Factors associated with healing of artificial ulcer after endoscopic submucosal dissection with reference to Helicobacter pylori infection, CYP2C19 genotype, and tumor location: Multicenter randomized trial.
OBJECTIVE
Healing speed of peptic ulcer is affected by a number of factors, including Helicobacter pylori (H. pylori) infection and intragastric pH. Acid inhibition exerted by proton pump inhibitors differs by CYP2C19 genotype. Herein, we investigated whether healing speed of artificial ulcers formed after endoscopic submucosal dissection (ESD) was influenced by H. pylori infection, CYP2C19 genotype, or other factors.


METHODS
A total of 96 H. pylori-positive patients with gastric tumors scheduled for ESD were randomly assigned to receive eradication therapy for H. pylori before ESD (pre-ESD eradication) (n = 44) or after (post-ESD eradication) (n = 52). Patients received eradication therapy consisting of lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 200 mg twice daily for 1 week. After ESD, lansoprazole 30 mg was given once daily for 8 weeks. Ulcer size was endoscopically measured on the next day and at 4 and 8 weeks after ESD.


RESULTS
Mean reduction rate of artificial ulcer area in the pre-ESD eradication group was 94.7% ± 5.5% at 4 weeks, which was similar to that in the post-ESD eradication group (94.7% ± 6.7%, P = 0.987), irrespective of CYP2C19 genotype. In multivariate analyses, location of gastric tumor (middle and upper, odds ratio: 4.05, 95% CI: 1.620-10.230, P = 0.003) was a factor for 97% reduction of artificial ulcer area at 4 weeks post-ESD, but CYP2C19 genotype and H. pylori infection were not.


CONCLUSIONS
Healing speed of ESD-induced artificial ulcer was affected by tumor location, but not by time of H. pylori eradication, resected size, or CYP2C19 genotype.
Department of Gastroenterology, Seirei Hamamatsu General Hospital.
Yashiro
Y
Yoshizawa
First Department of Medicine.
Mitsushige
M
Sugimoto
Department of Gastroenterology, Seirei Hamamatsu General Hospital.
Yoshihiko
Y
Sato
First Department of Medicine.
Shu
S
Sahara
First Department of Medicine.
Hitomi
H
Ichikawa
First Department of Medicine.
Takuma
T
Kagami
Department of Gastroenterology, Seirei Hamamatsu General Hospital.
Yoshisuke
Y
Hosoda
Department of Gastroenterology, Seirei Hamamatsu General Hospital.
Masaharu
M
Kimata
Department of Gastroenterology, Seirei Hamamatsu General Hospital.|First Department of Medicine.
Satoshi
S
Tamura
Department of Gastroenterology, Seirei Hamamatsu General Hospital.
Yousuke
Y
Kobayashi
Department of Endoscopic and Photodynamic Medicine.
Satoshi
S
Osawa
First Department of Medicine.
Ken
K
Sugimoto
First Department of Medicine.
Hiroaki
H
Miyajima
Center for Clinical Research, Hamamatsu University of Medicine, Hamamatsu, Japan.
Takahisa
T
Furuta
D000368:Aged; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D065731:Cytochrome P-450 CYP2C19 / Q000096:biosynthesis / Q000235:genetics*; D004273:DNA, Neoplasm / Q000235:genetics; D000069916:Endoscopic Mucosal Resection / Q000379:methods*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D013274:Stomach Neoplasms / Q000175:diagnosis / Q000209:etiology / Q000601:surgery*; D013276:Stomach Ulcer / Q000150:complications* / Q000175:diagnosis / Q000628:therapy
D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D004273:DNA, Neoplasm; D065731:Cytochrome P-450 CYP2C19
CYP2C19; Helicobacter pylori; artificial ulcer; endoscopic submucosal dissection; eradication