Реалии и перспективы применения калий-конкурентных блокаторов кислотопродукции в гастроэнтерологии - Журнал Терапевтический архив №8 Вопросы лечения 2025

Реалии и перспективы применения калий-конкурентных блокаторов кислотопродукции в гастроэнтерологии

Маев И.В., Андреев Д.Н., Заборовский А.В., Фоменко А.К. Реалии и перспективы применения калий-конкурентных блокаторов кислотопродукции в гастроэнтерологии. Терапевтический архив. 2025;97(8):611–617. DOI: 10.26442/00403660.2025.08.203381

© ООО «КОНСИЛИУМ МЕДИКУМ», 2025 г.

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Maev IV, Andreev DN, Zaborovskiy AV, Fomenko AK. Current status and prospects of using potassium-competitive acid blockers in gastroenterology. Terapevticheskii Arkhiv (Ter. Arkh.). 2025;97(8):611–617. DOI: 10.26442/00403660.2025.08.203381

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Аннотация

На протяжении последних десятилетий кислотопродукцию в желудке регулировали преимущественно с помощью ингибиторов протонной помпы (ИПП). Однако, несмотря на широкую распространенность и внушительную доказательную базу эффективности, ИПП имеют фармакокинетические и фармакодинамические ограничения, такие как медленное наступление действия, вариабельность ответа (зависимость от полиморфизмов CYP2C19) и потребность в активации кислой средой. Актуальность таких ограничений обусловила необходимость внедрения новых молекулярных подходов к ингибированию кислотопродукции, что привело к разработке препаратов принципиально иного механизма действия – калий-конкурентных блокаторов кислотопродукции (К-КБК), которые впервые интегрированы в клиническую практику в 2015 г. Механизм действия К-КБК основан на обратимом ионном взаимодействии с водородно-калиевой аденозинтрифосфатазой (Н⁺, К⁺-АТФазой) париетальных клеток желудка. Прямое ингибирование активного фермента позволяет достичь более быстрого и стойкого контроля над желудочной секрецией, включая ночную и постпрандиальную кислотопродукцию, что делает этот класс препаратов особенно актуальным в лечении гастроэзофагеальной рефлюксной болезни, язвенной болезни и в рамках эрадикации Helicobacter pylori. Последние метаанализы демонстрируют клинические преимущества К-КБК над ИПП при перечисленных патологических состояниях.

Ключевые слова: калий-конкурентный блокатор кислотопродукции, гастроэзофагеальная рефлюксная болезнь, эрозивный эзофагит, язвенная болезнь, Helicobacter pylori

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Over the past decades, acid production in the stomach has been regulated mainly by proton pump inhibitors (PPIs). However, despite their widespread use and solid evidence base for efficacy, PPIs have pharmacokinetic and pharmacodynamic limitations, such as a slow onset of action, response variability (dependent on CYP2C19 polymorphisms), and the need for activation in an acidic environment. These restrictions underscore the need for innovative molecular approaches to inhibiting acid production, which led to the development of a fundamentally different mechanism of action – potassium-competitive acid blockers (P-CABs), first introduced into clinical practice in 2015. The mechanism of action of P-CABs is based on a reversible ionic interaction with hydrogen potassium adenosine triphosphatase (H⁺/K⁺ ATPase) in parietal cells of the stomach. Direct inhibition of the active enzyme enables more rapid and sustained control of gastric secretion, including nocturnal and postprandial acid production, making this class of drugs particularly relevant in the treatment of gastroesophageal reflux disease, peptic ulcers, and in the eradication of Helicobacter pylori. Recent meta-analyses demonstrate the clinical benefits of P-CABs over PPIs for these indications.

Keywords: potassium-competitive acid blocker, gastroesophageal reflux disease, erosive esophagitis, peptic ulcer, Helicobacter pylori

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4. Maev IV, Andreev DN, Kucheryavyy YuA, Shaburov RI. Current Advances in the Treatment of Gastroesophageal Reflux Disease: A Focus on Esophageal Protection. Terapevticheskii Arkhiv (Ter. Arkh.). 2019;91(8):4-11 (in Russian). DOI:10.26442/00403660.2019.08.000387
5. Ivashkin VT, Lopina OD. Kletochnye mekhanizmy sekretsii solianoi kisloty i ingibitory protonnogo nasosa. In: Profilaktika i lechenie khronicheskikh zabolevanii verkhnikh otdelov zheludochno-kishechnogo trakta. Pod red. akad. RAMN VT Ivashkina. 2 ed. Moscow: MEDpress-inform, 2013 (in Russian).
6. Feldman M. American Journal of Gastroenterology lecture: Gastric acid secretion: Still relevant? Am J Gastroenterol. 2013;108:347-52. DOI:10.1038/ajg.2012.478
7. Spicer Z, Miller ML, Andringa A, et al. Stomachs of mice lacking the gastric H,K-ATPase α-subunit have achlorhydria, abnormal parietal cells, and ciliated metaplasia. J Biol Chem. 2000;275:21555-65. DOI:10.1074/jbc.M001558200
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10. Chu S, Schubert ML. Gastric secretion. Curr Opin Gastroenterol. 2012;28(6):587-93. DOI:10.1097/MOG.0b013e328358e5cc
11. He W, Liu W, Chew CS, et al. Acid secretion-associated translocation of KCNJ15 in gastric parietal cells. Am J Physiol Gastrointest Liver Physiol. 2011;301(4):G591-600. DOI:10.1152/ajpgi.00460.2010
12. Song P, Groos S, Riederer B, et al. Kir4.1 channel expression is essential for parietal cell control of acid secretion. J Biol Chem. 2011;286(16):14120-8. DOI:10.1074/jbc.M110.151191
13. Kopic S, Murek M, Geibel JP. Revisiting the parietal cell. Am J Physiol Cell Physiol. 2010;298:C1-10.
14. Kosiek O, Busque SM, Foller M, et al. SLC26A7 Can function as a chlorideloading mechanism in parietal cells. Pflugers Arch Eur J Physiol. 2007;454:989-98. Available at: https://link.springer.com/article/10.1007/s00424-007-0254-y. Accessed: 01.07.2025.
15. McDaniel N, Pace AJ, Spiegel S, et al. Role of Na-K-2Cl cotransporter-1 in gastric secretion of nonacidic fluid and pepsinogen. Am J Physiol Gastrointest Liver Physiol. 2005;289(3):G550-60. DOI:10.1152/ajpgi.00095.2005
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18. Yao X, Forte JG. Cell biology of acid secretion by the parietal cell. Annu Rev Physiol. 2003;65:103-31. DOI:10.1146/annurev.physiol.65.072302.114200
19. Schubert ML, Peura DA. Control of gastric acid secretion in health and disease. Gastroenterology. 2008;134(7):1842-60. DOI:10.1053/j.gastro.2008.05.021
20. Zhou R, Cao X, Watson C, et al. Characterization of protein kinase A-mediated phosphorylation of ezrin in gastric parietal cell activation. J Biol Chem. 2003;278(37):35651-9. DOI:10.1074/jbc.M303416200
21. Guyton and Hall: Textbook of Medical Physiology. 13 ed. Elsevier, 2016.
22. Hunt RH, Scarpignato C. Potent Acid Suppression with PPIs and P-CABs: What's New? Curr Treat Options Gastroenterol. 2018;16(4):570-90. DOI:10.1007/s11938-018-0206-y
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Авторы

И.В. Маев, Д.Н. Андреев*, А.В. Заборовский, А.К. Фоменко

ФГБОУ ВО «Российский университет медицины» Минздрава России, Москва, Россия
*dna-mit8@mail.ru

________________________________________________

Igor V. Maev, Dmitry N. Andreev*, Andrey V. Zaborovskiy, Aleksei K. Fomenko

Russian University of Medicine, Moscow, Russia
*dna-mit8@mail.ru

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