of preventing neoplasia and requires further evaluation by appropriately designed studies.

Identifying predictors for GHP recurrence is another important aspect discussed by Forte et al. They reported that recurrence was significantly more frequent in patients with cirrhosis, occurring in 79 % compared with 44 % of patients without cirrhosis. Although cirrhosis as a cause of GHPs has been reported in other studies [12] [13], higher recurrence rates have not been reported. The neoplastic potential of portal hypertensive polyps is low or nonexistent [14], as was also reported in the current study. Most polyps occur in advanced cirrhosis with a limited life expectancy. Opportunities for surveillance are higher given that these patients are already under surveillance for varices. Therefore, Forte et al. suggest that the threshold for endoscopic resection in patients with cirrhosis could be lower and possibly limited to GHPs with symptoms, and that surveillance with biopsies to detect early dysplasia may be adequate. This is a valid argument, which requires investigation in future studies.

GHPs are often red flags for associated gastric mucosal pathology such as H. pylori gastritis, autoimmune gastritis or intestinal metaplasia [7]. The presence of a GHP should therefore alert the endoscopist to examine the surrounding gastric mucosa carefully in order to identify these premalignant conditions [7]. IEE could prove particularly useful in this regard [10]. Eradication of associated H. pylori gastritis has been reported to resolve GHPs [15], and portal hypertensive polyps can regress after treatment of portal hypertension or after liver transplantation [12] [16]. Should therapy therefore be directed toward the underlying pathology rather than the polyp itself? Possibly yes, but more data on this subject are warranted.

In conclusion, the study by Forte et al. raises several relevant questions. Endoscopic resection of large GHPs has several limitations that clinicians need to recognize. Treatment of associated mucosal pathology should not be ignored in favor of endoscopic resection. The presence of liver cirrhosis could be a deterrent to performing endoscopic resection and patients may preferentially be offered surveillance. GHPs > 25 mm have high neoplastic potential and require endoscopic resection. However, in the absence of other high-risk features, particularly intestinal metaplasia, endoscopic resection for smaller lesions (10–25 mm) should be more selectively performed. Clear guidelines for patient selection for endoscopic resection in this group are currently lacking. Although IEE may assist in identifying high-risk patients, data are limited, and polyp size and presence of symptoms often govern the clinical decision. Hopefully, future research will provide more information on this topic. However, until such a time, the question “To be or not to be (resected),” could largely remain unanswered for large GHPs of size 10–25 mm.

Publication History

Article published online:
27 May 2020

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