Endoscopic submucosal dissection (ESD) is widely utilized for the treatment of large adenomas, submucosal lesions, and early gastric cancer. A significant artificial ulcer typically forms after ESD. Delayed or incomplete healing of these ulcers can result in complications such as delayed bleeding and perforation. However, a comprehensive review of the outcomes and risk factors related to ulcer healing following ESD is currently lacking.

To assess ulcer healing outcomes and identify risk factors associated with delayed ulcer healing.

Databases retrieved by computer include PubMed, EMBASE, The Cochrane Library, Web of Science, China National Knowledge Infrastructure, Wan Fang Data, and VIP. The study collects reports on ESD post-surgical ulcer healing outcomes and risk factors, using Stata 16.0 and RevMan 5.0 software for meta-analysis.

Our analysis included 12 studies, involving a total of 3430 patients. The meta-analysis revealed an overall healing rate of 65.55% for ulcers following ESD [odds ratio (OR) = 2.71; 95% confidence interval (CI): 2.45-3.00]. The healing rate within eight weeks was 48.32% (OR = 0.76; 95%CI: 0.35-1.66), while the rate beyond eight weeks was 88.32% (OR = 6.73; 95%CI: 3.82-11.87). Risk factors included Helicobacter pylori (H. pylori) infection (OR: = 5.32; 95%CI: 1.90-14.87; P = 0.001), ulcer size (OR = 2.08; 95%CI: 1.19-3.61; P = 0.01), lesion site (OR = 2.08; 95%CI: 1.19-3.11), and pathological type (OR = 1.64; 95%CI: 1.06-2.52). Diabetes (OR = 0.56; 95%CI: 0.05-5.80; P = 0.63) and duration of operation (OR = 1.00; 95%CI: 0.99-1.01; P = 0.96) were not significant factors.

The healing rate of ulcers following ESD is high after eight weeks. Risk factors affecting the healing process include H. pylori infection, ulcer size, lesion site, and pathological type.

Vonoprazan exhibits a more potent, rapid, and longer-lasting inhibitory effect on gastric acid secretion than proton pump inhibitors; however, whether it is more effective than PPI for treating endoscopic submucosal dissection (ESD)-induced artificial ulcers remains controversial.

This study aimed to assess and compare the effects of vonoprazan and lansoprazole for treating ESD-induced artificial ulcers.

This prospective, randomized controlled trial enrolled 149 patients who underwent ESD for the treatment of early gastric neoplasms from April 2015 to May 2017. They were randomly treated with either 20 mg/day vonoprazan (V group) or 30 mg/day lansoprazole (L group) orally. The primary end points were the area and shrinkage ratio of the ulcers at 4 and 8 weeks post-ESD.

Data from 127 patients were analyzed, which showed that the 4- and 8-week healing ratios were not significantly different between the V and L groups (4 weeks, 16.3 vs. 25.8%; 8 weeks, 86.9 vs. 90.9%, respectively). Similarly, the shrinkage ratio, categorized as less than 90%, 90% or more but less than 100%, or 100% at 4 weeks and as less than 100% or 100% at 8 weeks were not statistically different between the V and L groups (4 weeks: 12, 41, 8 vs. 13, 41, 12, p = 0.7246; 8 weeks: 9, 52 vs. 9, 57, p = 0.8568). Delayed bleeding was also not significantly different between both the groups (5.4 vs. 5.3%; p = 0.9844).

Vonoprazan is as effective as lansoprazole in treating ESD-induced ulcers.

Endoscopic submucosal dissection (ESD) has been developed for early gastric cancer (EGC). Helicobacter pylori eradication therapy has been reported to have a preventive effect against metachronous recurrence of EGC after ESD. However, the efficacy and safety of eradication therapy on ESD-induced ulcer healing are not clear. In a randomized control study, we compared the standard therapy (8-week proton pump inhibitor) and eradication therapy combined with subsequent treatment with 7-week rebamipide for healing ESD-induced ulcers.

A multicenter, randomized, open-label study was conducted. In group A, patients received 20 mg of omeprazole for 56 days. In group B, patients received 40 mg of omeprazole, 1,500 mg of amoxicillin, and 800 mg of clarithromycin for 7 days, and then 300 mg of rebamipide for 49 days. The primary end point was to evaluate the scarring ratio.

The scarring rate in group A was significantly higher than that in group B [85.0 % (34/40) vs. 56.8 % (21/37), P = 0.011]. The scarring rate of ulcers with an area ≥565.5 mm(2) in group A was significantly higher than that in group B [78.9 % (15/19) vs. 37.5 % (6/16), P = 0.018]. There was no significant difference between the groups in the scarring rate of smaller ulcers. No serious adverse events were observed in any of the patients in either group.

H. pylori eradication therapy and 7-week rebamipide monotherapy were not superior to PPI monotherapy, but this combination therapy for smaller sized ulcers was an optimal therapeutic option for healing. Serious adverse events were not observed in either group.

Gastric endoscopic submucosal dissection (ESD) causes artificial gastric ulcers and there is no consensus regarding the optimal perioperative management in terms of prevention of intra- or postoperative bleeding and promotion of healing. Traditionally, 8-week administration of proton pump inhibitors (PPI) and mucosal protective agents were used in the same way as for peptic ulcer management. However, recent studies have revealed that prior use of PPI might reduce intraoperative bleeding or early-phase postoperative bleeding, and combination of histamine-2 receptor antagonist (H2RA), and second-look endoscopy might have a similar effect on postoperative bleeding to PPI. Additionally, the advantage of PPI over H2RA is not proven and the optimal duration of PPI may be shortened until 2 weeks when the deteriorating factors for ESD ulcer are excluded. Furthermore, mucosal protective agents may facilitate ulcer healing. Further studies are needed to determine the optimal treatment protocol before and after ESD for both prevention of bleeding complication and promotion of ulcer healing, by using available antisecretory agents and mucosal protective agents.

Endoscopic submucosal dissection (ESD) is a novel endoscopic procedure first developed in the 1990s which enables en bloc resection of gastric neoplastic lesions that are difficult to resect via conventional endoscopic mucosal resection. However, given that ESD increases the risk of intra- and post-ESD delayed bleeding and that platelet aggregation and coagulation in artificial ulcers after ESD strongly depend on intragastric pH, faster and stronger acid inhibition via proton pump inhibitors (PPIs) and histamine 2-receptor antagonists (H(2)RAs) as well as endoscopic hemostasis by thermocoagulation during ESD have been used to prevent ESD-related bleeding. Because PPIs more potently inhibit acid secretion than H(2)RAs, they are often the first-line drugs employed in ESD treatment. However, acid inhibition after the initial infusion of a PPI is weaker in the early phase than that achievable with H(2)RAs; further, PPI effectiveness can vary depending on genetic differences in CYP2C19. Therefore, optimal acid inhibition may require tailored treatment based on CYP2C19 genotype when ESD is performed, with a concomitant infusion of PPI and H(2)RA possibly most effective for patients with the rapid metabolizer CYP2C19 genotype, while PPI alone may be sufficient for those with the intermediate or poor metabolizer genotypes.