Yoon Suk Jung

INTRODUCTION: Potassium-competitive acid blockers and proton pump inhibitors/sodium bicarbonate can rapidly increase intragastric pH. In this study, we aimed to compare the clinical outcomes of tegoprazan-based and esomeprazole/sodium bicarbonate–based triple therapies in the treatment of Helicobacter pylori infection. METHODS: We retrospectively reviewed the data of patients with H. pylori infection treated with a 14-day tegoprazan-based triple therapy or 14-day esomeprazole/sodium bicarbonate–based triple therapy. The primary end point was the H. pylori eradication rate with first-line treatment in an intention-to-treat analysis. Secondary end points included the eradication rate with first-line therapy in the per-protocol analysis and adverse events associated with eradication therapy. RESULTS: Of the 854 included patients, 435 were treated with tegoprazan-based therapy, and 419 received esomeprazole/sodium bicarbonate–based therapy. In the intention-to-treat population, no significant difference in eradication rate was detected between the tegoprazan-treated and esomeprazole/sodium bicarbonate–treated groups (78.6% [95% confidence interval (CI), 74.6–82.3%] vs 81.4% [95% CI, 77.4–84.9%], P = 0.313). The per-protocol analysis also revealed a similar eradication rate between groups (tegoprazan vs esomeprazole/sodium bicarbonate: 85.5% [95% CI, 81.8–87.5%] vs 87.8% [95% CI, 84.1–90.7%], P = 0.339). However, abdominal discomfort and diarrhea were more common in the esomeprazole/sodium bicarbonate–treated group than in the tegoprazan-treated group (abdominal discomfort: 1.1% vs 3.8%, P = 0.012; diarrhea: 9.9% vs 21.2%, P < 0.001). DISCUSSION: The efficacy of the esomeprazole/sodium bicarbonate–based triple therapy for H. pylori eradication was comparable with that of the tegoprazan-based triple therapy. However, esomeprazole/sodium bicarbonate–based therapy exhibited a higher risk of abdominal discomfort and diarrhea than tegoprazan-based therapy.

Background and Aim We evaluated the associations between gastric cancer (GC) family history (FH) and colorectal cancer (CRC) risk and between CRC FH and GC/gastric adenoma risk. Methods We used data of participants who underwent national cancer screening between 2013 and 2014. Participants with GC or CRC FH in first‐degree relatives ( n = 1 172 750) and those without cancer FH ( n = 3 518 250) were matched 1:3 by age and gender. Results Of the 1 172 750 participants with a FH, 871 104, 264 040, and 37 606 had FHs of only GC, only CRC, and both GC and CRC, respectively. The median follow‐up time was 4.8 years. GC and CRC FHs were associated with increased GC and CRC risks, respectively. GC FH was associated with CRC risk (adjusted hazard ratio 1.05; 95% confidence interval [CI] 1.01–1.10), whereas CRC FH was not associated with the risk of GC or gastric adenoma. However, gastric adenoma risk increased 1.62‐fold (95% CI 1.40–1.87) in participants with FHs of both GC and CRC, demonstrating a significant difference with the 1.39‐fold (95% CI 1.34–1.44) increase in participants with only GC FH. Furthermore, GC risk increased by 5.32 times (95% CI 1.74–16.24) in participants with FHs of both GC and CRC in both parents and siblings. Conclusions GC FH was significantly associated with a 5% increase in CRC risk. Although CRC FH did not increase GC risk, FH of both GC and CRC further increased the risk of gastric adenoma. FHs of GC and CRC may affect each other's neoplastic lesion risk.