PDF(Pubmed)
Abstract：
UNASSIGNED: Rising clarithromycin resistance undermines Helicobacter pylori (H. pylori) treatment efficacy. We aimed to determine clarithromycin\'s minimum inhibitory concentration (MIC) levels and identify specific mutation sites in the 23S ribosomal subunit (23S rRNA) that predict treatment outcomes in a 14-day regimen of clarithromycin bismuth quadruple therapy (amoxicillin 1g, clarithromycin 500 mg, rabeprazole 10 mg, and colloidal bismuth pectin 200 mg).
UNASSIGNED: We included adult H. pylori patients who hadn\'t previously undergone clarithromycin-based treatment, either as initial or rescue therapy. Exclusions were made for penicillin allergy, recent use of related medications, severe illnesses, or inability to cooperate. Patients underwent a 14-day clarithromycin bismuth quadruple therapy. Gastric mucosa specimens were obtained during endoscopy before eradication. MIC against amoxicillin and clarithromycin was determined using the E-test method. The receiver operating characteristic (ROC) curve helped to find the optimal clarithromycin resistance MIC breakpoint. Genetic sequences of H. pylori 23S rRNA were identified through Sanger Sequencing. (ChiCTR2200061476).
UNASSIGNED: Out of 196 patients recruited, 92 met the inclusion criteria for the per-protocol (PP) population. The overall intention-to-treat (ITT) eradication rate was 80.00 % (84/105), while the modified intention-to-treat (MITT) and PP eradication rates were 90.32 % (84/93) and 91.30 % (84/92) respectively. No amoxicillin resistance was observed, but clarithromycin resistance rates were 36.19 % (38/105), 35.48 % (33/93), and 34.78 % (33/92) in the ITT, MITT, and PP populations respectively. Compared with the traditional clarithromycin resistance breakpoint of 0.25 μg/mL, a MIC threshold of 12 μg/mL predicted better eradication. Among 173 mutations on 152 sites in the 23S rRNA gene, only the 2143A > G mutation could predict eradication outcomes (p < 0.000).
UNASSIGNED: Interpretation of elevated MIC values is crucial in susceptibility testing, rather than a binary \"susceptible\" or \"resistant\" classification. The 2143A > G mutation has limited specificity in predicting eradication outcomes, necessitating further investigation into additional mutation sites associated with clarithromycin resistance.
UNASSIGNED: We included adult H. pylori patients who hadn\'t previously undergone clarithromycin-based treatment, either as initial or rescue therapy. Exclusions were made for penicillin allergy, recent use of related medications, severe illnesses, or inability to cooperate. Patients underwent a 14-day clarithromycin bismuth quadruple therapy. Gastric mucosa specimens were obtained during endoscopy before eradication. MIC against amoxicillin and clarithromycin was determined using the E-test method. The receiver operating characteristic (ROC) curve helped to find the optimal clarithromycin resistance MIC breakpoint. Genetic sequences of H. pylori 23S rRNA were identified through Sanger Sequencing. (ChiCTR2200061476).
UNASSIGNED: Out of 196 patients recruited, 92 met the inclusion criteria for the per-protocol (PP) population. The overall intention-to-treat (ITT) eradication rate was 80.00 % (84/105), while the modified intention-to-treat (MITT) and PP eradication rates were 90.32 % (84/93) and 91.30 % (84/92) respectively. No amoxicillin resistance was observed, but clarithromycin resistance rates were 36.19 % (38/105), 35.48 % (33/93), and 34.78 % (33/92) in the ITT, MITT, and PP populations respectively. Compared with the traditional clarithromycin resistance breakpoint of 0.25 μg/mL, a MIC threshold of 12 μg/mL predicted better eradication. Among 173 mutations on 152 sites in the 23S rRNA gene, only the 2143A > G mutation could predict eradication outcomes (p < 0.000).
UNASSIGNED: Interpretation of elevated MIC values is crucial in susceptibility testing, rather than a binary \"susceptible\" or \"resistant\" classification. The 2143A > G mutation has limited specificity in predicting eradication outcomes, necessitating further investigation into additional mutation sites associated with clarithromycin resistance.
摘要：
■克拉霉素耐药性的上升破坏了幽门螺杆菌（H.幽门螺杆菌)治疗效果。我们旨在确定克拉霉素的最低抑制浓度（MIC）水平，并确定23S核糖体亚基（23SrRNA）中的特定突变位点，以预测克拉霉素铋四联疗法（阿莫西林1g，克拉霉素500毫克，雷贝拉唑10毫克，和胶体果胶铋200毫克)。
■我们包括以前没有接受克拉霉素治疗的成人幽门螺杆菌患者，作为初始或抢救治疗。排除了青霉素过敏，最近使用相关药物，严重的疾病,或者无法合作。患者接受了14天的克拉霉素铋四联疗法。根除前在内镜检查期间获得胃粘膜标本。使用E-test方法测定对阿莫西林和克拉霉素的MIC。受试者工作特征（ROC）曲线有助于找到最佳的克拉霉素抗性MIC断点。通过Sanger测序鉴定幽门螺杆菌23SrRNA的遗传序列。(ChiCTR2200061476)。
■在招募的196名患者中，92符合符合方案(PP)人群的纳入标准。整体意向治疗(ITT)根除率为80.00%(84/105),而改良意向治疗（MITT）和PP根除率分别为90.32％（84/93）和91.30％（84/92）。没有观察到阿莫西林耐药性，但克拉霉素耐药率为36.19%(38/105),35.48%（33/93），ITT中的34.78%(33/92)，米特,和PP种群分别。与传统克拉霉素耐药断点0.25μg/mL相比,12μg/mL的MIC阈值预测更好的根除。在23SrRNA基因152个位点的173个突变中，只有2143A>G突变可以预测根除结果(p<0.000)。
■对升高的MIC值的解释在敏感性测试中至关重要，而不是二进制的“易感”或“抗性”分类。2143A>G突变在预测根除结果方面具有有限的特异性，需要进一步研究与克拉霉素抗性相关的其他突变位点。
■我们包括以前没有接受克拉霉素治疗的成人幽门螺杆菌患者，作为初始或抢救治疗。排除了青霉素过敏，最近使用相关药物，严重的疾病,或者无法合作。患者接受了14天的克拉霉素铋四联疗法。根除前在内镜检查期间获得胃粘膜标本。使用E-test方法测定对阿莫西林和克拉霉素的MIC。受试者工作特征（ROC）曲线有助于找到最佳的克拉霉素抗性MIC断点。通过Sanger测序鉴定幽门螺杆菌23SrRNA的遗传序列。(ChiCTR2200061476)。
■在招募的196名患者中，92符合符合方案(PP)人群的纳入标准。整体意向治疗(ITT)根除率为80.00%(84/105),而改良意向治疗（MITT）和PP根除率分别为90.32％（84/93）和91.30％（84/92）。没有观察到阿莫西林耐药性，但克拉霉素耐药率为36.19%(38/105),35.48%（33/93），ITT中的34.78%(33/92)，米特,和PP种群分别。与传统克拉霉素耐药断点0.25μg/mL相比,12μg/mL的MIC阈值预测更好的根除。在23SrRNA基因152个位点的173个突变中，只有2143A>G突变可以预测根除结果(p<0.000)。
■对升高的MIC值的解释在敏感性测试中至关重要，而不是二进制的“易感”或“抗性”分类。2143A>G突变在预测根除结果方面具有有限的特异性，需要进一步研究与克拉霉素抗性相关的其他突变位点。
