Bor-Shyang Sheu

Impact of supplement with Lactobacillus- and Bifidobacterium-containing yogurt on triple therapy for Helicobacter pylori eradication

Aim : To test whether supplements of Lactobacillus‐ and Bifidobacterium‐containing yogurt (AB‐Yogurt) affect the success of Helicobacter pylori eradication.

Prevalence of primary fluoroquinolone resistance among clinical isolates of Helicobacter pylori at a University Hospital in Southern Taiwan.

Background:  Fluoroquinolone‐containing therapy is effective in eradicating Helicobacter pylori. However, the resistance rate of H. pylori to fluoroquinolones in Taiwan has not yet been reported. In this study, we aimed to investigate the susceptibility to antibiotics commonly used in eradication schedules and fluoroquinolones in H. pylori.

Splenic infarction after histoacryl injection for bleeding gastric varices

Gastric varix bleeding is a serious but relatively common complication in cirrhotic patients. Treatment is difficult not only because of the gastric intertwining venous network but also its isolated location in the cardia and fundus. The disappointing results with sclerosing agents in this situation have led to the introduction of tissue adhesive injection. A 93% success rate for initial hemostasis was achieved with N-butyl cyanoacrylate injection.1 The reported complications of this treatment include injection site ulcers, fever, chest pain, and thrombosis of the portal venous system.2 Splenic infarction as a complication had not been reported.

Resistance to metronidazole, clarithromycin and levofloxacin of Helicobacter pylori before and after clarithromycin‐based therapy in Taiwan

Background and Aim:  Clarithromycin‐based triple therapy has been commonly applied as the first‐line therapy for Helicobacter pylori eradication. Levofloxacin could serve as an alternative in either first‐line or second‐line regimens. This study surveyed the prevalence of levofloxacin resistance of H. pylori isolates in naive patients and in patients with a failed clarithromycin‐based triple therapy.

Interaction Between Host Gastric Sialyl-Lewis X and H. pylori SabA Enhances H. pylori Density in Patients Lacking Gastric Lewis B Antigen

OBJECTIVES:We tested whether the interaction between host gastric Lex antigen and the SabA protein of H. pylori determined gastric colonization density.METHODS:A total of 145 H. pylori-infected patients were assessed for their bacterial density and gastric Leb and sialyl-Lex expression. Their corresponding H. pylori isolates were tested for babA2 and sabA genotype by PCR. The sabA-genopositive PCR products were sequenced to check for mutations affecting SabA expression. The BabA and SabA expressions of each isolate were confirmed by Western blotting.RESULTS:All 145 H. pylori isolates were babA2-genopositive and expressed BabA. There were 116 (80%) sabA-genopositive isolates, but only 45 (31%) of the isolates expressed SabA. Sequence of sabA-genopositive PCR products was achieved in 92 isolates, of which 60% had regular CT repeat-pairs and the other 40% had a unique deletion of the CT repeats. Neither the deletion nor the different CT repeat-pairs in the sabA region were totally correlated with SabA expression, defined by Western blotting. H. pylori density was higher in those expressing gastric sialyl-Lex antigen (which interacts with SabA) (p < 0.001) only in those patients expressing weak or no gastric Leb antigen (which would interact with BabA), not in those with evident expression of gastric Leb antigen.CONCLUSIONS:In Taiwan, H. pylori isolates are 100% BabA-positive, but only 31% of them express SabA. The interaction between gastric sialyl-Lex and SabA of H. pylori determines the colonization density of patients expressing gastric Leb weakly or not at all.

Esomeprazole 40 mg twice daily in triple therapy and the efficacy of Helicobacter pylori eradication related to CYP2C19 metabolism

Aim : To determine whether an increased dosage of esomeprazole 40 mg twice daily in triple therapy improved the Helicobacter pylori eradication rate for patients with different genotypes of S‐mephenytoin 4′‐hydroxylase (CYP2C19).

Bacterial density of Helicobacter pylori predicts the success of triple therapy in bleeding duodenal ulcer

BACKGROUND We studied whether different initial bacterial densities of Helicobacter pylori would alter the eradication rate of H. pylori by triple therapy (amoxicillin 500 mg t.i.d. and metronidazole 500 mg t.i.d. for 14 days; bismuth subcitrate 120 mg t.i.d. for 28 days) in patients with duodenal ulcer bleeding. METHOD One hundred thirty-six cases with duodenal ulcer bleeding and H. pylori infection (proved by rapid urease test and histology during emergency endoscopy) were studied. One hundred twenty-seven of these patients completed a course of triple therapy. In each case, anti-H. pylori IgG titer, gastric biopsies for H. pylori density (score 1 to 5), and evaluation of severity of gastritis were collected at the first endoscopy and 1 month after completion of the triple therapy. RESULTS The ulcer healing rate was 84.3% (107 of 127) at the time of the second evaluation. The eradication rate of H. pylori was 76.4% (97 or 127). Eradication for H. pylori failed in 30 cases. In these eradication failure cases, initial serologic titer and density of H. pylori were higher than those of eradication success cases. The eradication rate of H. pylori decreased as the initial density of H. pylori increased (density of H. pylori: 1, 88.3%; 2, 83.8%; 3, 74.2%; 4, 68%; 5, 50%). At the second evaluation, the serologic titer was lower and continued to decline in eradication success cases whose mean residual titer ratio (100% x follow-up titer/initial titer) was lower than that of eradication failure cases (57.1% +/- 14.6% vs 107.1% +/- 24.1%, p < 0.001). The mean residual titer ratio also disclosed an upward trend as the density of H. pylori increased (density of H. pylori 1 to 5: 57.5%, 66.6%, 73.5%, 75.3%, 81.8%, respectively). CONCLUSIONS We suggest routine gastric biopsy to detect both the presence of H. pylori and its density inasmuch as quantitative results may predict the usefulness of triple therapy. The higher the H. pylori density, the less effective triple therapy will be at successful eradication of H. pylori.

Helicobacter pylori infection: An overview of bacterial virulence factors and pathogenesis

Helicobacter pylori pathogenesis and disease outcomes are mediated by a complex interplay between bacterial virulence factors, host, and environmental factors. After H. pylori enters the host stomach, four steps are critical for bacteria to establish successful colonization, persistent infection, and disease pathogenesis: (1) Survival in the acidic stomach; (2) movement toward epithelium cells by flagella-mediated motility; (3) attachment to host cells by adhesins/receptors interaction; (4) causing tissue damage by toxin release. Over the past 20 years, the understanding of H. pylori pathogenesis has been improved by studies focusing on the host and bacterial factors through epidemiology researches and molecular mechanism investigations. These include studies identifying the roles of novel virulence factors and their association with different disease outcomes, especially the bacterial adhesins, cag pathogenicity island, and vacuolating cytotoxin. Recently, the development of large-scale screening methods, including proteomic, and transcriptomic tools, has been used to determine the complex gene regulatory networks in H. pylori. In addition, a more available complete genomic database of H. pylori strains isolated from patients with different gastrointestinal diseases worldwide is helpful to characterize this bacterium. This review highlights the key findings of H. pylori virulence factors reported over the past 20 years.

Quadruple therapy containing amoxicillin and tetracycline is an effective regimen to rescue failed triple therapy by overcoming the antimicrobial resistance of Helicobacter pylori

Aim : To identify optimal antibiotics for second‐line quadruple therapy of Helicobacter pylori after failed 1‐week triple therapy.

Lactobacillus acidophilus ameliorates H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways.

BackgroundH. pylori infection may trigger Smad7 and NFκB expression in the stomach, whereas probiotics promote gastrointestinal health and improve intestinal inflammation caused by pathogens. This study examines if probiotics can improve H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways.ResultsChallenge with H. pylori increased IL-8 and TNF-α expressions but not TGF-β1 in MKN45 cells. The RNA levels of Smad7 in AGS cells increased after H. pylori infection in a dose-dependent manner. A higher dose (MOI 100) of L. acidophilus pre-treatment attenuated the H. pylori-induced IL-8 expressions, but not TGF-β1. Such anti-inflammatory effect was mediated via increased cytoplasmic IκBα and depletion of nuclear NFκB. L. acidophilus also inhibited H. pylori-induced Smad7 transcription by inactivating the Jak1 and Stat1 pathways, which might activate the TGF-β1/Smad pathway. L. acidophilus pre-treatment ameliorated IFN-γ-induced Smad7 translation level and subsequently reduced nuclear NF-κB production, as detected by western blotting.ConclusionsH. pylori infection induces Smad7, NFκB, IL-8, and TNF-α production in vitro. Higher doses of L. acidophilus pre-treatment reduce H. pylori-induced inflammation through the inactivation of the Smad7 and NFκB pathways.