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RESUMEN La información sobre la presentación y los factores predisponentes del síndrome de úlcera gástrica en mulas (SUGM) es escasa en comparación con el síndrome de úlcera gástrica en equinos (SUGE) y asnales. Debido a la naturaleza multifactorial de este síndrome, la helicobacteriosis ha sido estudiada en otras especies. El objetivo de este trabajo fue establecer la presencia de Helicobacter spp. en mucosa gástrica de mulas a través de la prueba rápida de la ureasa (PRU) y de análisis histopatológico. Menos del 27% de las muestras reaccionaron a la PRU, con tiempos prolongados de reacción, y al Agar Urea (prueba de oro), con menor porcentaje de positividad. La histopatología reveló procesos inflamatorios crónicos, sin presencia de bacterias curvoespiraladas. Las PRU no fueron conclusivas en la determinación de Helicobacter spp., comportamiento similar reportado en equinos. Se requieren exámenes diagnósticos más específicos y procedimientos complementarios orientados a explorar por regiones del estómago en la consideración del número de muestras representativas.

ABSTRACT Information on the presentation and predisposing factors of Mule Gastric Ulcer Syndrome (MGUS) is scarce, compared to Equine Gastric Ulcer Syndrome (EGUS) and donkeys. Within the multifactorial nature of this syndrome, helicobacteriosis has been studied in other species. The objective of this work was to establish the presence of Helicobacter spp. in gastric mucosa of mules, through the rapid urease test (RUT) and histopathological analysis. Less than 27% of the samples reacted to RUTs, with prolonged reaction times, and Urea Agar (gold test), with a lower percentage of positivity. Histopathology revealed chronic inflammatory processes, without the presence of curved-spiral bacteria. The RUTs were not conclusive in the determination of Helicobacter spp., a similar behavior reported in horses. More specific diagnostic tests and complementary procedures are required to explore the regions of the stomach in consideration of the number of representative samples.

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O objetivo deste trabalho foi relacionar os achados anatomopatológicos das lesões gástricas subclínicas de ocorrência natural em leitões com a presença, ou não, de Helicobacter spp. por meio da imuno-histoquímica. Foram utilizados 48 leitões de linhagem genética comercial. Os animais foram adquiridos em uma granja comercial, com peso médio de 34 Kg e idade média de 79 dias; após o abate, seus estômagos foram coletados e avaliados. Avaliações histopatológicas e imuno-histoquímicas foram realizadas em amostras das regiões anatômicas aglandular e glandular. Macroscopicamente, 34 (70,83%) leitões apresentaram lesões na região aglandular, enquanto que em 14 animais (29,17%) não foram encontradas alterações nesta região. Dos estômagos com lesão, 14 foram classificados como grau 1, seis como grau 2 e 14 como grau 3. Microscopicamente, 44 amostras (91,66%) apresentaram paraqueratose. Deste total, 22 apresentaram a forma discreta, 20 a moderada e dois a acentuada. Na avaliação macroscópica da porção glandular, 41 (85,4%) animais apresentaram alteração em pelo menos uma das três regiões, e em somente sete (14,6%) não foram encontradas lesões em nenhuma delas. Em 14 deles, houve aumento da atividade mucípara, em dois, houve erosão e, em cinco, hiperemia. As lesões na região glandular do estômago foram mais extensas no antro e no cárdia, seguidas do fundo. Em relação à análise imuno-histoquímica, 21 (43,8%) amostras tiveram resultados negativos em todas as regiões, e 24 (50%) foram positivas em pelo menos uma delas, sendo que nenhuma foi positiva em todas. Os achados anatomopatológicos demonstraram relação estatística com a bactéria e, sua imunomarcação não associada à lesão em certas regiões gástricas, demonstra seu caráter saprofítico e oportunista.

The aim of this study was to relate the anatomopathological findings of naturally occurring subclinical gastric lesions in piglets, with or without Helicobacter spp. through immunohistochemistry. Forty-eight piglets of commercial genetic lineage were used. The animals were acquired in a commercial farm, with an average weight of 34 kg and an average age of 79 days, and after slaughter, their stomachs were collected and evaluated. Samples from the glandular and aglandular anatomical regions were evaluated. Macroscopically, 34 (70.83%) samples had lesions on aglandular region, while 14 (29.17%) nothing had. Of the injured stomachs, 14 were classified as grade 1, six as grade 2 and 14 as grade 3. Microscopically, 44 samples (91.66%) showed parakeratosis. Of these, 22 showed a discreet manner, 20 moderate and two severe. In the glandular region, in 41 (85.4%) samples there was a change in at least one of the three regions, and only seven animals (14.6%) showed no change in any of the three. Fourteen samples showed increased muciparous activity, two showed erosion and five hyperemia. The lesions were higher in antral regions and cardic, followed the fundus. In relation to immunohistochemistry, 21(43.8%) samples were negative in all areas, 24 (50%) were positive in at least one, and none were positive in all. The anatomopathological findings showed a statistical relationship with the bacteria, and its immunostaining, not associated with gastric lesions in certain regions, demonstrates its saprophytic and opportunistic character.

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BACKGROUND/AIMS: Both bismuth-containing quadruple therapy and moxifloxacin-containing triple therapy have been suggested as second-line eradication therapy for Helicobacter pylori (H. pylori) infection. We aimed to evaluate the efficacy of 14-day moxifloxacin-containing triple therapy (14-EAM) in second-line H. pylori eradication in comparison to 7-day bismuth-containing quadruple therapy (7-RBMT). METHODS: From January 2011 to December 2015, a total of 569 patients who failed to respond to first-line triple therapy and who subsequently received second-line 7-RBMT or 14-EAM were retrospectively enrolled. The eradication rates were identified using per-protocol (PP) analysis. H. pylori eradication was confirmed by a 13C-urea breath test (UBiT-IR300®; Otsuka Electronics, Co., Ltd., Osaka, Japan) or a rapid urease test (CLOtest®; Delta West, Bentley, Australia) at least 4 weeks after completion of eradication therapy. RESULTS: A total of 487 and 82 patients received 7-RBMT and 14-EAM, respectively. PP eradication rates were 93.6% (366/391; 95% CI, 91.0–95.9%) with 7-RBMT and 73.8% (48/65; 95% CI, 63.1–84.6%) with14-EAM (p < 0.001). Therefore, the eradication rates with 7-RBMT were significantly higher than with 14-EAM according to the PP analysis. The adverse event rate was 17.1% (67/391) with 7-RBMT and 7.7% (5/65) with 14-EAM (p=0.065). In terms of risk factors, multivariate analysis revealed that 14-EAM (OR, 5.47; 95% CI, 2.74–10.93) was related to H. pylori eradication failure. CONCLUSIONS: 7-RBMT may be an effective second-line therapy in patients who failed to respond to first-line triple therapy in Korea, where there is a high prevalence of H. pylori infection.

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BACKGROUND/AIMS: The eradication of Helicobacter pylori (H. pylori) is an effective treatment in gastric mucosa-associated lymphoid tissue (MALT) lymphoma associated with H. pylori infection. However, the treatment strategy in gastric MALT lymphoma patients who are H. pylori-negative or unresponsive to H. pylori eradication therapy remains controversial. In this study, we investigated the clinical efficacy of treatments other than H. pylori eradication therapy in these groups of patients. METHODS: This was a retrospective single-center study based on the medical records of patients diagnosed with gastric MALT lymphoma at Yeungnam University Medical Center between January 2005 and December 2016. Patients were treated with H. pylori eradication therapy, chemotherapy, or radiotherapy according to their H. pylori infection status and stage of gastric MALT lymphoma. RESULTS: Of the 68 eligible patients, 50 were enrolled in the study. Of the 42 patients with H. pylori-positive gastric MALT lymphoma, 36 (81.7%) were treated with H. pylori eradication therapy as primary treatment and 25 (69.4%) achieved a complete response (CR). Patients without a CR after H. pylori eradication therapy (n=11, 30.6%) received radiotherapy as a secondary treatment. Two patients with H. pylori-positive gastric MALT lymphoma and eight with H. pylori-negative gastric MALT lymphoma received radiotherapy as the primary treatment. CR was achieved in all 21 patients treated with radiotherapy as primary or secondary treatment. The 5-year progression-free survival rate after radiotherapy was 92.9%. CONCLUSIONS: Radiotherapy may be a worthwhile treatment option in patients with H. pylori-negative MALT lymphoma or H. pylori-positive MALT lymphoma that is not responsive to H. pylori eradication therapy.

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PURPOSE: Helicobacter pylori (HP)-infected gastric cancer (GC) is known to be a fatal malignant tumor, but the molecular mechanisms underlying its proliferation, invasion, and migration remain far from being completely understood. Our aim in this study was to explore miR-1915 expression and its molecular mechanisms in regulating proliferation, invasion, and migration of HP-infected GC cells. MATERIALS AND METHODS: Quantitative real-time PCR and western blot analysis were performed to determine miR-1915 and receptor for advanced glycation end product (RAGE) expression in HP-infected GC tissues and gastritis tissues, as well as human gastric mucosal cell line GES-1 and human GC cell lines SGC-7901 and MKN45. CCK8 assay and transwell assay were performed to detect the proliferation, invasion, and migration capabilities. MiR-1915 mimics and miR-1915 inhibitor were transfected into GC cells to determine the target relationship between miR-1915 and RAGE. RESULTS: MiR-1915 was under-expressed, while RAGE was over-expressed in HP-infected GC tissues and GC cells. Over-expressed miR-1915 could attenuate cellular proliferation, invasion, and migration capacities. RAGE was confirmed to be the target gene of miR-1915 by bioinformatics analysis and luciferase reporter assay. Moreover, HP-infected GC cellular proliferation, invasion, and migration were inhibited after treatment with pcDNA-RAGE. CONCLUSION: MiR-1915 exerted tumor-suppressive effects on cellular proliferation, invasion, and migration of HP-infected GC cells via targeting RAGE, which provided an innovative target candidate for treatment of HP-infected GC.

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BACKGROUND: Helicobacter pylori increases production of reactive oxygen species (ROS), which activates inflammatory and carcinogenesis-related signaling pathways in gastric epithelial cells. Therefore, reducing ROS, by upregulating antioxidant enzyme, such as superoxide dismutase (SOD), may be a novel strategy to prevent H. pylori-associated gastric diseases. Astaxanthin is an antioxidant carotenoid that prevents oxidative stress-induced cell injury. The present study was aimed to determine whether H. pylori decreases SOD activity by changing the levels of SOD1/SOD2 and whether astaxanthin prevents changes in SOD levels and activity in H. pylori-infected gastric epithelial AGS cells. METHODS: AGS cells were pre-treated with astaxanthin for 3 hours prior to H. pylori infection and cultured for 1 hour in the presence of H. pylori. SOD levels and activity were assessed by Western blot analysis and a commercial assay kit, respectively. Mitochondrial ROS was determined using MitoSOX fluorescence. RESULTS: H. pylori decreased SOD activity and the SOD2 level, but increased mitochondrial ROS in AGS cells. The SOD1 level was not changed by H. pylori infection. Astaxanthin prevented H. pylori-induced decreases in the SOD2 level and SOD activity and reduced mitochondrial ROS in AGS cells. CONCLUSIONS: Consumption of astaxanthin-rich food may prevent the development of H. pylori-associated gastric disorders by suppressing mitochondrial oxidative stress.

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PURPOSE: Gastric adenocarcinoma of the fundic gland type (chief cell predominant type) (GA-FG-CCP) was first reported as a rare adenocarcinoma found in the normal fundic mucosa. Recent studies have proposed the possibility that GA-FG-CCPs were also generated in the atrophic mucosa after Helicobacter pylori (HP) eradication therapy. However, little is known on the endoscopic findings of GA-FG-CCP generated in the atrophic mucosa due to its extreme rarity. MATERIALS AND METHODS: A total of 8 patients who underwent endoscopic submucosal resection and were diagnosed with GA-FG-CCP generated in the HP-uninfected mucosa (4 cases, HP-uninfected group) or HP-eradicated atrophic mucosa (4 cases, HP-eradicated group) were retrospectively analyzed, and their endoscopic findings, including magnifying endoscopy with narrow band imaging (M-NBI), and pathological features were compared. RESULTS: While GA-FG-CCPs in the 2 groups displayed similar macroscopic appearance, M-NBI demonstrated that characteristic microvessels (tapered microvessels like withered branches) were specifically identified in the HP-eradicated group. Pathological investigation revealed that a decreasing number of fundic glands and thinned foveolar epithelium covering tumor ducts were thought to lower the thickness of the covering layer over tumor ducts in the HP-eradicated group. Moreover, dilation of vessels just under the surface of the lesions contributed to the visualization of microvessels by M-NBI. CONCLUSIONS: The change in background mucosa due to HP infection influenced the thickness of the covering layer over the tumor ducts and M-NBI finding of GA-FG-CCP.

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No abstract available.

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BACKGROUND/AIMS: Helicobacter pylori (H. pylori) eradication is known to be effective for reducing the size of gastric hyperplastic polyps (HPPs). This study investigated the change in size of gastric HPPs after H. pylori eradication.MATERIALS AND METHODS: This was a prospective study that enrolled 25 H. pylori-positive patients diagnosed as having HPPs at Korea University Guro Hospital between July 2015 and July 2016. If the patient wanted to receive eradication therapy, medication was given. If the patients refused eradication, only clinical follow-up was performed. All patients were subsequently followed up with endoscopic examination to determine any change in polyp size.RESULTS: Eighteen of the 25 H. pylori-positive patients diagnosed as having HPPs were given an eradication regimen, and 17 were confirmed to have achieved successful eradication. Twelve (70.8%) of the 17 patients in the eradication group showed ≥50% reduction in size, while two (25.0%) of the eight patients in the non-eradication group showed 50% reduction. The polyp regression rate was significantly higher in the eradication group (P=0.03). A multivariate analysis revealed that H. pylori eradication (OR, 40.047; 95% CI, 1.112~1442.767; P=0.044) and female sex (OR, 12.947; 95% CI, 1.038~161.503; P=0.047) were significant predictive factors of HPP regression.CONCLUSIONS: H. pylori eradication is an effective therapeutic modality for gastric HPP regression.

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Addressing the increasing antibiotic resistance, including clarithromycin resistance, which affects Helicobacter pylori (H. pylori) eradication therapy, is a challenge for clinicians. Antibiotic resistance is the main reason for H. pylori eradication failure and the resistance rate for clarithromycin may drastically increase, up to 38.5%, due to 23S ribosomal RNA point mutations. Therefore, the standard triple regimen is no longer suitable as the first-line treatment in most regions. However, there is a growing interest in personalized care for patients. Increased eradication rates of tailored therapy based on antibiotic susceptibility have been reported using nucleic acid-based techniques for clarithromycin resistance with a focus on the first-line eradication therapy of H. pylori infection. Herein, we discuss the eradication therapy for H. pylori, with a diagnostic test and appropriate treatment for clarithromycin resistance.

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Endoscopic submucosal dissection is widely accepted as standard treatment for early gastric cancer; however, long-term management of metachronous gastric cancer after endoscopic resection is an important issue that is gaining much attention. Several prospective and retrospective studies have reported that Helicobacter pylori (H. pylori) eradication can reduce the risk of metachronous gastric cancer after endoscopic resection. Although there is lack of sufficient data regarding this subject, a few studies have reported histologically proven improvement in atrophic gastritis and intestinal metaplasia following H. pylori eradication in patients undergoing endoscopic resection. Therefore, treatment for H. pylori eradication should be considered in this patient population to reduce the incidence of metachronous gastric cancer and improve long-term outcomes.(

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Helicobacter pylori (H. pylori) infection can cause gastric dysplasia and cancer via chronic inflammatory changes in the gastric mucosa that may lead to gastric atrophy and intestinal metaplasia. Many epidemiologic studies have demonstrated the prophylactic effects of H. pylori eradication on gastric cancer, and H. pylori eradication after endoscopic resection of early gastric cancer may prevent the occurrence of metachronous gastric cancer or dysplasia. Despite insufficient data on the effect of H. pylori eradication on gastric dysplasia and cancer before endoscopic resection, some studies have shown that H. pylori eradication can induce the regression or slow the progression of some gastric dysplasia. Therefore, eradication therapy before endoscopic resection may be effective in selected cases of low-grade dysplasia. However, endoscopic resection should be considered as the first-line treatment in high-grade dysplasia or early gastric cancer owing to the potential morphologic changes to some dysplasia or cancer that can be incurred by the eradication process, which may make it difficult to perform a subsequent endoscopic procedure.

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In order to investigate the antioxidant effect of alkylhydroxide peroxidase (ahpC) of Helicobacter pylori (H. pylori) 26695, an ahpC-deficient mutant (H. pylori 26695 ahpC::cat) was generated. ahpC-deficient mutant was grown slowly at lower pressure of oxygen (5% oxygen) compared to the H. pylori 26695. Whole cell proteins isolated form H. pylori 26695 and H. pylori 26695 ahpC::cat were analyzed by MALDI-TOF and tandem-MS. The expression of 15 proteins, including Ppa, HypB, GrpE, Elp, RecA, GroES, Mda66, RibE, NapA, GlnA, BioB, TrxB, Tsf, FumC and Icd, was more than doubled in H. pylori 26695 ahpC::cat. Production of 10 proteins such as UreG, FabE, Adk, Pnp, OorC, AtpA, AtpD, Nqq3, Pfr, and TagD decreased below 50% in H. pylori 26695 ahpC::cat compared to the H. pylori 26695. In microarray analysis, 9 genes including sul1, amiE, frxA, fecA, hyuA, and katA increased in transcription level in H. pylori 26695 ahpC::cat compared to H. pylori 26695. A total of 24 genes, including flaB, protein kinase C inhibitor, cag16, pabC, and sabA, reduced in transcription. 27 genes, including HP0889, showed common expression changes in ahpC, katA, and sodB-deficient mutations. As a result of this study, there were not many genes whose expression was commonly changed by the deletion of each of the three major antioxidant enzymes of H. pylori. These results showed the functions and regulation of the three antioxidant enzymes were different in H. pylori.

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No abstract available.

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BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infections, which cause a variety of gastrointestinal symptoms, are common in South Korea. Recent reports have shown a decline in the H. pylori eradication rates. β-caryophyllene is a natural bicyclic sesquiterpene that occurs in a wide range of plant species, such as cloves, basil, and cinnamon. β-caryophyllene has been reported to have anti-inflammatory and anti-bacterial effects. This study investigated the inhibitory effects of β-caryophyllene on H. pylori and its potential role as an alternative gastrointestinal drug.METHODS: This 8-week, randomized double-blind, placebo-controlled trial categorized subjects into a β-caryophyllene group (33 patients who received 126 mg/day of β-caryophyllene) and a placebo group (33 patients who received a placebo preparation). The inflammation level of H. pylori infiltration and the eradication rates were evaluated endoscopically and with the urea breath test (UBT) in both groups before and after administering the medication. The serum cytokine levels (tumor necrosis factor-α, and interleukin [IL]-1β and IL-6) were compared in both groups before and after administering the medication.RESULTS: Complete eradication was not observed in either group. Moreover, there was no significant change in the UBT and updated Sydney score. On the other hand, the β-caryophyllene group showed significant improvement in nausea (p=0.025) and epigastric pain (p=0.018), as well as a decrease in the serum IL-1β levels (p=0.038).CONCLUSIONS: β-caryophyllene improves dyspepsia symptoms and can be considered a useful supplementary treatment for gastrointestinal disease.

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PURPOSE: Few studies investigated roles of body mass index (BMI) on gastric cancer (GC) risk according to Helicobacter pylori infection status. This study was conducted to evaluate associations between BMI and GC risk with consideration of H. pylori infection information. MATERIALS AND METHODS: We performed a case-cohort study (n=2,458) that consists of a subcohort, (n=2,193 including 67 GC incident cases) randomly selected from the Korean Multicenter Cancer Cohort (KMCC) and 265 incident GC cases outside of the subcohort. H. pylori infection was assessed using an immunoblot assay. GC risk according to BMI was evaluated by calculating hazard ratios (HRs) and their 95% confidence intervals (95% CIs) using weighted Cox hazard regression model. RESULTS: Increased GC risk in lower BMI group (< 23 kg/m²) with marginal significance, (HR, 1.32; 95% CI, 0.98 to 1.77) compared to the reference group (BMI of 23-24.9 kg/m²) was observed. In the H. pylori non-infection, both lower (< 23 kg/m²) and higher BMI (≥ 25 kg/m²) showed non-significantly increased GC risk (HR, 10.82; 95% CI, 1.25 to 93.60 and HR, 11.33; 95% CI, 1.13 to 113.66, respectively). However, these U-shaped associations between BMI and GC risk were not observed in the group who had ever been infected by H. pylori. CONCLUSION: This study suggests the U-shaped associations between BMI and GC risk, especially in subjects who had never been infected by H. pylori.

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BACKGROUND/AIMS: Atrophic gastritis and intestinal metaplasia are sequential consequences of chronic Helicobacter pylori (H. pylori) infection. These conditions are well known to increase the risk of gastric adenocarcinoma development. Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is also a malignant consequence of H. pylori infection, but the relationship between gastric MALT lymphoma and atrophic gastritis-intestinal metaplasia has not been a focus of interest. We investigated the clinical characteristics of atrophic gastritis and intestinal metaplasia in patients with gastric MALT lymphoma. MATERIALS AND METHODS: A study was conducted by reviewing the electronic medical records of patients diagnosed as having gastric MALT lymphoma at an academic institute, the Yeouido St. Mary's Hospital, Seoul, Korea, between January 2001 and December 2018. RESULTS: Fifty-eight subjects were enrolled consecutively during the study period and analyzed retrospectively. The patients' mean age was 56.9 years old. The male-to-female ratio was 1.15 (31/27). On histological examination, background atrophic gastritis and intestinal metaplasia were detected in 26.8% (15/58) of cases. Serum pepsinogen I, II and gastrin levels, as serological markers of atrophy, were evaluated in 28 subjects. Three (5.2%) of the 28 cases were compatible with serological atrophic gastritis (pepsinogen I/II ratio of <3 and pepsinogen I level of <70 ng/mL). CONCLUSIONS: In patients with gastric MALT lymphoma, the prevalence of background mucosal atrophy or intestinal metaplasia was 26.8% on histological examination and 5.2% on serological analyses. These rates are lower than those in patients with gastric adenocarcinoma. This result suggests a different carcinogenic pathway of gastric MALT lymphoma from that of adenocarcinoma.