Trial reportBMC microbiology2008
Prevalence of A2143G mutation of H. pylori-23S rRNA in Chinese subjects with and without clarithromycin use history.
Trial report in BMC microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Antibiotic resistance in Helicobacter pylori: a genetic and physiological perspective.Gut pathogens · 2025Review
- Article
- Phenotypic and Genotypic Antibiotic Resistance Patterns inFrontiers in cellular and infection microbiology · 2020Article
- Increase in antibiotic resistantInfection and drug resistance · 2019Article
- Detection of 23SrRNA Mutations Strongly Related to Clarithromycin Resistance in Helicobacter pylori Strains Isolated From Patients in the North of Iran.Jundishapur journal of microbiology · 2016Article
- Functional and molecular surveillance of Helicobacter pylori antibiotic resistance in Kuala Lumpur.PloS one · 2014Article
- Characterization of human gastric carcinoma-related methylation of 9 miR CpG islands and repression of their expressions in vitro and in vivo.BMC cancer · 2012Article
- Nucleosomes correlate with in vivo progression pattern of de novo methylation of p16 CpG islands in human gastric carcinogenesis.PloS one · 2012Article
- Detection of A2142C, A2142G, and A2143G Mutations in 23s rRNA Gene Conferring Resistance to Clarithromycin among Helicobacter pylori Isolates in Kerman, Iran.Iranian journal of medical sciences · 2011Article
- Methylation of GATA-4 and GATA-5 and development of sporadic gastric carcinomas.World journal of gastroenterology · 2010Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA2143G mutation of 23S rRNA gene of H. pylori results in clarithromycin (CLR) resistance. To investigate the prevalence of the CLR resistance-related A2143G mutation of the H. pylori-specific 23S rRNA gene in Chinese subjects with and without CLR use history, 307 subjects received the treatment with amoxicillin and omeprazole (OA) and 310 subjects received a placebo in 1995, and 153 subjects received a triple therapy with OA and CLR (OAC) in 2000. DNA was extracted from fasting gastric juice at the end of the intervention trial in 2003. H. pylori infection was determined by H. pylori-specific 23S rRNA PCR, ELISA, and13C-urea breath test assays. Mutations of the 23S rRNA gene were detected by RFLP assays.
resultsThe presence of 23S rRNA due to H. pylori infection in the OA group remained lower than that in the placebo group 7.3 yrs after OA-therapy [51.1% (157/307) vs. 83.9% (260/310), p = 0.0000]. In the OAC group, the 23S rRNA detection rate was 26.8% (41/153) three yrs after OAC-treatment. The A2143G mutation rate among the 23S rRNA-positive subjects in the OAC group [31.7% (13/41)] was significantly higher than that in the OA group [10.2% (16/157)] and the placebo group [13.8% (36/260)]. The frequency of the AAGGG --> CTTCA (2222-2226) and AACC --> GAAG (2081-2084) sequence alterations in the OAC group was also significantly higher than those in the OA group and the placebo group.
conclusionPrimary prevalence of the A2143G mutation was 10~14% among Chinese population without history of CLR therapy. Administration of CLR to eliminate H. pylori infection increased the prevalence of the A2143G mutation in Chinese subjects (32%) significantly.
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