Determinación de Helicobacter spp. en mucosa gástrica glandular de muías a través de la prueba de la actividad de la ureasa e histopatología / Determination of Helicobacter spp. in glandular gastric mucosa of mules through the test of urease activity and histopathology

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.

Associação de alterações anatomopatológicas com o Helicobacter spp. por meio de análise imuno-histoquímica em estômagos de leitões / Association of anatomopathological changes with the Helicobacter spp. through immunohistochemical analysis in piglets stomachs

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.

Evaluating Diagnostic Tests for Helicobacter pylori Infection Without a Reference Standard: Use of Latent Class Analysis

Evaluation of diagnostic tests requires reference standards, which are often unavailable. Latent class analysis (LCA) can be used to evaluate diagnostic tests without reference standards, using a combination of observed and estimated results. Conditionally independent diagnostic tests for Helicobacter pylori infection are required. We used LCA to construct a reference standard and evaluate the capability of non-invasive tests (stool antigen test and serum antibody test) to diagnose H. pylori infection compared with the conventional method, where histology is the reference standard. A total of 96 healthy subjects with endoscopy histology results were enrolled from January to July 2016. Sensitivity and specificity were determined for the LCA approach (i.e., using a combination of three tests as the reference standard) and the conventional method. When LCA was used, sensitivity and specificity were 83.8% and 99.4% for histology, 80.0% and 81.9% for the stool antigen test, and 63.6% and 89.3% for the serum antibody test, respectively. When the conventional method was used, sensitivity and specificity were 75.8% and 71.1% for the stool antigen test and 77.7% and 60.7% for the serum antibody test, respectively. LCA can be applied to evaluate diagnostic tests that lack a reference standard.

Helicobacter pylori testing in a population of Korean patients with pernicious anemia

No abstract available.

Comparison of 7- and 14-Day Eradication Therapy for Helicobacter pylori with First- and Second-Line Regimen: Randomized Clinical Trial

Helicobacter pylori inhibited cell proliferation in human periodontal ligament fibroblasts through the Cdc25C/CDK1/cyclinB1 signaling cascade

PURPOSE: Several studies have shown that the oral cavity is a secondary location for Helicobacter pylori colonization and that H. pylori is associated with the severity of periodontitis. This study investigated whether H. pylori had an effect on the periodontium. We established an invasion model of a standard strain of H. pylori in human periodontal ligament fibroblasts (hPDLFs), and evaluated the effects of H. pylori on cell proliferation and cell cycle progression. METHODS: Different concentrations of H. pylori were used to infect hPDLFs, with 6 hours of co-culture. The multiplicity of infection in the low- and high-concentration groups was 10:1 and 100:1, respectively. The Cell Counting Kit-8 method and Ki-67 immunofluorescence were used to detect cell proliferation. Flow cytometry, quantitative real-time polymerase chain reaction, and western blots were used to detect cell cycle progression. In the high-concentration group, the invasion of H. pylori was observed by transmission electron microscopy. RESULTS: It was found that H. pylori invaded the fibroblasts, with cytoplasmic localization. Analyses of cell proliferation and flow cytometry showed that H. pylori inhibited the proliferation of periodontal fibroblasts by causing G2 phase arrest. The inhibition of proliferation and G2 phase arrest were more obvious in the high-concentration group. In the low-concentration group, the G2 phase regulatory factors cyclin dependent kinase 1 (CDK1) and cell division cycle 25C (Cdc25C) were upregulated, while cyclin B1 was inhibited. However, in the high-concentration group, cyclin B1 was upregulated and CDK1 was inhibited. Furthermore, the deactivated states of tyrosine phosphorylation of CDK1 (CDK1-Y15) and serine phosphorylation of Cdc25C (Cdc25C-S216) were upregulated after H. pylori infection. CONCLUSIONS: In our model, H. pylori inhibited the proliferation of hPDLFs and exerted an invasive effect, causing G2 phase arrest via the Cdc25C/CDK1/cyclin B1 signaling cascade. Its inhibitory effect on proliferation was stronger in the high-concentration group.

The Effect of Trimebutine and/or Helicobacter pylori Eradication on the Gastroesophageal Reflux Disease, Irritable Bowel Syndrome, and Functional Dyspepsia Overlapping Disorders

No abstract available.

Can Helicobacter pylori Eradication Regress Gastric Hyperplastic Polyps?

No abstract available.

Effectiveness of Helicobacter pylori Eradication before Endoscopic Resection

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.

Helicobacter pylori Eradication after Endoscopic Resection of Gastric Epithelial Neoplasms

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.(

Eradication Therapy for Helicobacter pylori with Diagnostic Test for Clarithromycin Resistance

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.

Change in Size of Gastric Hyperplastic Polyps after Helicobacter pylori Eradication: A Prospective Study

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.

Up-Regulation of MiR-1915 Inhibits Proliferation, Invasion, and Migration of Helicobacter pylori-Infected Gastric Cancer Cells via Targeting RAGE

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.

Clinical Efficacy of Radiotherapy in Helicobacter pylori Negative or Unresponsive to Eradication Therapy Primary Gastric Mucosa-Associated Lymphoid Tissue Lymphoma / 대한소화기학회지

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.

Effect of 7-day Bismuth Quadruple Therapy versus 14-day Moxifloxacin Triple Therapy for Second-line Helicobacter pylori Eradication Therapy / 대한소화기학회지

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.

Can Helicobacter pylori Infection Accelerate the Healing of Nonsteroidal Anti-inflammatory Drugs-induced Peptic Ulcer and Bleeding?

No abstract available.

Proteome Analysis of Alkylhydroxide Peroxidase-Deficient Isogenic Mutant of Helicobacter pylori 26695

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.

Risk of Peptic Ulcer Bleeding Associated with Helicobacter pylori Infection, Nonsteroidal Anti-inflammatory Drugs, and Low-dose Aspirin Therapy in Peptic Ulcer Disease: A Case-control Study

BACKGROUND/AIMS: The association between Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose aspirin therapy as a risk factor for peptic ulcer bleeding (PUB) remains unclear. This study investigated the risk of PUB associated with H. pylori infection and NSAID or low-dose aspirin therapy in patients with PUD. MATERIALS AND METHODS: This case-control study investigated 340 patients with PUB between 2012 and 2016. The control group comprised age and sex-matched patients with endoscopically documented non-bleeding ulcers. Using logistic regression analysis, the adjusted odds ratio (AOR) was calculated for the risk of PUB. RESULTS: Of the patients investigated, 57.9% in the study group and 51.8% in the control group were diagnosed with H. pylori infection (P=0.106). Logistic regression analysis showed synergistic interaction between H. pylori infection and low-dose aspirin therapy. Multivariate analysis showed that low-dose aspirin (AOR 3.92, P < 0.001), NSAIDs (AOR 2.98, P=0.001), warfarin (AOR 14.57, P=0.011), gastric ulcer (compared with duodenal ulcer) (AOR 1.65, P=0.01), and smoking (AOR 1.97, P=0.004) increased the risk of PUB compared with the risk of PUD. CONCLUSIONS: Both NSAIDs and aspirin are independent risk factors for bleeding in patients with PUD. Additionally, low-dose aspirin therapy concomitant with H. pylori infection produced a synergistic effect. Therefore, H. pylori eradication may be crucial in aspirin users. Moreover, a proton pump inhibitor should be prescribed in patients with a history of bleeding ulcers who need long-term NSAID treatment.

Periodic Methylation Patterns in the Background Mucosa of Gastric Cancer

BACKGROUND/AIMS: Gastrointestinal glandular stem cells renew every 8 years. New stem cells with impeded housekeeping gene methylation have unstable phenotypes and are prone to transform into malignant cells. Age-related changes in methylation in the gastric mucosa were evaluated to define the period of cancer-prone stem cell replacement. MATERIALS AND METHODS: Endoscopic biopsy specimens of normal-appearing gastric mucosa were obtained from 148 Helicobacter pylori-negative controls, 124 H. pylori-positive controls, and 69 gastric cancer patients with closed-type mucosal atrophy. Methylation-variable sites of two stomach-specific genes (TFF2 and TFF3) and four housekeeping genes (CDH1, ARRDC4, MMP2, and CDKN2A) were analyzed using radioisotope-labeled methylation-specific polymerase chain reaction. Age-related methylation was evaluated depending on the gastric mucosal atrophy at 2-year intervals. RESULTS: TFF2 methylation peaked periodically at 40 to 41, 48 to 49, 56 to 57, and 64 to 65 years of age in H. pylori-negative controls. Periodic peaks of TFF2 methylation were also found in H. pylori-positive controls. Housekeeping-gene methylation troughed at 48 to 49, 56 to 57, and 68 to 69 years of age in cancer patients. Trough methylation of CDH1 and ARRDC4 was lower in cancer patients than in H. pylori-positive controls. CONCLUSIONS: Methylation peaks of stomach-specific TFF2 in controls and methylation troughs of housekeeping genes in cancer patients were found every 8 years. Periodic methylation patterns may be used to identify individuals at high risk for gastric cancer.

Eradication Rates of 10-day Sequential Therapy for Helicobacter pylori: Results of an 8-year Prospective Study Conducted at a Tertiary Korean Hospital / 대한소화기학회지

BACKGROUND/AIMS: The Helicobacter pylori (H. pylori) eradication rate of standard triple therapy is unsatisfactory in Korea, and sequential therapy (SQT) has been suggested to be a practical first-line alternative regimen. The aim of this prospective study was to document changes in annual eradication rates of SQT. METHODS: A total of 983 H. pylori-positive subjects were enrolled from 2010 to 2018 and their data were subjected to intention-to-treat (ITT) and per-protocol (PP) analysis. All subjects received 10-day sequential therapy consisting of 40 mg esomeprazole and 1 g amoxicillin b.i.d for 5 days followed by 40 mg esomeprazole b.i.d, 500 mg clarithromycin b.i.d and 500 mg metronidazole t.i.d for 5 days. The 13C-urea breath test, rapid urease test (CLO test®), and histology were used to confirm eradication. Compliance and side effects were also investigated. RESULTS: ITT and PP eradication rates of SQT were 69.9% (687 of 983) and 87.1% (657 of 754), respectively. The annual eradication rate of ITT remained consistent over the 8-year study period (p for trend=0.167), whereas PP analysis showed the eradication rate increased (p for trend=0.042). The overall adverse event rate for SQT was 41.7% (410 subjects). CONCLUSIONS: Despite high antibiotic resistance rates in Korea, the eradication rate of SQT did not decrease over the 8-year study period.