Combination Treatment with Ranitidine Is Highly Efficient Against Helicobacter pylori Despite Negative Impact of Macrolide Resistance

Helicobacter ◽  
1997 ◽  
Vol 2 (4) ◽  
pp. 188-193 ◽  
Author(s):  
Kristina Hultén ◽  
Bernhard Jaup ◽  
Bo Stenquist ◽  
Lars Engstrand
1997 ◽  
Vol 41 (12) ◽  
pp. 2724-2728 ◽  
Author(s):  
A Occhialini ◽  
M Urdaci ◽  
F Doucet-Populaire ◽  
C M Bébéar ◽  
H Lamouliatte ◽  
...  

Resistance of Helicobacter pylori to macrolides is a major cause of failure of eradication therapies. Single base substitutions in the H. pylori 23S rRNA genes have been associated with macrolide resistance in the United States. Our goal was to extend this work to European strains, to determine the consequence of this mutation on erythromycin binding to H. pylori ribosomes, and to find a quick method to detect the mutation. Seven pairs of H. pylori strains were used, the parent strain being naturally susceptible to macrolides and the second strain having acquired an in vivo resistance during a treatment regimen that included clarithromycin. The identity of the strains was confirmed by random amplified polymorphic DNA testing with two different primers, indicating that resistance was the result of the selection of variants of the infecting strain. All resistant strains were found to have point mutations at position 2143 (three cases) or 2144 (four cases) but never on the opposite DNA fragment of domain V of the 23S rRNA gene. The mutation was A-->G in all cases except one (A-->C) at position 2143. Using BsaI and BbsI restriction enzymes on the amplified products, we confirmed the mutations of A-->G at positions 2144 and 2143, respectively. Macrolide binding was tested on purified ribosomes isolated from four pairs of strains with [14C]erythromycin. Erythromycin binding increased in a dose-dependent manner for the susceptible strain but not for the resistant one. In conclusion we suggest that the limited disruption of the peptidyltransferase loop conformation, caused by a point mutation, reduces drug binding and consequently confers resistance to macrolides. Finally, the macrolide resistance could be detected without sequencing by performing restriction fragment length polymorphism with appropriate restriction enzymes.


1997 ◽  
Vol 41 (11) ◽  
pp. 2550-2553 ◽  
Author(s):  
K Hultén ◽  
A Gibreel ◽  
O Sköld ◽  
L Engstrand

Helicobacter pylori strains from seven patients treated with clarithromycin were investigated for development, mechanism, and stability of resistance. Genetic relatedness between pre- and posttreatment isolates was shown by arbitrary primed PCR. Clarithromycin resistance was associated with A-to-G transitions at either position 2143 or 2144 or at both positions 2116 and 2142. In four cases, the mutations were homozygous. The Cla(r) phenotype was stable after 50 subcultivations in vitro. No erythromycin-modifying enzymes or rRNA methylases were found by biological assays, PCR and sequencing, or cloning methods.


2007 ◽  
Vol 39 (9) ◽  
pp. 757-763 ◽  
Author(s):  
Hedvig Jakobsson ◽  
Karin Wreiber ◽  
Katja Fall ◽  
Björn Fjelstad ◽  
Olof Nyrén ◽  
...  

1999 ◽  
Vol 43 (7) ◽  
pp. 1779-1782 ◽  
Author(s):  
Leen-Jan van Doorn ◽  
Yvette J. Debets-Ossenkopp ◽  
Armelle Marais ◽  
Ricardo Sanna ◽  
Francis Mégraud ◽  
...  

ABSTRACT A PCR-based reverse hybridization system (research prototype kit INNO-LiPA for H. pylori resistance) was developed and evaluated for simultaneous detection of 23S ribosomal DNA point mutations, associated with macrolide resistance in Helicobacter pylori. Fifty-seven H. pylori strains (51 natural, 6 laboratory-derived artificial, 52 resistant, and 5 susceptible strains) were tested by PCR-LiPA (detecting mutations A2115→G, G2141→A, A2142→G, A2142→C, A2143→G, A2143→C, and A2143→T), DNA sequencing, restriction fragment length polymorphism, and/or hybridization to oligonucleotide probes. Results were highly concordant, but PCR-LiPA appears to be more sensitive for the simultaneous detection of multiple mutants.


Helicobacter ◽  
2021 ◽  
Author(s):  
Lucie Bénéjat ◽  
Astrid Ducournau ◽  
Chloé Domingues‐Martins ◽  
Mélanie Lecoeur ◽  
Alice Blosse ◽  
...  

2017 ◽  
Vol 95 (1) ◽  
pp. 15-22
Author(s):  
Vadim A. Akhmedov ◽  
O. V. Gaus

This review article highlights the modern views of manifestations associated with Hp infection. The data are presented about the negative impact of the infection on the state of the musculoskeletal system, the development of migraine, progression of diffuse liver disease and the risk of developing liver cancer. The paper also provides information on the possible effects of Helicobacter pylori infection on the formation of halitosis, tympanosclerosis, male reproductive health disorders, colorectal cancer, Alzheimer's and Parkinson's disease, pre-eclampsia during pregnancy, and idiopathic chronic urticaria. In addition, the negative relationship between Hp infection, bronchial asthma, and inflammatory bowel disease is considered.


Digestion ◽  
2021 ◽  
pp. 1-7
Author(s):  
Sho Suzuki ◽  
Chika Kusano ◽  
Toshiki Horii ◽  
Ryoji Ichijima ◽  
Hisatomo Ikehara

<b><i>Background:</i></b> <i>Helicobacter pylori</i> eradication treatments are widely performed to improve gastric mucosal inflammation, promote ulcer healing, and reduce the incidence of gastric cancer. However, there are several issues associated with <i>H. pylori</i> eradication treatment. First, various treatment regimens are currently used worldwide, and the standard treatment varies with region and country. Second, the antimicrobial resistance of <i>H. pylori</i> is increasing due to indiscriminate antibiotic use. Finally, gut microbiota dysbiosis is potentially induced by <i>H. pylori</i> treatment. <b><i>Summary:</i></b> Based on current international guidelines and a network meta-analysis comparing the effects of various treatment regimens, nonbismuth quadruple therapies for 10–14 days and vonoprazan-based triple therapy for 7 days are the currently recommended <i>H. pylori</i> treatment regimens. These regimens show good eradication rates of approximately 90%, even in areas where antimicrobial-resistant strains are highly prevalent. However, these regimens still have inherent drawbacks that may promote further increases in antimicrobial resistance and induce gut microbiota dysbiosis because of the empiric use of multiple antibiotics. <b><i>Key Message:</i></b> The ideal concept for the present and future <i>H. pylori</i> eradication treatment involves “a simple, cost-effective strategy that fosters compliance without having a negative impact on the gut microbiota or contributing to future antimicrobial resistance.” One interesting possibility that may fulfill this concept is a dual therapy involving vonoprazan and amoxicillin. This is the simplest treatment regimen that provides acceptable eradication rates, improves safety and tolerability, and minimizes the potential for increasing antimicrobial resistance or causing gut microbiota dysbiosis.


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