The Influence of in Vitro Nitroimidazole Resistance on The Efficacy of Nitroimidazole-Containing Anti- Helicobacter Pylori Regimens: A Meta-Analysis

Wouden, EJ van der; Thijs, J. C.; Zwet, AA van; Sluiter, Willem; Kleibeuker, Jan H.

doi:10.1111/j.1572-0241.1999.01202.x

Cited by 48 publications

(16 citation statements)

References 71 publications

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“…This finding is in contrast with results from previous studies demonstrating the negative effect of different levels of metronidazole resistance on PPI‐based triple therapy 11, 13, 16, 17 . Moayyedi et al .…”

Section: Discussioncontrasting

confidence: 99%

“…Several studies have established that primary resistance to clarithromycin in H. pylori is a strong predictive factor for therapeutic failure in clarithromycin containing regimens 10–13 . On the contrary, conflicting results have been reported on the impact of primary metronidazole resistance on treatment outcome, especially in treatment combinations containing both nitroimidazole and clarithromycin 11, 13–17 . Prevalence of primary clarithromycin resistance in H. pylori is still relatively low at 3–13% in both industrialized and developing countries 11, 15, 18–21 .…”

Section: Introductionmentioning

confidence: 99%

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The importance of the level of metronidazole resistance for the success of Helicobacter pylori eradication

Wheeldon

Granström

Hoang

et al. 2004

Aliment Pharmacol Ther

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SUMMARYAims: To evaluate the role of antibiotic susceptibility for the treatment outcome of proton pump inhibitordependent and independent Helicobacter pylori eradication regimens. Methods: In a placebo-controlled clinical study of peptic ulcer patients with H. pylori infection, patients were randomized to receive lansoprazole, clarithromycin and tinidazole twice-daily, clarithromycin and tinidazole once-daily with lansoprazole or with placebo. Helicobacter pylori status was assessed by culture and antibiotic susceptibility by E-test minimal inhibitory concentration (MIC) in 205 clinical isolates. Results: Primary resistance to clarithromycin and metronidazole was 1 and 76%, respectively. In metronidazole susceptible strains eradication rates were similar at > 90% for all treatment groups (P ¼ 0.49).With low-level metronidazole resistance (4 lg/ mL < MIC < 256 lg/mL), eradication rates were similar at >75% (P ¼ 0.80). The major difference was found at high-level metronidazole resistance (MIC ‡ 256 lg/mL) with 95%, 58% and 21% eradication in the lansoprazole, clarithromycin and tinidazole twice-daily, lansoprazole, clarithromycin and tinidazole once-daily and placebo, clarithromycin and tinidazole once-daily groups, respectively (P < 0.001). Conclusion: In the absence of antibiotic resistance, a once-daily therapy of only clarithromycin and tinidazole can achieve a high rate of H. pylori eradication. Such a combination could offer a simpler and cheaper treatment option for developing countries. The standard, twice-daily proton pump inhibitor-based triple therapy was shown to be efficient in H. pylori eradication even in the presence of high-level metronidazole resistance.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The importance of the level of metronidazole resistance for the success of Helicobacter pylori eradication

Wheeldon

Granström

Hoang

et al. 2004

Aliment Pharmacol Ther

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“…Metronidazole resistance also plays a role because resistance was shown to reduce eradication rates of clarithromycin triple therapy by 18% . Still, several studies have suggested adequate (76–82%) eradication rates among metronidazole‐resistant compared with metronidazole‐susceptible strains (), which may be a function of the ability to overcome metronidazole resistance with more frequent dosing, longer durations of therapy, and concomitant therapy with a PPI or bismuth …”

Section: Penicillin Allergymentioning

confidence: 99%

Treatment of Helicobacter pylori in Special Patient Populations

et al. 2019

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Helicobacter pylori infection can lead to gastritis, gastric and duodenal ulcers, and gastric cancer. Consequently, complete eradication is the goal of therapy. First‐line therapy for H. pylori infection includes clarithromycin triple therapy (clarithromycin, proton pump inhibitor [PPI], and amoxicillin or metronidazole), bismuth quadruple therapy (bismuth salt, PPI, tetracycline, and metronidazole or amoxicillin), or concomitant therapy (clarithromycin, PPI, amoxicillin, and metronidazole). However, many patients have relative contraindications to the antibiotics included in these regimens, making therapy selection difficult. Furthermore, failure of initial therapy makes selection of second‐line therapy challenging due to concerns for potential resistance to agents included in the initial regimen. This review discusses H. pylori microbiology, including antibiotic resistance, and summarizes the existing evidence for first‐ and second‐line treatment regimens that may be considered for special populations such as patients with penicillin allergies, patients with or at risk for QTc‐interval prolongation, and patients who are pregnant, breastfeeding, or elderly.

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“…The bacterial cells then entered vacuoles and remained viable for at least 48 h. However, replication of the internalized H. pylori cells was not observed in the study, perhaps because of the short monitoring time and because the intracellular milieu was not suitable for bacterial replication (Amieva et al, 2002). Nonetheless, a most recent study found that H. pylori could proliferate in cells: two cells lines (AGS and MKN45) were evaluated in gentamicin protection experiments, revealing that H. pylori could proliferate after entering the cells, with the maximum number of bacterial cells observed after 6–12 h (van der Wouden et al, 1999; Rokkas et al, 2009; Chu et al, 2010). Zhang et al (2015) also observed this phenomenon in their study, whereby H. pylori attached to the cell membrane and combined with cellular microvilli after 2.5 h of infection.…”

Section: Cellular Invasion Of H Pylorimentioning

confidence: 99%

Adhesion and Invasion of Gastric Mucosa Epithelial Cells by Helicobacter pylori

Huang

Wang

Cheng

et al. 2016

Front. Cell. Infect. Microbiol.

105

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Helicobacter pylori is the main pathogenic bacterium involved in chronic gastritis and peptic ulcer and a class 1 carcinogen in gastric cancer. Current research focuses on the pathogenicity of H. pylori and the mechanism by which it colonizes the gastric mucosa. An increasing number of in vivo and in vitro studies demonstrate that H. pylori can invade and proliferate in epithelial cells, suggesting that this process might play an important role in disease induction, immune escape and chronic infection. Therefore, to explore the process and mechanism of adhesion and invasion of gastric mucosa epithelial cells by H. pylori is particularly important. This review examines the relevant studies and describes evidence regarding the adhesion to and invasion of gastric mucosa epithelial cells by H. pylori.

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The Influence of in Vitro Nitroimidazole Resistance on The Efficacy of Nitroimidazole-Containing Anti- Helicobacter Pylori Regimens: A Meta-Analysis

Abstract: NIR decreases treatment efficacy. Treatment duration and choice of other drugs influence the impact of NIR on treatment efficacy. If NIR is present, a nitroimidazole-containing regimen should be avoided or a quadruple regimen should be given for > 1 wk.

Cited by 48 publications

References 71 publications

The importance of the level of metronidazole resistance for the success of Helicobacter pylori eradication

The importance of the level of metronidazole resistance for the success of Helicobacter pylori eradication

Treatment of Helicobacter pylori in Special Patient Populations

Adhesion and Invasion of Gastric Mucosa Epithelial Cells by Helicobacter pylori

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