Gastric ulcer healing after treatment of endoscopic submucosal dissection in Japanese: comparison of H(2) receptor antagonist and proton pump inhibitor administration

Abstract

Endoscopic submucosal dissection has made it possible to resect large lesions during a single operation. The present study was undertaken to compare the time taken for recovery from artificial ulcers after endoscopic submucosal dissection between an H(2) Receptor Antagonist treatment group and a Proton Pump Inhibitor treatment group, focusing on analysis of the time course of reduction rate in ulcer area. The powerful acid suppression by Proton Pump Inhibitor may not be needed to treat Japanese post-endoscopic submucosal dissection ulcer which usually develops after early gastric carcinoma in the mucosa of low acid secretory capacity. The study involved 60 patients with 69 artificial ulcers following endoscopic submucosal dissection for the treatment of tumors remaining in the gastric mucosa. Of all lesions, 36 were allocated to the H(2) Receptor Antagonist group and 33 to the Proton Pump Inhibitor group. Patients in both groups underwent endoscopy at 4 and 8 weeks after the start of administration. There were no significant differences between two groups and ulcer healing rates were similar in the two groups. The efficacy of H(2) Receptor Antagonists in curing this type of ulcer can thus be expected to be comparable to that of Proton Pump Inhibitors.

Keywords: H2 receptor antagonist; endoscopic submucosal dissection; gastric ulcer healing; proton pump inhibitor.

Fig. 1

Trial profile. The flow diagram of this study. (PPI group, H₂RA group)

Fig. 2

The ESD procedure and hemostasis. a: A IIa gastric tumor with the long axis of 10 mm at anterior pylorus. b: The lesion dyed with indigocarmine. c: Marking outer margin of the lesion by a coagulation wave. d: Inflation of the mucosa around the lesion by local injection of solution. e: The lesion after circumferential incision. f: Dissection of the lesion by IT-knife2. g: The lesion during dissection. h: An ulcer floor formed immediately after ESD. i: Hemostasis of vessels in the ulcer floor.

Fig. 3

Study protocol. Patients were not fed for 2 days after ESD procedures and received roxatidine acetate hydrochloride, an intravenous H₂RA given at a dosage of 150 mg/day during the fasting period. Then, both patient groups received an anti-ulcer drug orally for 8 weeks; the H₂RA group received roxatidine 150 mg/day and the PPI group received rabeprazole 10 mg/day. Patients in both groups underwent upper gastrointestinal endoscopy at 4 and 8 weeks after the start of administration.

Fig. 4

Measurement of ulcer size. The ESD-induced ulcer size was assessed by area; long and short axes (mm) of an assumed ellipse were measured using an endoscope and measuring equipment, and the ulcer size was calculated.

Fig. 5

A case treated with H₂RA (Roxatidine). a: IIa early gastric cancer at the lesser curvature of gastric angle. b: The lesion was dyed with indigocarmine. c: Immediately after ESD, an ulcer floor was formed. d: Two days after ESD, there was white moss in the ulcer floor. e: Four weeks after ESD, the ulcer floor shrunk and was surrounded by regenerating epithelium. f: Eight weeks after ESD, the ulcer floor disappeared and turned into a scar.