Potential factors of Helicobacter pylori resistance to clarithromycin.

Q2 Pharmacology, Toxicology and Pharmaceutics
Svetlana Serebrova, Daria Kurguzova, Lyudmila Krasnykh, Galina Vasilenko, Vladimir Drozdov, Natalia Lazareva, Eugenia Shikh, Marina Zhuravleva, Svetlana Rykova, Natalia Eremenko, Elena Kareva, Karin Mirzaev, Dmitriy Sychev, Alexey Prokofiev
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引用次数: 1

Abstract

Objectives: A comparative dissolution kinetics test (CDKT) and bioequivalence studies of generic proton pump inhibitors (PPIs) do not model pharmacological acid suppression (PAS) and pathological duodenogastric reflux (PDGR). This study aimed to model them in CDKT to assess drugs stability and potential pantoprazole-clarithromycin interactions.

Methods: In CDKT, PDGR (dissolution medium pH 7.00 ± 0.05, preexposure at pH 1.20 ± 0.05) and PAS (pH 4.00 ± 0.05) were modelled for original pantoprazole (OP) and its generics (GP1-4). In CDKT with high-performance liquid chromatography, dissolution gastric medium in adequate (pH 4.00 ± 0.05) and inadequate (pH 1.20 ± 0.05) PAS were modelled for original clarithromycin (OC) and its generics (GC1-4).

Results: After exposure in pH 7.00 ± 0.05, pantoprazole was released from GP1 within 10 min in the amount of 68.8%. In рН 4.00 ± 0.05, 83.0% and 81.5% of pantoprazole were released from GP1 and GP4. When OP, GP2 and GP3 were placed in pH 7.00 ± 0.05, pantoprazole was released in amount: 99.4%, 88.0% and 98.2%. Clarithromycin releasing from OC, GC1, GC2, GC3, GC4 in pH 4.00 ± 0.05 was 93.5%, 91.6%, 92.9%, 79.4% and 83.0%. In pH 1.20 ± 0.05: 9.7%, 6.7%, 8.5%, 33.3%, 28.8%.

Conclusions: Destruction of enteric coats of some local pantoprazole generics in CDKT-models might be a potential factor for inadequate therapy.

幽门螺杆菌对克拉霉素耐药的潜在因素。
目的:通用质子泵抑制剂(PPIs)的比较溶解动力学试验(CDKT)和生物等效性研究没有模拟药理学抑酸(PAS)和病理性十二指肠胃反流(PDGR)。这项研究的目的是在CDKT中对它们进行建模,以评估药物稳定性和潜在的泮托拉唑-克拉霉素相互作用。方法:在CDKT中,对原泮托拉唑(OP)及其仿制药(GP1-4)进行PDGR(溶解介质pH 7.00±0.05,预暴露pH 1.20±0.05)和PAS (pH 4.00±0.05)模型建立。在CDKT高效液相色谱法中,对原克拉霉素(OC)及其仿制药(GC1-4)在适当(pH 4.00±0.05)和不适当(pH 1.20±0.05)PAS条件下的胃培养基溶出度进行了模拟。结果:pH为7.00±0.05后,泮托拉唑在10 min内从GP1释放,释放量为68.8%。在рН 4.00±0.05时,GP1和GP4分别释放了83.0%和81.5%的泮托拉唑。当OP、GP2和GP3置于pH为7.00±0.05时,泮托拉唑的释放量分别为99.4%、88.0%和98.2%。pH为4.00±0.05时OC、GC1、GC2、GC3、GC4的克拉霉素释放量分别为93.5%、91.6%、92.9%、79.4%和83.0%。在pH值1.20±0.05:9.7%,6.7%,8.5%,33.3%,28.8%。结论:cdkt模型中局部泮托拉唑类药物肠粘膜破坏可能是治疗不充分的潜在因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Drug metabolism and personalized therapy
Drug metabolism and personalized therapy Pharmacology, Toxicology and Pharmaceutics-Pharmacology, Toxicology and Pharmaceutics (all)
CiteScore
2.30
自引率
0.00%
发文量
35
期刊介绍: Drug Metabolism and Personalized Therapy (DMPT) is a peer-reviewed journal, and is abstracted/indexed in relevant major Abstracting Services. It provides up-to-date research articles, reviews and opinion papers in the wide field of drug metabolism research, covering established, new and potential drugs, environmentally toxic chemicals, the mechanisms by which drugs may interact with each other and with biological systems, and the pharmacological and toxicological consequences of these interactions and drug metabolism and excretion. Topics: drug metabolizing enzymes, pharmacogenetics and pharmacogenomics, biochemical pharmacology, molecular pathology, clinical pharmacology, pharmacokinetics and drug-drug interactions, immunopharmacology, neuropsychopharmacology.
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