Effect of Triple Therapy (Antibiotics plus Bismuth) on Duodenal Ulcer Healing

Graham, David Y.; Lew, Ginger M.; Evans, Dolores G.; Evans, Doyle J.; Klein, Peter

doi:10.7326/0003-4819-115-4-266

Cited by 206 publications

(71 citation statements)

References 14 publications

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“…Helicobacter pylori is a causative agent for duodenal and peptic ulcers (17,49), and infection with H. pylori is a risk factor for gastric adenocarcinoma (14) and for B-cell MALT lymphoma (37). H. pylori infection in Western countries occurs in up to 50% of the population (16) and may reach 90 to 100% in developing countries (15), where antibiotic resistance rates are also high (15).…”

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Helicobacter pylori Flagellar Hook-Filament Transition Is Controlled by a FliK Functional Homolog Encoded by the Gene HP0906

et al. 2005

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Helicobacter pylori is a human gastric pathogen which is dependent on motility for infection. The H. pylori genome encodes a near-complete complement of flagellar proteins compared to model enteric bacteria. One of the few flagellar genes not annotated in H. pylori is that encoding FliK, a hook length control protein whose absence leads to a polyhook phenotype in Salmonella enterica. We investigated the role of the H.

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Helicobacter pylori Flagellar Hook-Filament Transition Is Controlled by a FliK Functional Homolog Encoded by the Gene HP0906

et al. 2005

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“…Subsequently, an RCT of both colloidal bismuth subcitrate and cimetidine, alone or in combination with tinidazole, confirmed that colloidal bismuth subcitrate and tinidazole cleared the infection in almost 75% of patients [7] . With the addition of a second antibiotic, tetracycline or amoxicillin, eradication rates in later RCTs exceeded 80% [8][9][10] . However, there were some problems associated with bismuth-based triple therapy, which included the number of tablets patients were required to take, the duration of therapy, and side effects such as altered taste, nausea, and diarrhoea.…”

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Adverse events with bismuth salts for Helicobacter pylori eradication: Systematic review and meta-analysis

Ford

Malfertheiner²,

Giguere³

et al. 2008

WJG

110

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INTRODUCTIONBismuth salts have been used for centuries in medicine. From a gastroenterology perspective these drugs have been used to treat peptic ulcer disease, dyspepsia, parasitic infections, microscopic colitis, and infectious diarrhoea [1] . The discovery of Helicobacter pylori (H pylori) in 1983 by Warren and Marshall revolutionised the management of peptic ulcer disease [2] , and led to a renewed interest in bismuth compounds, largely because bismuth was found to inhibit the growth of H pylori and was effective in eradicating the organism (when combined with antibiotics or in combination with antibiotics and acid suppression therapy [3,4] ). The first randomised controlled trial (RCT) of bismuth in H pylori-positive individuals suggested that bismuth was superior to erythromycin monotherapy in eradicating the infection [5] . A further RCT of 6 wk of colloidal bismuth subcitrate versus cimetidine, in H pylori-positive duodenal ulcer patients, demonstrated that bismuth successfully eradicated the bacterium in up to 50% of patients [6] . Subsequently, an RCT of both colloidal bismuth subcitrate and cimetidine, alone or in combination with tinidazole, confirmed that colloidal bismuth subcitrate and tinidazole cleared the infection in almost 75% of patients [7] . With the addition of a second antibiotic, tetracycline or amoxicillin, eradication rates in later RCTs exceeded 80% [8][9][10] . However, there were some problems associated with bismuth-based triple therapy, which included the number of tablets patients were required to take, the duration of therapy, and side effects such as altered taste, nausea, and diarrhoea. Abstract AIM: To assess the safety of bismuth used in Helicobacter pylori (H pylori ) eradication therapy regimens. METHODS:We conducted a systematic review and meta-analysis. MEDLINE and EMBASE were searched (up to October 2007) to identify randomised controlled trials comparing bismuth with placebo or no treatment, or bismuth salts in combination with antibiotics as part of eradication therapy with the same dose and duration of antibiotics alone or, in combination, with acid suppression. Total numbers of adverse events were recorded. Data were pooled and expressed as relative risks with 95% confidence intervals (CI). RESULTS: We identified 35 randomised controlled trials containing 4763 patients. There were no serious adverse events occurring with bismuth therapy. There was no statistically significant difference detected in total adverse events with bismuth [relative risk (RR) = 1.01; 95% CI: 0.87-1.16], specific individual adverse events, with the exception of dark stools (RR = 5.06; 95% CI: 1.59-16.12), or adverse events leading to withdrawal of therapy (RR = 0.86; 95% CI: 0.54-1.37).CONCLUSION: Bismuth for the treatment of H pylori is safe and well-tolerated. The only adverse event occurring significantly more commonly was dark stools.

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“…H. pylori infection elicits gastric inflammation and may cause gastritis, peptic ulcers, duodenal ulcers, and gastric adenocarcinoma (5,10,20,59). The motility of H. pylori is an essential requirement for colonization of the gastric niche (13,14).…”

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Posttranscriptional Regulation of Flagellin Synthesis in Helicobacter pylori by the RpoN Chaperone HP0958

et al. 2008

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The Helicobacter pylori protein HP0958 is essential for flagellum biogenesis. It has been shown that HP0958 stabilizes the 54 factor RpoN. The aim of this study was to further investigate the role of HP0958 in flagellum production in H. pylori. Global transcript analysis identified a number of flagellar genes that were differentially expressed in an HP0958 mutant strain. Among these, the transcription of the major flagellin gene flaA was upregulated twofold, suggesting that HP0958 was a negative regulator of the flaA gene. However, the production of the FlaA protein was significantly reduced in the HP0958 mutant, and this was not due to the decreased stability of the FlaA protein. RNA stability analysis and binding assays indicated that HP0958 binds and destabilizes flaA mRNA. The HP0958 mutant was successfully complemented, confirming that the mutant phenotype described was due to the lack of HP0958. We conclude that HP0958 is a posttranscriptional regulator that modulates the amount of the flaA message available for translation in H. pylori.

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Effect of Triple Therapy (Antibiotics plus Bismuth) on Duodenal Ulcer Healing

Abstract: Combined therapy with anti-H. pylori agents and ranitidine was superior to ranitidine alone for duodenal ulcer healing. Our results indicate that H. pylori plays a role in duodenal ulcer disease.

Cited by 206 publications

References 14 publications

Helicobacter pylori Flagellar Hook-Filament Transition Is Controlled by a FliK Functional Homolog Encoded by the Gene HP0906

Helicobacter pylori Flagellar Hook-Filament Transition Is Controlled by a FliK Functional Homolog Encoded by the Gene HP0906

Adverse events with bismuth salts for Helicobacter pylori eradication: Systematic review and meta-analysis

Posttranscriptional Regulation of Flagellin Synthesis in Helicobacter pylori by the RpoN Chaperone HP0958

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