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Background and AimPBK‐1701TC is a novel sulfate tablet‐based that contains 320 mg of simethicone and delivers 90% of the salt and water delivered by oral sulfate solution (OSS) preparation. This study evaluated the efficacy, safety, and tolerability of PBK‐1701TC compared with OSS in bowel preparation for colonoscopy.MethodsThis randomized, multicenter, phase 3 non‐inferiority trial included adults aged 19 years or older with a body mass index of 19–30 kg/m2 undergoing colonoscopy at five university hospitals in Korea. The primary efficacy endpoint was successful bowel‐cleansing rate, defined as Harefield Cleansing Scale grade A or B as evaluated by blinded central readers. Secondary endpoints included the presence of residual air bubbles. Adverse events and laboratory evaluations were monitored to assess safety. Tolerability was assessed via participant interview.ResultsOverall, 235 participants were randomized, and 224 were included in the per‐protocol analysis (PBK, 112; OSS, 112). Successful bowel cleansing was achieved for 95.5% (107/112) in the PBK group, which was non‐inferior to the OSS group (98.2%, 110/112) with a difference of −2.7% (one sided 97.5% confidence limit, −8.1%). The participants in the PBK group had fewer intraluminal bubbles (0.9% vs 81.3%, P < 0.001) and reported a lower incidence of nausea and vomiting, with better acceptance, taste, and willingness to repeat the regimen than those in the OSS group (all P < 0.05).ConclusionThe novel sulfate tablet, PBK‐1701TC, was non‐inferior to OSS with respect to bowel‐cleansing efficacy and exhibited better safety and tolerability in adults undergoing colonoscopy.

BackgroundWe investigated the inhibitory effect of pantoprazole on signal transducer and activator of transcription 3 (STAT3) activity and invasiveness of gastric adenocarcinoma cells, and the role of SH2-containing protein tyrosine phosphatase 1 (SHP-1) in mediating role.MethodsWe used AGS and MKN-28 cells because of reduced SHP-1 and preserved p-STAT3 expression. Western blot, wound closure assay, Matrigel invasion assay and 3-D culture invasion assay were performed. Pharmacologic inhibitor of SHP-1 and siRNA were used for validation of the role of SHP-1.ResultsWe observed that pantoprazole at 40, 80, and 160 μg/ml upregulated SHP-1 and downregulated p-STAT3 expression in a dose-dependent manner in AGS and MKN-28 cells. Furthermore, pantoprazole significantly downregulated mesenchymal markers (Snail1 and vimentin), upregulated epithelial marker (E-cadherin), and inhibited migration and invasion of AGS and MKN-28 cells. To validate the role of SHP-1 in inhibition of STAT3 activity by pantoprazole in gastric cancer cells, we performed pharmacologic inhibition (pervanadate) or knockdown of SHP-1 before pantoprazole treatment, which significantly attenuated the suppression of p-STAT3 and anti-migration and invasion effect by pantoprazole in AGS cells. In xenograft tumor model, tumor volume was significantly reduced by intraperitoneal injection of pantoprazole, with upregulation of SHP-1 and downregulation of p-STAT3, which were attenuated by concomitant injection of pervanadate.ConclusionOur data suggest that the inhibitory effect of pantoprazole on cellular migration and invasion might be through inducing SHP-1 in gastric cancer cells.

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Nonsteroidal anti-inflammatory drugs (NSAIDs) and low-dose aspirin (LDA) are the main causes of peptic ulcer (PU), and cause major complication such as bleeding and perforation. The interaction of Helicobacter pylori infection with NSAIDs or LDA is complex and remains unclear. However, H. pylori infection may play additive, synergistic, or antagonistic roles in the development of drug-induced PU. H. pylori infection and NSAID use are independent risk factors for the development of PU, which is thought to be a synergistic effect. Eradication of H. pylori significantly reduces the incidence of PU in NSAID-naïve patients. However, the effect of secondary prevention is controversial, especially in chronic NSAID users. The use of a gastroprotective agent such as a proton pump inhibitor (PPI) is mandatory to prevent the recurrence of PU in patients with a previous history, especially in chronic NSAID users. H. pylori infection may also increase the risk of LDA-associated complicated and uncomplicated PU, including the risk of upper gastrointestinal bleeding. In patients taking LDA, H. pylori eradication alone may prevent the recurrence of PU bleeding. However, PPI maintenance is necessary with concomitant use of an NSAID, steroid, anticoagulant, or other antiplatelet agents. (Korean J Helicobacter Up Gastrointest Res 2018;18:89-94)