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Currently, no consensus exists on optimal treatment for post-endoscopic submucosal dissection (ESD) gastric ulcer. This study aims to compare rebamipide and tegoprazan combination therapy with tegoprazan monotherapy for post-ESD ulcer healing. Between May 2022 and September 2023, 140 patients (141 lesions) who underwent ESD for gastric epithelial neoplasms at five tertiary hospitals were randomly assigned to tegoprazan monotherapy or combination therapy groups. The size, stage and healing quality of the post-ESD ulcers were assessed at weeks 4 and 8. Modified intention-to-treat (mITT) and per-protocol analyses included 132 and 121 lesions, respectively. The ulcer healing rate at week 4 was significantly higher in the combination therapy group than in the tegoprazan monotherapy group (96.4% vs. 93.6%, P  = 0.02 in mITT). Combination therapy significantly predicted higher-than-average ulcer healing at week 4 (odds ratio 2.28, 95% confidence interval 1.04–5.02, P  = 0.04). The proportion of flat ulcer scar at week 8 was significantly higher in the combination group than in the tegoprazan monotherapy group (73.8% vs. 48.4%, P  = 0.007). Combination treatment with rebamipide and tegoprazan led to faster ulcer healing and the development of high-quality post-ESD scars compared to tegoprazan monotherapy.

The term Equine Gastric Ulcer Syndrome (EGUS) was first used in 1999 to describe gastric ulceration in the horse.1 However, as discussed by Merritt,2 the terminology is commonly misused. The committee reinforces the importance of distinguishing between diseases of the squamous and glandular mucosa because, as discussed in this statement, important differences exist between the two. In human medicine, the term peptic ulcer disease (PUD) is used as an umbrella term to describe erosive and ulcerative diseases of the stomach and it is recognized that a large number of individual diseases are present under the term.3 Furthermore, while some different diseases might share similarities in pathophysiology and treatment regimens, it is recognized in human medicine that the direct extrapolation of either from one specific disease (such as NSAID-associated ulceration) to another (such as Helicobacter pylori associated ulceration) is inappropriate.3

Background Patients with high Rockall scores have increased risk of ulcer rebleeding after 3-day esomeprazole infusions. Objective To investigate whether double oral esomeprazole given after a 3-day esomeprazole infusion decreases ulcer rebleeding for patients with high Rockall scores. Design We prospectively enrolled 293 patients with peptic ulcer bleeding who had achieved endoscopic haemostasis. After a 3-day esomeprazole infusion, patients with Rockall scores ≥6 were randomised into the oral double-dose group (n=93) or the oral standard-dose group (n=94) to receive 11 days of oral esomeprazole 40 mg twice daily or once daily, respectively. The patients with Rockall scores <6 served as controls (n=89); they received 11 days of oral esomeprazole 40 mg once daily. Thereafter, all patients received oral esomeprazole 40 mg once daily for two more weeks until the end of the 28-day study period. The primary end point was peptic ulcer rebleeding. Results Among patients with Rockall scores ≥6, the oral double-dose group had a higher cumulative rebleeding-free proportion than the oral standard-dose group (p=0.02, log-rank test). The proportion of patients free from recurrent bleeding during the 4th–28th day in the oral double-dose group remained lower than that of the group with Rockall scores <6 (p=0.03, log-rank test). Among patients with Rockall scores ≥6, the rebleeding rate was lower in the oral double-dose group than in the oral standard-dose group (4th–28th day: 10.8% vs 28.7%, p=0.002). Conclusions Double oral esomeprazole at 40 mg twice daily after esomeprazole infusion reduced recurrent peptic ulcer bleeding in high-risk patients with Rockall scores ≥6. Trial registration number NCT01591083.

Gastric ulcers occur due to an imbalance between harmful and protective factors. This study aimed to examine the effect of L-arginine on ethanol-induced gastric ulcers in rats. In this study, 30 male Wistar rats were divided into five groups: a control group that received saline, group 1 which was treated with 70% ethanol to induce gastric ulcers, group 2 that received saline along with L-arginine at a dose of 500 mg/kg administered intraperitoneally, group 3 that was given ethanol along with L-arginine at the same dose but administered orally, and group 4 which received ethanol together with omeprazole at a dose of 10 mg/kg administered intraperitoneally. After the ethanol treatment induced ulceration, gastric lesions were evaluated, and assays were performed to measure antioxidant enzyme levels, malondialdehyde (MDA) levels, and the gene expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS). Treatment with L-arginine or omeprazole reduced ethanol-induced gastric damage by lowering the ulcer index, increasing gastric pH, improving antioxidant status (decreased MDA, increased SOD and CAT), and modulating NO and iNOS levels. L-arginine showed protective effects comparable to those of omeprazole. This study shows that L-arginine can effectively reduce gastric mucosal injury caused by ethanol, achieving results comparable to those of omeprazole. The protective effects of L-arginine are likely due to its ability to enhance antioxidant defenses, regulate gastric acidity, and modulate nitric oxide pathways. These findings highlight the potential therapeutic role of L-arginine in managing gastric ulcers.

Background Equine gastric ulcer syndrome (EGUS) adversely affects the health, welfare, and performance of sports horses, requiring gastroscopy for definitive diagnosis. Owners frequently consider girth aversion as highly suggestive of EGUS. Objectives To evaluate whether owner‐reported clinical signs or fecal occult blood tests (FOBTs) can help identify horses needing gastroscopy for EGUS diagnosis or monitoring treatment, thereby reducing unnecessary procedures in unaffected horses. Animals Eighty competition dressage horses referred by veterinarians for EGUS evaluation. Methods Case–control study including questionnaire, clinical examination, gastroscopy, and FOBT. Based on gastroscopic findings, horses were classified as cases (presenting equine squamous gastric disease, equine glandular gastric disease, or both) or controls (no lesions). Nineteen horses underwent a follow‐up examination after EGUS treatment. Predictive values of clinical signs and fecal hemoglobin were assessed using the Wilson–Brown method, and group differences were analyzed using Mann–Whitney and Fisher's exact tests. Results Fifty‐five horses (69%) had EGUS. The most commonly reported clinical signs in this cohort included girth aversion (78%), poor performance (33%), and weight loss (30%), with no differences between groups (p = 0.44–0.99). Neither clinical signs nor FOBT had sufficient sensitivity or specificity for EGUS screening. Among the 19 horses reevaluated after treatment, resolution of clinical signs did not reliably predict mucosal healing, with poor agreement between owner‐reported clinical response and gastroscopic outcome. Conclusions and Clinical Importance In competition dressage horses, owner‐reported clinical signs and FOBT results are unreliable predictors of EGUS or treatment outcomes. Gastroscopy remains essential for accurately diagnosing and monitoring EGUS in sports horses.

Ethanol consumption is one of the common causative agents implicated in gastric ulcer development. Oxidative stress plays a major role in the induction and development of gastric ulceration. NADPH oxidases (NOXs) and Nuclear factor erythroid 2-related factor 2 (Nrf2) are key players in ethanol-induced ulcers. High-mobility group box 1 (HMGB1), a ubiquitous nuclear protein, mediates various inflammation functions. However, the role of HMGB1 in ethanol-induced gastric ulcer is not yet elucidated. Raspberry Ketone (RK) is a natural phenolic compound with antioxidant and anti-inflammatory properties. In the present study, absolute ethanol (7.5 ml/kg) was used to induce gastric ulceration in rats. Raspberry Ketone (RK) (50 mg/kg) was given orally one hour before the administration of absolute ethanol. Interestingly, ethanol-induced gastric ulcer was associated with Nrf2 downregulation, which was correlated with NOX-1, 2 NOX-4, and HMGB1 upregulation, and was significantly reversed by RK pre-treatment. RK pre-treatment provided 80% gastroprotection. Gastroprotective properties of RK were mediated via antioxidant, anti-inflammatory (suppression of NF-kB and tumor necrosis factor-α), and antiapoptotic activities (reduction of Bax/Bcl2 ratio). Gastroprotective properties of RK were confirmed by histopathological examination. In conclusion, this study is the first to provide evidence to the role of HMGB1 in ethanol-induced gastric ulcer, and the crosstalk of Nrf2, NOXs and HMGB1. It also demonstrates that RK represents a promising gastroprotective activity comparable to omeprazole.

The primary objective of our research is to investigate the gastroprotective impact of Ficus. carica L. latex extract (FCL). Metabolic profiling based on HR- LCMS for the extract led to the annotation of 20 compounds. Additionally, the gastro-protective activity of the latex extract was evaluated in vivo using male albino rats. FCL significantly alleviated the indomethacin-induced ulceration and reduced the ulcer index. Furthermore, the inflammation caused by indomethacin was seen to diminish due to the downregulation of the production of certain genes (IL-6, and TNF-α, IL-1β). Besides, FCL considerably reduced the elevated TGF-β, and IGF-1, COX-2 relative gene expression. Likewise, FCL dramatically raised EGF and KGF relative gene expression, demonstrating its beneficial impact in ulcer healing. The antioxidant ability of FCL was assessed by in vitro experiments utilizing hydrogen peroxide and superoxide radical scavenging, which demonstrated significant antioxidant capacity. Employing network pharmacology, we identified 10 hub genes central to peptic ulcer disease and conducted molecular docking studies screening interactions between FCL extract compounds and these hubs along with anti-inflammatory targets including FGFR, TGF-βR, IGFR-1R and IL-1R1 involved in ulcer healing. Additionally, an in-silico study using annotated FCL compounds highlighted Ficuseptin-C, Ficuseptin-B and Ficusin-A in the extract may contribute to its antiulcer properties. The present study highlighted the potential of FCL as a promising natural gastro-protective agent.

Naringenin is a major flavanone found in grapes, tangelos, blood oranges, lemons, pummelo, and tangerines. It is known to have anti-inflammatory, antioxidant, anticancer, antimutagenic, antifibrogenic, and antiatherogenic pharmacological properties. This study aims to investigate the anti-inflammatory effects of naringenin in ethanol-induced gastric damage in vivo and ethanol-stimulated KATO III cells in vitro. Our results showed that pretreatment with naringenin significantly protected mice from ethanol-induced hemorrhagic damage, epithelial cell loss, and edema with leucocytes. It reduced gastric ulcers (GU) by suppressing ethanol-induced nuclear factor-κB (NF-κB) activity and decreasing the levels of nitric oxide (NO), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-8 (IL-8), and myeloperoxidase (MPO). In addition, pretreatment with naringenin might inhibit the secretion of TNF-α, IL-6, and IL-8, as well as the proteins cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) via the suppression of NF-κB and mitogen-activated protein kinase (MAPK) signaling in ethanol-stimulated stomach epithelial KATO III cells. Together, the results of this study highlight the gastroprotective effect of naringenin in GU of mice by inhibiting gastric secretion and acidity, reducing inflammation and oxidative stress, suppressing NF-κB activity, and restoring the histological architecture. These findings suggested that naringenin has therapeutic potential in the alleviation of ethanol-induced GU.

Innovative treatment strategies are required for stomach ulcers because of their multifactorial nature. Nanotechnology has emerged as a promising and transformative platform for the formulation and targeted delivery of therapeutic agents. The gastroprotective potential of both in its free form and encapsulated in calcium alginate beads was evaluated against ethanol-induced gastric ulceration in rats. Phytol-loaded nanoemulsions were incorporated into alginate beads to achieve controlled release. Alginate beads showed a pH-dependent release pattern. The release behavior showed a higher release rate at pH 6.8 than at pH 1.2. Phytol release kinetics followed the Korsmeyer-Peppas model, indicating a release mechanism governed by diffusion and polymer relaxation. Rats were pretreated with Phytol and/or nano-Phytol at 10 or 20 mg/kg doses administered one hour before ethanol exposure. Gastric ulcer was induced by administration of EtOH (1 mL/kg, p.o.) 0.5 h after NG-nitro-L-Arginine Methyl Ester (L-NAME) or Aminoguanidine (AMG) injection. Phytol treatment led to a reduction in ulcer index and severity and improved stomach gross morphology. Also, interleukin-6 (IL-6) gastric contents were reduced, whereas transforming growth factor β (TGF-β1) was elevated, and histopathological features were ameliorated. Western blot analysis revealed that nano-Phytol exerted greater inhibitory effects on caspase-3 and Nuclear Factor kappa B (NF-κB) than unformulated Phytol. Interestingly, Phytol's pharmacological effects on ulcers were enhanced by its nanoformulation in a dose-dependent way without exhibiting any toxicity symptoms. Confocal laser scanning microscopy (CLSM) confirmed significantly improved tissue penetration of nano-Phytol within the stomach layers compared to the Phytol. The Phytol or nano-Phytol gastroprotective effects were modified via the co-administration of L-NAME and AMG. The nano-Phytol formulation significantly enhanced the gastroprotective effect of Phytol against ethanol-induced gastric ulcers, primarily through modulation of the nitric oxide (NO) synthase pathway, suppression of inflammation, and upregulation of the growth factor TGF-β1.

BackgroundThe recommendation of second look endoscopy (SLOGD) in selected patients at high risk for rebleeding has been inconclusive. This study aimed to evaluate the benefit of SLOGD in selected patients predicted at high risk of recurrent bleeding.MethodsFrom a cohort of 939 patients with bleeding peptic ulcers who underwent endoscopic hemostasis, we derived a 9-point risk score (age > 60, Male, ulcer ≥ 2 cm in size, posterior bulbar or lesser curve gastric ulcer, Forrest I bleeding, haemoglobin < 8 g/dl) to predict recurrent bleeding. We then validated the score in another cohort of 1334 patients (AUROC 0.77). To test the hypothesis that SLOGD in high-risk patients would improve outcomes, we did a randomized controlled trial to compare scheduled SLOGD with observation alone in those predicted at high risk of rebleeding (a score of ≥ 5). The primary outcome was clinical bleeding within 30 days of the index bleed.ResultsOf 314 required, we enrolled 157 (50%) patients (SLOGD n = 78, observation n = 79). Nine (11.8%) in SLOGD group and 14 (18.2%) in observation group reached primary outcome (absolute difference 6.4%, 95% CI − 5.0% to 17.8%). Twenty-one of 69 (30.4%) patients who underwent SLOGD needed further endoscopic treatment. No surgery for bleeding control was needed. There were 6 vs. 3 of 30-day deaths in either group (p = 0.285, log rank). No difference was observed regarding blood transfusion and hospitalization.ConclusionsIn this aborted trial that enrolled patients with bleeding peptic ulcers at high-risk of recurrent bleeding, scheduled SLOGD did not significantly improve outcomes.ClinicalTrials.gov:NCT02352155.