Search Results (612)

Malignant gastric outlet obstruction (MGOO) is a serious complication arising from advanced gastric or pancreatic head cancer, significantly impairing patients’ quality of life by disrupting oral intake and inducing severe gastrointestinal symptoms. With benign causes such as peptic ulcer disease on the decline, malignancies now account for 50–80% of gastric outlet obstruction (GOO) cases globally. This review outlines the pathophysiology, evolving epidemiology, and treatment modalities for MGOO. Therapeutic approaches include conservative management, endoscopic stenting, surgical gastrojejunostomy (GJ), stomach partitioning gastrojejunostomy (SPGJ), and endoscopic ultrasound-guided gastroenterostomy (EUS-GE). While endoscopic stenting offers rapid symptom relief with minimal invasiveness, it has higher rates of re-obstruction. Surgical options like GJ and SPGJ provide more durable palliation, especially for patients with longer expected survival. SPGJ, a modified surgical technique, demonstrates reduced incidence of delayed gastric emptying and may improve postoperative oral intake and survival compared to conventional GJ. EUS-GE represents a promising, minimally invasive alternative that combines surgical durability with endoscopic efficiency, although long-term data remain limited. Treatment selection should consider patient performance status, tumor characteristics, prognosis, and institutional resources. This comprehensive review underscores the need for individualized, multidisciplinary decision-making to optimize symptom relief, nutritional status, and overall outcomes in patients with MGOO. Full article

Background/Objectives: Helicobacter pylori (H. pylori) is a common gastric pathogen linked to gastritis, gastroduodenal ulcers, and gastric cancer. Rising antimicrobial resistance (AMR) poses challenges for effective treatment and has prompted the WHO to classify H. pylori as a high-priority pathogen. This study aimed to detect the prevalence of AMR genes in H. pylori-positive gastric samples from patients in Algarve, Portugal, where regional data is scarce. Methods: Eighteen H. pylori-positive gastric biopsy samples from patients undergoing upper gastrointestinal endoscopy were analyzed. PCR and sequencing were used to identify genes associated with resistance to amoxicillin (Pbp1A), metronidazole (rdxA, frxA), tetracycline (16S rRNA mutation) and clarithromycin (23S rRNA). Sequence identity and homologies were verified using tBLASTx and the Comprehensive Antibiotic Resistance Database (CARD). Results: Out of the 18 H. pylori-positive samples, 16 (88.9%) contained at least one AMR gene. The most frequent genes were rdxA (83.3%) and frxA (66.7%) for metronidazole resistance, and the 16S rRNA mutation (66.7%) for tetracycline. Resistance to amoxicillin and clarithromycin was detected in 27.8% and 16.7% of cases, respectively. Most samples (72.2%) had multiple resistance genes. A significantly strong association was found between female sex and the presence of the rdxA gene (p = 0.043). Conclusions: The study reveals a high prevalence of H. pylori resistance genes in Algarve, particularly against metronidazole and tetracycline. These findings highlight the need for local surveillance and tailored treatment strategies. Further research with larger populations is warranted to assess regional resistance patterns and improve eradication efforts. Full article

Background/Objectives: This study investigated the timing of adverse events (AEs) after carbon-ion radiotherapy (CIRT) for hepatocellular carcinoma (HCC) and identified the risk factors for biliary stricture post CIRT. Methods: This retrospective study included 103 patients with HCC who had undergone CIRT (60 Gy/4 fractions). The onset, frequency, and grade of AEs after CIRT were analyzed. HCC was classified into perihilar and distal types to assess the frequency of biliary stricture, and the risk factors for biliary stricture were investigated. Results: AEs after CIRT were more frequent in patients with liver dysfunction, skin redness/dermatitis, and pigmentation. Biliary stricture occurred long after CIRT (3.0–17.0 months). Most AEs were of grade 1–2. Grade ≥ 3 AEs included biliary stricture (2.9%) and radiation gastric ulcer (1.0%), whereas grade 5 AEs included biliary stricture (1.9%). Biliary stricture was exclusively observed in patients with perihilar-type HCC. Among patients with perihilar-type HCC, those having a tumor in the portal vein trunk branch area were more prone to biliary stricture than those with a tumor in the primary portal vein branch area (p = 0.0018), and all grade ≥ 3 biliary strictures (2.9%) were observed in the portal vein trunk branch area. Patients with perihilar-type HCC and biliary stricture were more likely to have macrovascular invasion (p = 0.0052) and previous local therapy targeting the perihilar region (p = 0.0371) than those without biliary stricture. Conclusions: This study reported the detailed data of AEs post CIRT for HCC and the risk factors for biliary stricture post CIRT. Full article

This study arises from the search for non-invasive diagnostic alternatives for equine gastric ulceration (EGUS), which is prevalent, clinically variable and only confirmed by gastroscopy. The aim is to quantify five salivary biomarkers (IL1-F5, PIP, CA VI, serotransferrin, albumin) under clinical conditions by validated assays and analyse their diagnostic value. Horses were grouped in No EGUS (neither clinical signs of EGUS nor gastric lesions), EGUS non-clinical (apparently no clinical signs of EGUS but with gastric lesions), and EGUS clinical (obvious clinical signs of EGUS and with gastric lesions). The concentration of 5 analytes could be quantified using sandwich ELISA assays, with high precision (CV: 6.79–12.38%) and accuracy (>95%). Mean salivary levels of IL1-F5, CA-VI, serotransferrin and albumin were significantly higher in EGUS clinical horses compared to No EGUS horses, whereas PIP showed no statistical significance. EGUS non-clinical horses showed statistical differences with No EGUS horses for PIP and albumin. In addition, IL1-F5, CA-VI, serotransferrin and albumin showed moderate accuracy to distinguish between No EGUS and EGUS clinical horses (AUC ≥ 0.8), with sensitivity and specificity greater than 77% and 65%, respectively. Therefore, these biomarkers could be a promising starting point for screening horse that might have EGUS in practice. Full article

Gaultherin [methyl salicylate 2-O-β-D-xylopyranosyl-(1→6)-β-D-glucopyranoside] is a natural salicylate found in some plant species belonging primarily to the Ericaceae and Rosaceae families. Biological studies conducted since the beginning of the 21st century have suggested the potential use of gaultherin in treating various diseases related to inflammation and oxidative stress, including rheumatoid arthritis, sciatica, neuralgia, and muscular pain. The accumulated results indicated a targeted range of biological effects, particularly anti-inflammatory, antipyretic, and anti-rheumatic properties associated with reduced adverse outcomes. The molecular mechanisms involve the influence on several signalling pathways, including NF-κB, MAPK, and potentially AMPK, as well as the inhibition of critical pro-inflammatory enzymes, such as COX-2. This inhibition is achieved without affecting the COX-1 isoform, thereby preventing side effects such as bleeding ulcers or intracranial haemorrhage. This overview summarises the current knowledge about pharmacokinetics, molecular mechanisms, pharmacology, and biocompatibility of gaultherin. Additionally, four methods for isolating gaultherin from plant material and its distribution within the plant kingdom were the focal points of review and discussion. The paper also describes significant differences between synthetic aspirin and natural gaultherin in their biological potential and side effects, resulting from their different mechanisms of action. As a prodrug of salicylic acid, gaultherin releases salicylic acid gradually through enzymatic hydrolysis in the gastrointestinal tract. This controlled release minimises direct gastric irritation and accounts for its superior gastrointestinal safety profile compared to aspirin. Unlike aspirin, which irreversibly inhibits COX-1 and can lead to serious side effects with chronic use, gaultherin selectively inhibits COX-2 while sparing COX-1. These properties position gaultherin as a compelling natural alternative for patients requiring long-term anti-inflammatory therapy with reduced risk of gastrointestinal or bleeding complications. Full article

Helicobacter pylori infection represents one of the most prevalent and persistent bacterial infections worldwide, closely linked to a spectrum of gastroduodenal diseases, including chronic gastritis, peptic ulceration, and gastric cancer. Recent advances have shed light on the critical role of endogenous lectins, particularly galectins, in modulating host–pathogen interactions within the gastric mucosa. Galectins are β-galactoside-binding proteins with highly conserved structures but diverse biological functions, ranging from regulation of innate and adaptive immunity to modulation of cell signaling, apoptosis, and epithelial integrity. This review provides a comprehensive synthesis of current knowledge on the involvement of key galectin family members—especially Galectin-1, -2, -3, -8, and -9—in the context of H. pylori infection. Their dual roles in enhancing mucosal defense and facilitating bacterial persistence are examined along with their contributions to immune evasion, inflammation, and gastric carcinogenesis. Understanding the interplay between galectins and H. pylori enhances our knowledge of mucosal immunity. This interaction may also reveal potential biomarkers for disease progression and identify novel therapeutic targets. Modulating galectin-mediated pathways could improve outcomes in H. pylori-associated diseases. Full article

Nonsteroidal anti-inflammatory drug-based therapies are the cause of 20–30% cases of gastric lesions in chronic users worldwide. Co-medication with omeprazole (OMP) is the most commonly used option to prevent these lesions, although this carries risks of its own; thus, alternatives are being explored, such as dietary antioxidant therapies. The objective of this study was to evaluate the gastroprotective activity of quinoa (Chenopodium quinoa Willd.) on ibuprofen (IBP)-induced gastric ulcers in a rat model. Quinoa cookies were formulated with heat-treated quinoa using microwave radiation. The intestinal bioaccessibility of phenols and flavonoids, and the antioxidant activity of microwaved quinoa cookies (MQCs) were notably higher than quinoa cookies without thermal treatment (RQCs): 132% TPC, 52% TFC, 1564% TEAC vs. 67% TPC, 24% TFC, and 958% TEAC, respectively. Basal diets were supplemented with MQCs (20%) and quercetin (Q, 0.20%) as a reference flavonoid and administered for 30 days. Gastric lesions were induced by intragastric IBP doses, with OMP treatment as a positive control. Gastric damage index (macroscopic study), histological score (microscopic study), and plasma antioxidant enzyme activity (SOD and CAT) were evaluated. Macroscopic results showed that the addition of MQCs, Q, and OMP decreased the gastric damage index (GDI) by 50%, 40%, and 3%, respectively, as compared to IBP (GDI 100%). Histological analyses showed neutrophil infiltration and congested blood vessels in IBP-treated tissues; in contrast, the experimental diet groups showed lower infiltration for MQC > OMP > Q, respectively. A significant increase in SOD and CAT enzyme activity was observed in the MQC and Q groups as compared to the IBP group. We conclude that a reduction in the GDI and histological score was observed in IBP-induced murine models fed diets containing 20% MQC and 0.20% Q, demonstrating a preventive gastroprotective effect. Full article

H. pylori infects over half of the global population and is associated with various gastric and extra-gastric diseases. Other species, such as zoonotic non-Helicobacter pylori Helicobacters (NHPHs), have shown similar associations with gastritis and MALT lymphoma and H. pylori-negative cases with gastric disease have been identified, including gastric MALT lymphoma, chronic gastritis, and gastroduodenal ulcers. Accurate identification of these species is of great relevance but remains challenging using conventional diagnostic methods. This cross-sectional study aimed to determine the prevalence of H. pylori and NHPH infections, comparing standard histological protocols with molecular techniques. Between December 2024 and February 2025, 54 adult patients undergoing upper gastrointestinal endoscopy (UGE) with gastric biopsy in three hospitals in Algarve, Portugal were recruited. Endoscopic assessment was performed, and gastric biopsies were collected for histological and molecular analysis. DNA was extracted from antral biopsies and analyzed by conventional PCR to detect H. pylori and NHPH. H. pylori diagnostic techniques were compared, descriptive plus statistical analysis was performed, and p-values < 0.05 were considered to be statistically significant. Fifty-four patients were included in the study, with 51.9% of them presenting symptoms. Endoscopic gastritis was observed in 66.7% of patients, while histological gastritis was present in 88.9%, with statistically significant differences between the two diagnostic techniques (p = 0.004). Helicobacter spp. were identified in 44.4% (24/54) of the patients. H. pylori was detected in 42.6% of the patients by Modified Giemsa stain and in 33.3% by PCR. H. bizzozeronii was found in 35.9% of the patients, with 22.2% showing mixed infections. This study reveals a significant prevalence of Helicobacter spp. in patients from the Algarve region, with both H. pylori and zoonotic H. bizzozeronii detected. This is the first report of H. bizzozeronii DNA detection in gastric biopsies via PCR from patients undergoing UGE in Portugal, highlighting the need to consider NHPH in clinical diagnosis. It is important to include molecular methods in routine diagnostics and the need for broader studies to assess regional and national trends in Helicobacter infections besides H. pylori. Full article

Uncaria tomentosa (Ut) is a Rubiaceae widely used in Peru’s traditional medicine. It is mainly known by the vernacular name of Cat’s claw due to its morphological aspects and is found in tropical low mountain forests of Central and South America. A decoction of Ut bark, root and leaves is used traditionally for different health problems, including arthritis, weakness, viral infections, skin disorders, abscesses, allergies, asthma, cancer, fevers, gastric ulcers, haemorrhages, inflammations, menstrual irregularity, rheumatism, urinary tract inflammation and wounds, among others, which gave rise to scientific and commercial interest. The present paper reviews research progress relating to the ethnobotany, phytochemistry and pharmacology of Ut, and some promising research routes are also discussed. We highlight the centrality of its different biological activities, such as antioxidant, anti-inflammatory, antiproliferative, antiviral, and antinociceptive, among others. Recently, studies of the health effects of this plant suggest that novel nutraceuticals can be obtained from it and applied as a preventive or prophylaxis strategy before the start of conventional drug therapy, especially for patients who are not prone to conventional pharmacological approaches to diseases. The present work emphasizes the current pharmacological properties of Uncaria tomentosa, evidencing its therapeutic benefits and encouraging further research on this medicinal plant. Full article

Rare presentations are surprising and may disturb the day-to-day routine of a medical unit; however, they are expected (not as individual entities, but as a group of “uncommon causes”). While reviewing the literature in relation to three clinical cases of upper gastrointestinal bleeding (UGIB) encountered in our institution—gastric metastases of breast cancer (GMB), pyloric gland adenoma, and gastrointestinal stromal tumor (GIST)—we identified seven and 29 case reports for the first two entities, and over 100 publications addressing GIST. This prompted a shift in focus from novel reporting to diagnostic contextualization. We found it difficult to obtain an overview of the spectrum of UGIB etiologies, as most publications refer to a few individual entities or to a subgroup of rare causes. The narrative review we conducted arose from this particular research methodology. Based on a broad literature search, UGIB etiologies were organized in five categories (lesions of the mucosa, neoplasms, vascular causes, bleeding predisposition, and external sources of bleeding). In the management of patients with UGIB, the underlying etiology deviates from the classic peptic ulcer disease/esophageal varices dyad in approximately half of the cases. This underscores the need for heightened clinical vigilance, particularly in complex scenarios, where endoscopic findings, imaging results, and histopathological interpretations may be unexpected or prone to misinterpretation. As an illustration, we conducted two systematic reviews of case reports of bleeding GMB and PGA. Our findings support a proactive diagnostic and research mindset and advocate for improved awareness of uncommon UGIB etiologies. Full article

Background: Helicobacter pylori infection is widely prevalent across the globe and is a major etiological agent of various gastric pathologies. This bacterium colonizes the human stomach, where it induces a range of mucosal abnormalities observable upon clinical examination. Accordingly, the present study aimed to assess the prevalence and clinical implications of H. pylori infection among patients undergoing endoscopic evaluation. Method: A cross-sectional study was conducted from January to May 2019 at endoscopy service-providing health institutions. Sociodemographic and clinical data were collected. Gastric biopsies were collected during endoscopic procedures and immediately inoculated into brain–heart infusion broth and plated out. Then, phenotypic bacterial identification was done. The collected data have been analyzed using SPSS version 23. A logistic regression model was used for association determination. Result: Among the 135 individuals enrolled in the study, 59.3% are male, and 40.7% are female, with a mean age of 45 years. H. pylori is isolated in 17.8% of participants (24/135). Notably, the majority of these isolates 71% (17/24) are from male participants, while 29% (7/24) are from females. A statistically significant association is identified between H. pylori infection and both high salt intake [AOR = 3.3; 95% CI: 1.5–10.8; p = 0.04] and the presence of duodenal ulcers [AOR = 3.8; 95% CI: 1.2–11.9; p = 0.02]. The highest prevalence of H. pylori is observed among patients diagnosed with atrophic pangastritis. Conclusions: The prevalence of H. pylori among the study participants is comparatively low. However, a significant association was observed between H. pylori infection and both high dietary salt intake and the presence of duodenal ulcers. Full article

Helicobacter pylori is a gastric pathogen implicated in peptic ulcer disease and gastric cancer. The increasing prevalence of antibiotic-resistant strains underscores the urgent need for alternative therapeutic strategies. In this study, we investigated the chemical composition and antibacterial activity of an aqueous extract from Caulerpa lentillifera (sea grape), a farm-cultivated edible green seaweed collected from Krabi Province, Thailand. Ultra-high-performance liquid chromatography–tandem mass spectrometry (UHPLC-MS/MS) revealed that the extract was enriched in bioactive nucleosides and phenolic compounds. In vitro assays demonstrated dose-dependent inhibition of H. pylori growth following exposure to sea grape extract. Furthermore, untargeted intracellular metabolomic profiling of H. pylori cells treated with the extract uncovered significant perturbations in central carbon and nitrogen metabolism, including pathways associated with the tricarboxylic acid (TCA) cycle, one-carbon metabolism, and alanine, aspartate, and glutamate metabolism. Pyrimidine biosynthesis was selectively upregulated, indicating a potential stress-induced shift toward nucleotide salvage and DNA repair. Of particular note, succinate levels were markedly reduced despite accumulation of other TCA intermediates, suggesting disruption of electron transport-linked respiration. These findings suggest that bioactive metabolites from C. lentillifera impair essential metabolic processes in H. pylori, highlighting its potential as a natural source of antimicrobial agents targeting bacterial physiology. Full article

Helicobacter pylori (H. pylori) is one of the most prevalent chronic bacterial infections globally, significantly contributing to gastritis, peptic ulcers, and gastric malignancies. Its pathogenesis involves a complex array of virulence factors—including cagA, vacA, and urease—which facilitate mucosal colonization, immune evasion, and persistent inflammation. A major challenge in vaccine development is the bacterium’s ability to manipulate both innate and adaptive immune responses, resulting in limited natural clearance and long-term persistence. This review synthesizes H. pylori pathogenesis and host immune dynamics, highlighting their implications for vaccine design. By elucidating the molecular and cellular mechanisms underlying host–pathogen interactions, we explore how these insights inform antigen selection, adjuvant optimization, and delivery strategies. By integrating basic science with translational objectives, this review aims to support the development of an effective H. pylori vaccine, addressing global health needs, particularly in regions with a high infection burden and limited access to treatment. Full article

Background and Objectives: Chronic mucosal infection with Helicobacter pylori (H. pylori) plays a key role in the development of gastroduodenal disorders such as chronic gastritis, peptic ulcers, gastric lymphoma, and gastric cancer by triggering local immune responses and inducing hypoxic and inflammatory conditions in the gastric mucosa. This study aims to evaluate the potential diagnostic value of hypoxia-inducible factors HIF-1α and HIF-2α, along with transmembrane prolyl 4-hydroxylase (P4H-TM), as biomarkers in H. pylori-positive patients. Additionally, the study investigates the association between these markers and alterations in lipid profiles, as well as their involvement in the molecular mechanisms underlying gastric conditions like gastritis, particularly in the context of H. pylori infection. Materials and Methods: This study was conducted at Istanbul Avcılar Murat Kölük State Hospital’s General Surgery Outpatient Clinic. A total of 60 participants were included: 40 patients diagnosed with chronic gastritis (20 H. pylori-positive and 20 H. pylori-negative) and 20 healthy controls confirmed negative by 13C-urea breath test. Blood samples were collected for ELISA analysis of HIF-1α, HIF-2α, and P4H-TM levels. Additionally, lipid profiles were measured and compared among the groups. Results: No significant differences were found among the groups in terms of demographic factors such as age, sex, or body mass index (BMI). However, significant variations were observed in the levels of HIF-1α, HIF-2α, and P4H-TM across all groups (p < 0.001 for each marker). These markers were substantially elevated in the H. pylori-positive gastritis group compared to both the H. pylori-negative and healthy control groups. Receiver Operating Characteristic (ROC) curve analysis revealed that all evaluated markers exhibited strong diagnostic accuracy in differentiating H. pylori-positive individuals from other groups. HIF-1α (AUC: 0.983) and HIF-2α (AUC: 0.981) both achieved 100% sensitivity with specificities of 93.3% and 91.1%, respectively. P4H-TM showed an AUC of 0.927, with 85% sensitivity and 95.6% specificity. Conclusions: These findings indicate that HIF-1α, HIF-2α, and P4H-TM may serve as effective biomarkers for diagnosing H. pylori-positive patients and may be linked to changes in lipid metabolism. The elevated expression of these markers in response to H. pylori infection highlights their potential roles in the inflammatory and hypoxic pathways that contribute to the pathogenesis of gastric diseases such as gastritis. Full article

Equine gastric disease (EGD) is a common condition in performance horses (Equus caballus), potentially compromising behaviour, performance, and welfare. EGD is often attributed to high-starch, high-sugar feeds and limited forage. Evidence for diet-induced changes on digestive microbiota is lacking. Nine elite showjumping horses were housed at the same performance yard with standardised diet and management throughout the study. Horses were transitioned from a high-sugar and -starch (31%) feed to a low-starch and -sugar (16.5%) concentrate feed. Gastroscopies, blood, and faecal samples were taken pre- and 12 weeks post-diet change. Squamous and glandular ulceration was blindly graded a posteriori using 0–4 scores and faecal microbiota profiled using 16S rRNA gene amplicon sequencing. Total (t_(1,8) = −6.17, p < 0.001; Pre: 4 [0–5], Post: 1 [0–2]), squamous (t_(1,8) = −5.32, p < 0.001; Pre: 1 [0–3], Post: 0 [0–1]), and glandular (t_(1,8) = −2.53, p = 0.04; Pre: 2.5 [0–4], Post: 0 [0–2]) disease improved following the introduction of a low-starch diet. Diet change did not impact microbiota communities (PERMANOVA: F_(1,16) = 1.37, p = 0.15, r² = 0.08), but Firmicute to Bacteroidota (F/B) ratio reduced (t_(1,8) = −3.13, p = 0.01; Pre: 2.07 ± 0.21 vs. Post: 1.29 ± 0.14). Lower F/B ratios were associated with reduced total EGD scores (ChiSq_(1,17) = 3.83, p = 0.05). Low-starch diets did not influence faecal microbiota diversity but aided gastric disease healing and reduced F/B ratios in elite showjumpers during a competition season without medication. Full article