Purpose: The aim of this study is to summarize cancer risk among patients with clinical indications of immunosuppressive and antineoplastic drugs in Korea, which are pharmaceuticals defined as group 1 by International Agency for Research on Cancer. Materials and Methods: We conducted a nationwide population-based retrospective cohort study using the Korean National Health Insurance Service claims data from 2002 to 2018. Patients with clinical indications for group 1 pharmaceuticals from 2002 to 2017 were selected as baseline population, and followed up until 2018. Cox proportional hazards regression model was used to analyze the risk of cancer and dose-response relationship between group 1 pharmaceuticals and cancer. Results: Azathioprine use increased the risk of skin and hematologic cancer (hazard ratio [HR], 4.63; 95% confidence interval [CI], 2.91 to 7.39 and HR, 3.15; 95% CI, 2.41 to 4.13). Cyclosporine use increased the risk of skin and hematologic cancer (HR, 2.30; 95% CI, 1.79 to 2.95 and HR, 2.96; 95% CI, 2.59 to 3.40). Cyclophosphamide use increased the risk of bladder and hematologic cancer (HR, 2.69; 95% CI, 1.92 to 3.78 and HR, 3.83; 95% CI, 3.20 to 4.59). Chlorambucil use increased the risk of hematologic cancer (HR, 3.51; 95% CI, 2.53 to 4.87) and melphalan use increased the risk of hematologic cancer (HR, 16.31; 95% CI, 13.41 to 19.85). Methoxsalen use increased the risk of skin cancer (HR, 2.32; 95% CI, 1.36 to 3.95). Conclusion Group 1 pharmaceuticals were associated with increased risk of cancer. The results are expected to help establish alternative clinical strategies and policies for patients with clinical indications of group 1 pharmaceuticals, by continuous risk analysis and discussions on the surveillance systems.

Background: It is unclear whether long-term use of proton pump inhibitors (PPIs) has a potential carcinogenic effect on the colorectum. Methods: We reviewed a consecutive series of neurosurgery outpatients who underwent two or more colonoscopies between January 2014 and April 2023. Patients in whom the timing of endoscopy was not in accordance with the guidelines and those without a history of previous endoscopy were excluded. In the second colonoscopy, the risk of adenomatous colon polyps was evaluated depending on whether the patient had taken a PPI. Results: In total, 520 patients were enrolled. In the multivariate analysis related to the risk of adenomatous colon polyps, age and aspirin use for >5 years were identified as significant factors. After excluding patients who had taken aspirin for >5 years, the patients were divided into three groups: those who had taken PPIs for >12 months, those who had taken PPIs for >3 months but <12 months, and those who had not taken PPIs. The risk of adenomatous colon polyps in these groups was 35.2%, 32.8%, and 22.8%, respectively (p=0.10). In the post-hoc analysis, there was a significant difference between patients who took PPIs and those who did not (p=0.03). In the multivariate analysis, a history of PPI use for >12 months was a significant risk factor for the development of advanced colon polyps (p=0.03). Conclusion Prolonged PPI use appears to increase the risk of developing adenomatous and advanced colon polyps.

Background: It is unclear whether long-term use of proton pump inhibitors (PPIs) has a potential carcinogenic effect on the colorectum. Methods: We reviewed a consecutive series of neurosurgery outpatients who underwent two or more colonoscopies between January 2014 and April 2023. Patients in whom the timing of endoscopy was not in accordance with the guidelines and those without a history of previous endoscopy were excluded. In the second colonoscopy, the risk of adenomatous colon polyps was evaluated depending on whether the patient had taken a PPI. Results: In total, 520 patients were enrolled. In the multivariate analysis related to the risk of adenomatous colon polyps, age and aspirin use for >5 years were identified as significant factors. After excluding patients who had taken aspirin for >5 years, the patients were divided into three groups: those who had taken PPIs for >12 months, those who had taken PPIs for >3 months but <12 months, and those who had not taken PPIs. The risk of adenomatous colon polyps in these groups was 35.2%, 32.8%, and 22.8%, respectively (p=0.10). In the post-hoc analysis, there was a significant difference between patients who took PPIs and those who did not (p=0.03). In the multivariate analysis, a history of PPI use for >12 months was a significant risk factor for the development of advanced colon polyps (p=0.03). Conclusion Prolonged PPI use appears to increase the risk of developing adenomatous and advanced colon polyps.

Background: It is unclear whether long-term use of proton pump inhibitors (PPIs) has a potential carcinogenic effect on the colorectum. Methods: We reviewed a consecutive series of neurosurgery outpatients who underwent two or more colonoscopies between January 2014 and April 2023. Patients in whom the timing of endoscopy was not in accordance with the guidelines and those without a history of previous endoscopy were excluded. In the second colonoscopy, the risk of adenomatous colon polyps was evaluated depending on whether the patient had taken a PPI. Results: In total, 520 patients were enrolled. In the multivariate analysis related to the risk of adenomatous colon polyps, age and aspirin use for >5 years were identified as significant factors. After excluding patients who had taken aspirin for >5 years, the patients were divided into three groups: those who had taken PPIs for >12 months, those who had taken PPIs for >3 months but <12 months, and those who had not taken PPIs. The risk of adenomatous colon polyps in these groups was 35.2%, 32.8%, and 22.8%, respectively (p=0.10). In the post-hoc analysis, there was a significant difference between patients who took PPIs and those who did not (p=0.03). In the multivariate analysis, a history of PPI use for >12 months was a significant risk factor for the development of advanced colon polyps (p=0.03). Conclusion Prolonged PPI use appears to increase the risk of developing adenomatous and advanced colon polyps.

Background: It is unclear whether long-term use of proton pump inhibitors (PPIs) has a potential carcinogenic effect on the colorectum. Methods: We reviewed a consecutive series of neurosurgery outpatients who underwent two or more colonoscopies between January 2014 and April 2023. Patients in whom the timing of endoscopy was not in accordance with the guidelines and those without a history of previous endoscopy were excluded. In the second colonoscopy, the risk of adenomatous colon polyps was evaluated depending on whether the patient had taken a PPI. Results: In total, 520 patients were enrolled. In the multivariate analysis related to the risk of adenomatous colon polyps, age and aspirin use for >5 years were identified as significant factors. After excluding patients who had taken aspirin for >5 years, the patients were divided into three groups: those who had taken PPIs for >12 months, those who had taken PPIs for >3 months but <12 months, and those who had not taken PPIs. The risk of adenomatous colon polyps in these groups was 35.2%, 32.8%, and 22.8%, respectively (p=0.10). In the post-hoc analysis, there was a significant difference between patients who took PPIs and those who did not (p=0.03). In the multivariate analysis, a history of PPI use for >12 months was a significant risk factor for the development of advanced colon polyps (p=0.03). Conclusion Prolonged PPI use appears to increase the risk of developing adenomatous and advanced colon polyps.

Objectives: A significant number of patients with gastroesophageal reflux disease (GERD) experience refractory symptoms despite conventional doses of a proton pump inhibitor (PPI). Potassium-competitive acid blockers (PCABs) directly inhibit H+,K+-ATPase in a reversible manner and more profoundly inhibit acid secretion. However, the efficacy of PCABs in the treatment of refractory symptoms has not been thoroughly studied. Methods: This consecutive study was conducted between March 2020 and March 2023; patients with refractory symptoms were enrolled. Esophagogastroduodenoscopy, ambulatory esophageal pH measurements, and manometry were performed. Double split doses of rabeprazole (20 mg) or tegoprazan (50 mg) were prescribed for 2 weeks, and the symptoms were subsequently evaluated. A positive response was defined as more than 50% improvement in the visual analog scale scores for symptom severity. Results: A total of 63 patients were enrolled. In the group that received a double split dose of PPI (n=33), the positive response rate was 63.6% (21/33). There were 18 cases of abnormal acid exposure (excessive esophageal acid exposure time [AET] >4.0%); the positive response rate was 50.0% (9/18). In the group treated with PCAB (n=30), the positive response rate was 80.0% (24/30) (p=0.15). There were 19 cases of abnormal acid exposure; the positive response rate was 84.2% (16/19). The difference was statistically significant in favor of the PCAB group (p=0.02). Conclusions In patients with refractory GERD symptoms, PCAB therapy had effects corresponding to those of a double split dose of PPIs. PCAB therapy was therefore deemed superior to PPIs, especially in patients with abnormal AETs

Background/Aims: The effects of probiotic supplementation on Helicobacter pylori (H. pylori) eradication therapy are not completely understood. In this study, we investigated the effects of continuous probiotic administration on eradication rates, recrudescence, and symptom response following completion of a course of H. pylori therapy. Methods: This prospective, randomized, double-blind placebo-controlled trial was performed between June 2018 and 2020. Twohundred seventy patients who received a standard triple regimen for H. pylori eradication, were included in the study. Participants were randomized to receive a probiotic as adjunctive therapy (Enterococcus faecium 4.5×108 and Bacillus subtilis 5.0×107; Medilac-S®, Hanmi Pharmaceuticals, Seoul, Korea) or a placebo (one tablet thrice daily) for 28 days, following H. pylori eradication. Participants who showed successful eradication underwent a repeat 13C-urea breath test after 6 months. Results: Eradication rates in the probiotic and placebo groups were 77.1% and 72.4%, respectively (P=0.48) using per-protocol analysis. Using intention-to-treat analysis, eradication rates were 67.4% and 65.9%, respectively (P=0.43). Of 149 patients who were followed-up after 6 months, four patients had recrudescence (2.7%). Recrudescence rates did not differ between the probiotic and placebo groups. Of the 76 patients who had non-ulcer dyspepsia, 60 (78.9%) showed symptom resolution after 6 months. This beneficial effect was most pronounced in patients with postprandial distress syndrome (P=0.02). Conclusions Consecutive probiotic supplementation following H. pylori eradication therapy did not increase eradication rates or decrease recrudescence rates.

Chronic inflammation due to a Helicobacter pylori (H. pylori) infection is a representative cause of gastric cancer that can promote gastric carcinogenesis by abnormally activating immune cells and increasing the inflammatory cytokines levels. H. pylori infections directly cause DNA double-strand breaks in gastric epithelial cells and genetic damage by increasing the enzymatic activity of cytidine deaminase. Eventually, gastric cancer is induced through dysplasia. Hypermethylation of tumor suppressor genes is an important cause of gastric cancer because of a H. pylori infection. In addition, the changes in gastric microbiota and the mucosal inflammatory changes associated with a co-infection with the Epstein-Barr virus are associated with gastric cancer development. DNA damage induced by H. pylori and the subsequent responses of gastric stem cells have implications for gastric carcinogenesis. Although the pathogenesis of H. pylori has been established, many uncertainties remain, requiring more study.

Background/Aims: Compared with other regimens, concomitant therapy (CT) used as a first-line regimen for Helicobacter pylori (H. pylori) infection is associated with higher eradication rates. We compared the efficacy of tailored therapy (TT) using bismuth added to standard triple therapy (STT) with CT. Methods: This consecutive study performed between September 2020 and 2021 included 210 patients with H. pylori infection. Two participating gastroenterologists prescribed TT and CT. Multiplex PCR assays were performed before eradication therapy to identify the relevant point mutations and confirm clarithromycin resistance in the TT group (n=105). Patients who showed negative PCR results received 14-day STT and those with positive PCR results received a 14-day regimen of bismuth added to STT. The other group (n=105) received 10-day CT. Results: Based on per-protocol analysis, eradication rates in the TT and CT groups were 89.2% (91/102) and 81.6% (84/103), respectively. We observed no statistically significant intergroup differences in eradication rates (P=0.12). The frequency of estimated clarithromycin resistance confirmed using multiplex PCR assays was 32.4% (34/105), and the eradication rate associated with bismuth add-on STT was 76.5% (26/34) in patients with clarithromycin resistance. Conclusions Considering the current and emerging trends in antibiotic resistance, a therapeutic strategy using TT (bismuth add-on STT) is recommended to minimize unnecessary administration of antibiotics.