High prevalence of <i>Helicobacter pylori</i> infection with dual resistance to metronidazole and clarithromycin in Hong Kong

Wang, W. H.; Wong, Bcy; Mukhopadhyay, Asish K.; Berg, Douglas E.; Cho, C. H.; Lai, K. C.; Hu, Whc; Fung, F. M. Y.; Hui, W. M.; Lam, Shiu‐Kum

doi:10.1046/j.1365-2036.2000.00795.x

Cited by 99 publications

(110 citation statements)

References 31 publications

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“…Therefore we need to find means to attenuate gastric inflammation and provide cytoprotection against H. pyloriinduced cytotoxicity. 23 Our study showed H. pylori-associated chronic active gastritis and gastric carcinogenesis to be effectively suppressed by oral administration of canolol at 0.1% in the diet. In addition, iNOS, COX-2, and inflammatory cytokine IL-1b, IL-12 and TNF-a mRNA expression levels were substantially decreased after canolol administration in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 89%

4‐Vinyl‐2,6‐dimethoxyphenol (canolol) suppresses oxidative stress and gastric carcinogenesis in Helicobacter pylori‐infected carcinogen‐treated Mongolian gerbils

Cao

Tsukamoto

Seki

et al. 2008

Intl Journal of Cancer

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Oxidative stress is linked to gastric carcinogenesis because of its ability to damage DNA. Here we examined antioxidative and antiinflammatory effects of 4-vinyl-2,6-dimethoxyphenol (canolol), a recently identified potent antioxidative compound obtained from crude canola oil, on Helicobacter (H.) pylori-induced gastritis and gastric carcinogenesis using a Mongolian gerbil model. The animals were allocated to H. pylori-infection alone (12 weeks) or H. pylori 1 N-methyl-N-nitrosourea (MNU) administration (52 weeks). After oral inoculation of H. pylori, they were fed for 10 and 44 weeks with or without 0.1% canolol. H. pylori-induced gastritis, 5 0 -bromo-2 0 -deoxyuridine (BrdU) labeling and scores for cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) immunohistochemistry were attenuated in the canololtreated groups. Expression of interleukin-1b (IL-1b), tumor necrosis factor-a (TNF-a), COX-2 and iNOS mRNA in the gastric mucosa, and serum 8-hydroxy-2 0 -deoxyguanosine (8-OHdG), anti-H. pylori IgG and gastrin levels were also significantly lower in canolol-treated groups. Furthermore, the incidence of gastric adenocarcinomas was markedly reduced in the H. pylori 1 MNU 1 canolol-treated group [15.0% (6/40)] compared to the control group [39.4% (13/33)] (p < 0.05). These data indicate canolol to be effective for suppressing inflammation, gastric epithelial cell proliferation and gastric carcinogenesis in H. pylori-infected Mongolian gerbils. Interestingly, the viable H. pylori count was not changed by the canolol containing diet. Thus, the data point to the level of inflammation because of H. pylori rather than the existence of the bacteria as the determining factor. Importantly, canolol appears to suppress induction of mRNAs for inflammatory cytokines. ' 2007 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 89%

4‐Vinyl‐2,6‐dimethoxyphenol (canolol) suppresses oxidative stress and gastric carcinogenesis in Helicobacter pylori‐infected carcinogen‐treated Mongolian gerbils

Cao

Tsukamoto

Seki

et al. 2008

Intl Journal of Cancer

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“…20 Amoxicillin resistance is uncommon. According to the latest research from Taiwan 21 and Hong Kong, 22 primary resistance to metronidazole, clarithromycin and amoxicillin was found in 32%, 6% and 0%, and 56%, 2% and 0.4%, respectively. Furazolidone is an old and cheap but effective antimicrobial with bactericidal or bacteriostatic activity against many Grampositive and Gram-negative bacteria.…”

Section: Discussionmentioning

confidence: 99%

One‐week regimens containing ranitidine bismuth citrate, furazolidone and either amoxicillin or tetracycline effectively eradicate Helicobacter pylori: a multicentre, randomized, double‐blind study

Lü¹,

Zhang²,

Hu³

et al. 2001

Aliment Pharmacol Ther

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Background: The metronidazole resistance of Helicobacter pylori strains has increased rapidly. Aim: To evaluate the efficacy and safety of new 1‐week regimens containing ranitidine bismuth citrate, furazolidone and either amoxicillin or tetracycline. Methods: One hundred and twenty patients with H. pylori‐positive inactive duodenal ulcer or non‐ulcer dyspepsia diagnosed by endoscopy were recruited randomly to receive one of two regimens for 7 days: ranitidine bismuth citrate, 350 mg b.d., furazolidone, 100 mg b.d., and either amoxicillin, 1000 mg b.d. (n=60), or tetracycline, 500 mg b.d. (n=60). H. pylori infection was identified by rapid urease testing and histology. 13C‐Urea breath test was performed to evaluate the cure of H. pylori infection at least 4 weeks after completion of triple therapy. Results: The eradication rates of H. pylori by ranitidine bismuth citrate–furazolidone–amoxicillin and ranitidine bismuth citrate–furazolidone–tetracycline regimens were 82% and 85% (P > 0.05), respectively, by intention‐to‐treat analysis, and 85% and 91% (P > 0.05), respectively, by per protocol analysis. Adverse effects were mild in both ranitidine bismuth citrate–furazolidone–amoxicillin and ranitidine bismuth citrate–furazolidone–tetracycline groups. Conclusions: One‐week regimens containing ranitidine bismuth citrate, furazolidone and amoxicillin or tetracycline are well tolerated and effective for the eradication of H. pylori.

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“…The prevalence of resistance to these anti-microbial agents varies with gender, ethnic group and country of origin (Table 1) [41] . It was recently reported from Hong Kong that almost 50% of pre-treatment strains of H. pylori were resistant to metronidazole and over 10% to clarithromycin [42] . The efficacy of treatment for H. pylori is significantly decreased in the presence of pre-treatment anti-microbial resistance and the likelihood of this should influence the chosen regimen (Table 1, Figure 1) [5,41] .…”

Section: H Pylori Eradication Treatmentmentioning

confidence: 99%

“…Eradication is defined as negative tests for the bacterium four weeks, or longer, after the end of antimicrobial therapy [42] . Failure to detect H. pylori on tests done less than four weeks after the end of therapy may give false negative results because clearance, or uppression of H. pylori may occur during treatment, followed by rapid recrudescence of the original infection.…”

Section: H Pylori Eradication Treatmentmentioning

confidence: 99%

“…The most overall effective H. pylori eradication regimens reported to date combine either a PPI (esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole) or RBC with two of the following: amoxycillin, clarithromycin, or a nitroimidazole (metronidazole or tinidazole) [5,42,[43][44][45][46][47][48][49] ( Table 2). These regimens are commonly prescribed for one week and the tablets are taken twice daily.…”

Section: Low-dose Triple Therapymentioning

confidence: 99%

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Treatment of Helicobacter pylori

Harris¹

2001

WJG

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High prevalence of Helicobacter pylori infection with dual resistance to metronidazole and clarithromycin in Hong Kong

Cited by 99 publications

References 31 publications

4‐Vinyl‐2,6‐dimethoxyphenol (canolol) suppresses oxidative stress and gastric carcinogenesis in Helicobacter pylori‐infected carcinogen‐treated Mongolian gerbils

4‐Vinyl‐2,6‐dimethoxyphenol (canolol) suppresses oxidative stress and gastric carcinogenesis in Helicobacter pylori‐infected carcinogen‐treated Mongolian gerbils

One‐week regimens containing ranitidine bismuth citrate, furazolidone and either amoxicillin or tetracycline effectively eradicate Helicobacter pylori: a multicentre, randomized, double‐blind study

Treatment of Helicobacter pylori

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