Multiple Genetic Analysis System-Based Antibiotic Susceptibility Testing in Helicobacter pylori and High Eradication Rate With Phenotypic Resistance-Guided Quadruple Therapy

Dong, Fangyuan; Ji, Danian; Huang, Ruoyu; Zhang, Fan; Huang, Yiqin; Xiang, Ping; Kong, Mimi; Li, Nan; Zeng, Xianping; Wu, Yong; Bao, Zhijun

doi:10.1097/md.0000000000002056

Cited by 25 publications

(26 citation statements)

References 22 publications

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“…In addition, regarding the molecular mechanisms, some genetic mutations have been identified. Mutations occurring in the 2-oxoglutarate:acceptor oxidoreductase ( oorD ) gene, including A041G , A122G , C349A(G) , A78G , A112G , A335G , C156T and C165T , and in the pyruvate oxidoreductase ( porD ) gene, including G353A , A356G , C357T , C347T , C347G and C346A , are possibly related to the resistance[ 2 , 3 ]. The oor and por genes are involved in the generation of acetyl coenzyme A (acetyl-CoA) and succinyl-CoA[ 4 ].…”

Section: To the Editormentioning

confidence: 99%

Resistance of Helicobacter pylori to furazolidone and levofloxacin: A viewpoint

Zamani

Rahbar

Shokri‐Shirvani

2017

WJG

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In their review, Arslan et al[1] did not describe the status of Helicobacter pylori (H. pylori) treatment with furazolidone and the resistance to this antibiotic. We have presented different surveys showing the resistance of H. pylori to furazolidone from Asia and South America. The resistance rates varied but were mostly low (< 5%). There are not enough data on its efficacy and resistance in the United States and Europe. H. pylori mutations occurring in the oorD gene, including A041G, A122G, C349A(G), A78G, A112G, A335G, C156T and C165T, and in the porD gene, including G353A, A356G, C357T, C347T, C347G and C346A, have been indicated to be possibly related to the observed resistance. Additionally, to complete Arslan et al’s statement regarding levofloxacin resistance, it should be noted that compound mutations of N87A, A88N and V65I at codon Asn-87 were recently observed in the gyrA gene for the first time. However, the results on these topics are not sufficient, and more worldwide studies are suggested.

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Section: To the Editormentioning

confidence: 99%

Resistance of Helicobacter pylori to furazolidone and levofloxacin: A viewpoint

Zamani

Rahbar

Shokri‐Shirvani

2017

WJG

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“…The genotypic determination of antimicrobial resistance has made possible the elucidation of the molecular mechanisms of H. pylori resistance to antimicrobials such as clarithromycin, tetracycline, metronidazole, among others [22][23][24][25][26][27]. Resistance to clarithromycin has resulted from 3 points mutations A2142G, A2142C, and A2143G in 23S rDNA in the gene encoding the peptidyl transferase enzyme especially in the V domain (mutations too named like A2146C, A2146G, and A2147G) [28].…”

Section: Introductionmentioning

confidence: 99%

Surveillance of the Antimicrobial Resistance Rates of <b><i>Helicobacter pylori</i></b> Ten Years Later in the Western Central Region, Colombia

Bedoya-Gómez

Aldana

Moncayo

et al. 2019

Dig Dis

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Background: Helicobacter pylori is a bacterium associated with gastroduodenal disease and gastric cancer. Empirical therapy in the treatment of H. pylori infection increases the risk of apparition of antimicrobial drug resistance. In a previous report, in H. pylori clinical isolates, resistance rates to commonly used antimicrobial drugs were as follows: metronidazole 82%, clarithromycin 3.8%, and amoxicillin 1.9%. The aim was to establish the variation of resistance rates and the detection of H. pylori genetic mutations isolated from dyspeptic patients. Methods: Antimicrobial susceptibility profiles were performed by the E-test method for metronidazole, clarithromycin, amoxicillin, and tetracycline in 61 clini-cal isolates. Sequencing was performed to detect mutations associated with resistance to clarithromycin. Results: According to our results, resistance rates found in the 61 isolates were 78.60% for metronidazole and 8.20% for clarithromycin. None of the studied isolates had resistance to tetracycline and amoxicillin. Secondary resistance rates displayed an increase when compared to primary rates for metronidazole (87.50 vs. 77.35%) and for clarithromycin (25.66 vs. 5.66%). Of 5 isolates resistant to clarithromycin, 3 had the A2143G mutation. By comparing the results in this work with previous reports, antimicrobial drug resistance rates did not show major modifications for metronidazole, amoxicillin, and tetracycline during the last 10 years. For clarithromycin, the resistance rate showed a moderate increase; nevertheless, it remains low (< 15%) and this change was not statistically significant. Conclusion: Together, all findings in this work indicate that these antimicrobial drugs can still be used as first line of defense on infected patients living in this region of the country.

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“…Antibiotic resistance of H. pylori strains, though, is not limited to clarithromycin. The following rates of H. pylori resistance were reported in a 2015 report from Shanghai, China: clarithromycin 40.0 %, amoxicillin 4.4 %, metronidazole 53.3 %, tetracycline 0 %, and levofloxacin 55.6 % [15]. While testing for clarithromycin resistance alone will provide important information, to treat H. pylori gastritis as an infectious disease will require available testing for not only clarithromycin, but also for other commonly used antibiotics.…”

Section: How the Article Addresses The Controversiesmentioning

confidence: 99%