[喀山地区幽门螺旋杆菌对抗生素产生耐药性的突变率]。

Pub Date : 2024-09-14 DOI:10.26442/00403660.2024.08.202813
E A Kupriyanova, S R Abdulkhakov, R К Ismagilova, D D Safina, A R Akhtereeva, R R Galimova, A G Safin, T V Grigoryeva, R А Abdulkhakov
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引用次数: 0

摘要

背景:目的:研究喀山上消化道疾病患者中导致克拉霉素和左氧氟沙星耐药性的幽门螺杆菌点突变的发生率:研究对象包括2019-2021年在喀山联邦大学附属医院(俄罗斯喀山)接受上消化道内窥镜检查的203名消化不良症状患者。使用PureLink Genomic DNA Mini Kits(美国赛默飞世尔科技公司)从胃窦粘膜活检组织中分离DNA。聚合酶链反应使用 23S 基因 V 区和编码 gyrA 基因区的 A 亚基 DNA 回旋酶特异性引物进行。获得的 DNA 片段在 3730 DNA 分析仪上进行测序。对序列进行了搜索,以找出导致幽门螺杆菌对克拉霉素(A2143G、A2142G 和 A2142C193 突变)和左氧氟沙星(gyrA 基因突变)产生耐药性的点突变:结果:通过聚合酶链反应,47.78%的活检标本检测出幽门螺杆菌。具有克拉霉素耐药性突变的幽门螺杆菌菌株比例为 17.53%。在 12.37% 的样本中发现了 gyrA 基因的氨基酸替换。在两个幽门螺杆菌菌株(2.06%)中,发现了对克拉霉素和左氧氟沙星的双重耐药性:结论:在喀山接受检查的患者中,幽门螺杆菌对克拉霉素和左氧氟沙星产生耐药性的突变发生率很高。
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[The prevalence of mutations underlying development of Helicobacter pylori resistance to antibiotics in Kazan].

Background: One of the reasons for the decrease of Helicobacter pylori eradication effectiveness is its resistance to antibiotics.

Aim: To examine the prevalence of H. pylori point mutations responsible for clarithromycin and levofloxacin resistance among the patients with upper gastrointestinal (GI) tract disorders in Kazan.

Materials and methods: The study included 203 patients with symptoms of dyspepsia who underwent upper GI endoscopy at the University Hospital of Kazan Federal University (Kazan, Russia) in 2019-2021. DNA isolation from gastric antrum mucosal biopsies was performed using PureLink Genomic DNA Mini Kits (Thermo Fisher Scientific, USA). Polymerase chain reaction was performed using primers specific for the V-region of the 23S gene and the A subunit DNA gyrase encoding gyrA gene region. The sequencing of obtained DNA fragments was performed on 3730 DNA Analyzer. The sequences were searched for point mutations responsible for H. pylori resistance to clarithromycin (A2143G, A2142G and A2142C193 mutations) and levofloxacin (mutations of the gyrA gene).

Results: H. pylori was detected in 47.78% of biopsy specimens using polymerase chain reaction. The proportion of H. pylori strains with mutations leading to clarithromycin resistance was 17.53%. Amino acid substitutions in the gyrA gene were found in 12.37% of samples. In case of two H. pylori strains (2.06%), dual resistance to clarithromycin and levofloxacin was found.

Conclusion: So high incidence of mutations underlying the development of H. pylori resistance to clarithromycin and levofloxacin was observed among examined patients in Kazan.

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