NSAIDs including loxoprofen increase the risk of UGIB in Japan as in Western countries, with a similar magnitude of association. There was no evidence of biological interaction between NSAIDs and H. pylori infection.
Background:Deep learning is a type of artificial intelligence (AI) that imitates the neural network in the brain. We generated an AI to diagnose Helicobacter pylori (H. pylori) infection using blue laser imaging (BLI)-bright and linked color imaging (LCI). The aim of this pilot study was to establish an AI diagnosing system that predicts H. pylori infection status using endoscopic images to improve the accuracy and productivity of endoscopic examination.Methods:A total of 222 enrolled subjects (105 H. pylori-positive) underwent esophagogastroduodenoscopy and a serum test for H. pylori IgG antibodies. During esophagogastroduodenoscopy, an endoscopist sequentially took 3 still images of the lesser curvature of the stomach using white light imaging (WLI), BLI-bright, and LCI. EG-L580NW endoscopic equipment (FUJIFILM Co., Japan) was used for the study. The specifications of the AI were as follows: operating system, Linux; neural network, GoogLeNet; framework, Caffe; graphic processor unit, Geforce GTX TITAN X (NVIDIA Co., USA).Results:The area under the curve (AUC) on receiver operating characteristics analysis was 0.66 for WLI. In contrast, the AUCs of BLI-bright and LCI were 0.96 and 0.95, respectively. The AUCs obtained for BLI-bright and LCI were significantly larger than those for WLI (P<0.01).Conclusions:The results demonstrate that the developed AI has an excellent ability to diagnose H. pylori infection using BLI-bright and LCI. AI technology with image-enhanced endoscopy is likely to become a useful image diagnostic tool.
Summary
Background
Vonoprazan is a new potassium‐competitive acid blocker for treatment of acid‐related diseases.
Aim
To conduct two randomised‐controlled trials, to evaluate the non‐inferiority of vonoprazan vs. lansoprazole, a proton pump inhibitor, for treatment of gastric ulcer (
GU
) or duodenal ulcer (
DU
).
Methods
Patients aged ≥20 years with ≥1 endoscopically‐confirmed
GU
or
DU
(≥5 mm white coating) were randomised 1:1 using double‐dummy blinding to receive lansoprazole (30 mg) or vonoprazan (20 mg) for 8 (
GU
study) or 6 (
DU
study) weeks. The primary endpoint was the proportion of patients with endoscopically confirmed healed
GU
or
DU
.
Results
For
GU
, 93.5% (216/231) of vonoprazan‐treated patients and 93.8% (211/225) of lansoprazole‐treated patients achieved healed
GU
; non‐inferiority of vonoprazan to lansoprazole was confirmed [difference = −0.3% (95%
CI
−4.750, 4.208);
P
= 0.0011]. For
DU
, 95.5% (170/178) of vonoprazan‐treated patients and 98.3% (177/180) of lansoprazole‐treated patients achieved healed
DU
; non‐inferiority to lansoprazole was not confirmed [difference = −2.8% (95%
CI
−6.400, 0.745);
P
= 0.0654]. The incidences of treatment‐emergent adverse events were slightly lower for
GU
and slightly higher for
DU
with vonoprazan than with lansoprazole. There was one death (subarachnoid haemorrhage) in the vonoprazan group (
DU
). The possibility of a relationship between this unexpected patient death and the study drug could not be ruled out. In both studies, increases in serum gastrin levels were greater in vonoprazan‐treated vs. lansoprazole‐treated patients; levels returned to baseline after treatment in both groups.
Conclusions
Vonoprazan 20 mg has a similar tolerability profile to lansoprazole 30 mg and is non‐inferior with respect to
GU
healing and has similar efficacy for
DU
healing.
BackgroundThe efficacy of low-dose lansoprazole has not been established for the prevention of recurrent gastric or duodenal ulcers in those receiving long-term low-dose aspirin (LDA) for cardiovascular and cerebrovascular protection. This study sought to examine the efficacy of low-dose lansoprazole (15 mg once daily) for the secondary prevention of LDA-associated gastric or duodenal ulcers.MethodsPatients were randomized to receive lansoprazole 15 mg daily (n = 226) or gefarnate 50 mg twice daily (n = 235) for 12 months or longer in a prospective, multicenter, double-blind, randomized active-controlled trial, followed by a 6-month follow-up study with open-label lansoprazole treatment. The study utilized 94 sites in Japan and 461 Japanese patients with a history of gastric or duodenal ulcers who required long-term LDA therapy for cardiovascular and cerebrovascular disease.ResultsThe primary endpoint was the development of gastric or duodenal ulcers. The cumulative incidence of gastric or duodenal ulcers on days 91, 181, and 361 from the start of the study was calculated by the Kaplan–Meier method as 1.5, 2.1, and 3.7%, respectively, in the lansoprazole group versus 15.2, 24.0, and 31.7%, respectively, in the gefarnate group. The risk of ulcer development was significantly (log-rank test, P < 0.001) lower in the lansoprazole group than in the gefarnate group, with the hazard ratio being 0.099 (95% confidence interval [CI] 0.042–0.230).ConclusionLansoprazole was superior to gefarnate in reducing the risk of gastric or duodenal ulcer recurrence in patients with a definite history of gastric or duodenal ulcers who required long-term LDA therapy.Electronic supplementary materialThe online version of this article (doi:10.1007/s00535-011-0397-7) contains supplementary material, which is available to authorized users.
Curative treatment of H. pylori infection is useful in preventing ulcer recurrence. Gastric ulcer is more likely to relapse than duodenal ulcer. Recurrent ulcer tended to recur at the site of the original ulcers.
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