Helicobacter pylori eradication rates with concomitant and tailored therapy based on 23S rRNA point mutation: A multicenter randomized controlled trial

Abstract

Background:We evaluated the efficacy of tailored therapy based on point mutation presence identified with the dual-priming oligonucleotide (DPO)-based multiplex polymerase chain reaction (PCR) method compared with concomitant therapy. Materials and methods:Subjects were randomly assigned concomitant therapy (amoxicillin 1 g, clarithromycin 500 mg, metronidazole 500 mg, and lansoprazole 30 mg twice/day for 14 days) or tailored therapy (amoxicillin 1 g, clarithromycin 500 mg, and lansoprazole 30 mg twice/day for 14 days in point mutation-negative subjects; and amoxicillin 1 g, metronidazole 500 mg, and lansoprazole 30 mg twice/ day for 14 days in point mutation-positive subjects). Results:A total of 397 and 352 subjects were included in the intention-to-treat (ITT) and per-protocol (PP) analyses, respectively. Point mutations were identified in 25.9% of the subjects. The overall eradication rate was not significantly different between the groups by ITT (86.2% vs 81.6%, P = .132) and PP analyses (90.2% vs 86.5%, P = .179). There was no significant difference in the eradication rates between the groups in both the point mutation-negative subjects (91.7% vs 87.3%, P = .154) and the point mutation-positive subjects (71.2% vs 64.7%, P = .312). The eradication rates were significantly lower in the point mutation-positive subjects than in the point mutation-negative subjects in both the concomitant and tailored therapy groups.Conclusions: Tailored therapy based on point mutation presence identified with the DPO-based multiplex PCR method was as effective as concomitant therapy. The eradication rates of both therapy regimens were suboptimal in point mutation-positive subjects. K E Y W O R D Sconcomitant therapy, eradication, point mutation, tailored therapy

Molecular Assessment of Resistance to Clarithromycin in Helicobacter pylori Strains Isolated from Patients with Dyspepsia by Fluorescent In Situ Hybridization in the Center of Iran

“…Based on the Maastricht V consensus reports, the above treatment is appropriate in countries with less than 15% resistance to clarithromycin. There are numerous, important factors (human and bacterial) in reducing the effect of H. pylori treatment, of which the antibiotic resistance seems to be the most significant [7,8].…”

Empirical or susceptibility-guided treatment forHelicobacter pyloriinfection? A comprehensive review

“…We have just performed (in 2020) an updated meta-analysis comparing empirical versus susceptibility-guided treatment of H. pylori , 59 including 40 studies. 60–100 When only assessing first-line treatments, better efficacy results were obtained, overall, with the susceptibility-guided strategy (although the results were borderline statistically significant). However, when considering only empirical up-to-date first-line quadruple regimens (that is excluding the suboptimal triple therapies) no differences in efficacy were found versus the susceptibility-guided group.…”

Validation of loop‐mediated isothermal amplification to detect Helicobacter pylori and 23S rRNA mutations: A prospective, observational clinical cohort study

“…11 However, H pylori is difficult to culture in clinical settings because it requires microaerobic and high-CO 2 culture conditions. 11 Several lines of evidence suggest that the 2143A > G mutation in H pylori 23S ribosomal RNA (rRNA) is related to clarithromycin resistance and eradication failure, [12][13][14][15] and screening for this mutation is likely to be an effective alternative method to identify clarithromycin resistance in H pylori. 12 We previously reported that the presence of 2143G in H pylori 23S rRNA is an independent risk for eradication failure, which reached approximately 60% in response to clarithromycin-based triple therapy, and patients with 2143A-2182C mutations showed a moderate risk with approximately 10% eradication failure.…”

“…11 Several lines of evidence suggest that the 2143A > G mutation in H pylori 23S ribosomal RNA (rRNA) is related to clarithromycin resistance and eradication failure, [12][13][14][15] and screening for this mutation is likely to be an effective alternative method to identify clarithromycin resistance in H pylori. 12 We previously reported that the presence of 2143G in H pylori 23S rRNA is an independent risk for eradication failure, which reached approximately 60% in response to clarithromycin-based triple therapy, and patients with 2143A-2182C mutations showed a moderate risk with approximately 10% eradication failure. 15 However, the polymerase chain reaction (PCR)-based method to amplify DNA fragments and identify targeted mutations is also time-consuming, 16 and it is emerged the need for simple method to detect mutations.…”