We found that the most common symptoms of GPs were nausea, anemia and abdominal pain.The increasing incidence of gastric polyps in recent years may be attributed to the following reasons: a) an increasing number of people undergo endoscopy for health check-ups; b) environment and diet components have changed with socioeconomic development; and c) advances in endoscopic technology and its wide application have increased the positivity rate. The detection rate of gastric polyps was reported to be 6.35% in a population in the United States[11,12]; in China, it ranges from 1% to 4.3%. Literature has shown that gastric polyps are more common in females. It has been reported that the male : female ratio was 1:1:22 in a population (n=440) in Sichuan Province , 1:1.58 in an analysis including 36,650 patients , and 1:2.1 in 2643 patients in Guangdong Province .
Helicobacter pylori (H. pylori) infection can cause an inflammatory reaction of the mucosa, and a polyp may form due to overgrowth of cells during the recovery period[16,17]. In fact, hyperplastic polyps are by-products of the damaged mucosa during its healing. According to literature, the vast majority of fundic gland polyps occur in patients who are not infected with H. pylori[19,20]. In addition, long-term duodenal reflux can cause chronic inflammation, gastric pit cell hyperplasia, atypical hyperplasia, polyps, and other lesions[21,22]. Large amounts of gastric reflux can cause inflammatory changes in the mucosa; also, it can alter the acid-base balance in the stomach, leading to excessive secretion of gastrin, which, to a certain extent, promotes cell proliferation and thus triggers the forming of hyperplastic polyps[24,25].
Use of PPI can affect the course of FGP. Prolonged PPI administration results in the increased number and volume of FGP, whereas PPI reduction and withdrawal are associated with gradually decreased number and volume of FGP. It has been found patients taking PPI for less than 1 year will not develop FGP; however, long-term PPI therapy increases the risk of polyps (in particular, it is associated with a 4-fold increased risk for FGP). This phenomenon is considered to be a cystic change caused by the chronic stimulation of gastric mucosa by a high level of gastrin. Animal experiments have revealed that gastrin can promote the growth of parietal cells by increasing their height and size. When the parietal cells in the neck of gland are enlarged, they may block the opening of the gland and increase the pressure inside the gland, leading to the development of cystic changes and eventually the forming of polyps.
In recent years, the incidence of FGP has markedly increased in Western countries, accounting for more than 70% of GP. It has been reported that FGP is not associated with H. pylori but with PPI therapy. FGP may be resolved with the withdrawal of PPI, and therefore it is speculated that the pathogenesis of FGP may be related to the inhibition of gastric acid secretion. Long-term PPI use can lead to hypergastrinemia, which promotes the cystic dilatation of gastric glands to form polyps.
However, HP development is associated with H. pylori infection and hypergastrinemia . In our study, FGPs were found in eight patients. It is known that H. pylori infection reduces FGP formation, and these polyps are common in H. pylori-negative patients . This low incidence may be related to high rates of H. pylori infection in China. However, even in countries with high H. pylori infection rates, FGP frequency may be high, but these polyp have not been observed in several studies . Frequency of FGPs is related to long-term PPI use. No increased risk of short-term use has been observed. The most common reason for EGD surgery is complaints of indigestion. The frequency of FGPs in our patients was low; probably because they had been treated with PPIs for a short time. Also, because these polyps are so small, they may be missed during EGD surgery or may be neglected due to their indistinct endoscopic appearance.
In our study, 20 (5.2%) patients had FHPs. These lesions are considered to be precursors of HPs, although it is unclear how long FHPs take to change to HPs. The lesions may be stable or may grow or shrink. However, whether they are HP precursors is still controversial. It has been shown that the basic structure and cytological criteria of FHPs and HPs can be easily distinguished by biopsy material obtained by endoscopic forceps. These lesions are not the result of HP precursors . FHPs are common lesions in research. In our study, APs were detected in eight patients. Aps have been shown to account for 2.1% of GPs . These polyps are more common in patients with stomach cancer and have high malignant potential of 6.8–55.3% . Lesion size, height of atypical hyperplasia and presence of intestinal epithelium are risk factors for malignant tumor development. Even adenomas with low displacement during long-term follow-up have malignant potential. Therefore, it is recommended to remove these lesions . In addition, IFP was detected in one patient in our study. These polyps are not always diagnosed as endoscopic biopsies because they are local . Because our case was not diagnosed by endoscopic biopsy, it was diagnosed after surgical removal .
A total of 128 patients (33.3%) underwent snare polypectomy in our study. One patient required endoscopic control of bleeding. Low rates of hemorrhage caused by endoscopic polypectomy can be treated by sclerotherapy, endoclip or endoloop procedures. No death or perforation occurred in any patient. Snare polypectomy is a safe and effective way to diagnose and treat polyps.
In conclusion, the GP frequency in our study was low (3.84%). HP polyps were the most common types of gastric polyps. Of note, as GPs may have a risk of developing adenocarcinoma or precancerous lesions, we suggest that appropriate GP resection technology ( such as biopsy forceps or mesenchymal resection) should be applied.