State of acid-producing function of the stomach in patients with helicobacter pylori-associated gastroduodenal ulcer disease and no response to eradication therapy
https://doi.org/10.21518/2079-701X-2018-6-174-179
Abstract
This paper deals with the second phase of the prospective, randomized comparative study of the efficacy and safety of the hybrid eradication therapy (ET) regimen in patients with H. pylori-associated gastroduodenal ulcer. Objective: Evaluation of the acid-forming function of the stomach with a pharmacological proton pump inhibitor (PPI) test in patients with H. pylori-associated gastroduodenal ulcer disease and no response to eradication therapy. Materials and methods. 19 patients were enrolled in this study after the failed ET using any of the following three regimens: standard triple regimen, four-component therapy with bismuth agents, hybrid regimen; in all regimens, omeprazole (20 mg b.i.d.) was used as an IPP. All patients underwent a 48-hour intragastric pH-meter (Gastroscan-GEM device, Istok-System, Russia) to assess the initial state of the acid-forming function of the stomach during the first day and the subsequent pharmacological PPI test (omeprazole 20 mg b.i.d.) on the second day. The minimum, maximum and average pH values in the cardia and body of the stomach, as well as the time with pH> 4 in the body of the stomach during the entire study period (48 hours) were analysed. Results. Median time average with pH> 4 in the body of the stomach for the first day of the study (before PPI administration) was 1.0 hour (IQR from 0.0 to 1.5), and against a pharmacological test – 15.5 hours (IQR from 11.1 to 16.5). At the same time, an adequate alkalization of the gastric environment under pressure of IPP therapy was identified in 12 patients, when the pH level> 4 in the body of the stomach was maintained for 16–17 hours. In 7 patients, pH> 4 was maintained for less than 16 hours, which is a symptom of insufficient antisecretory effect. During this study, no PPI resistance was revealed. The conclusion. Evaluation of the state of the acid-forming function of the stomach with pharmacological tests upon conduct of the 48-hour pH-metry makes it possible to evaluate the antisecretory effect of the used PPI and, thus, to predict the probability of effective eradication.
About the Authors
G. L. YurenevRussian Federation
MD, Prof.
E. V. Partsvania-Vinogradova
Russian Federation
D. N. Andreev
Russian Federation
PhD in medicine
D. T. Dicheva
Russian Federation
PhD in medicine
I. V. Maev
Russian Federation
Acad. of RAS, MD, Prof.
References
1. Maev IV, Samsonov AA, Andreev DN. Stomach diseases. Moscow: GEOTAR-Media, 2015.
2. Chan FK, Lau JY. Peptic Ulcer Disease. In.: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. Edited by Mark Feldman, Law rence S Friedman, Laurence J Brandt. 10th ed. 2015.
3. Lanas A, Chan FK. Peptic ulcer disease. Lancet, 2017, 390(10094): 613-624.
4. Maev IV, Samsonov AA, Andreev DN. Helicobacter pylori infection. Moscow: GEOTAR-Media, 2016.
5. Malfertheiner P, Link A, Selgrad M. Helicobacter pylori: perspectives and time trends. Nat Rev Gastroenterol Hepatol, 2014, 11(10): 628-38.
6. Guide on Internal Medicine. Edited by Arutyunova GP, Martynova AI, Spassky AA. M., 2015.
7. Andreev D. Helicobacter pylori Eradication Therapy: Current Regimens. Adv Res Gastroentero Hepatol, 2017, 7(2): 555710.
8. Malfertheiner P, Megraud F, O’Morain CA et al. Management of Helicobacter pylori infection-the Maastricht V/Florence Consensus Report. Gut, 2017, 66(1): 6-30.
9. Fallone CA, Chiba N, van Zanten SV et al. The Toronto Consensus for the Treatment of Helicobacter pylori Infection in Adults. Gastroenterology, 2016, 151(1): 51-69.e14.
10. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol, 2017, 112(2): 212-239.
11. Labenz J. Current role of acid suppressants in Helicobacter pylori eradication therapy. Best Pract Res Clin Gastroenterol, 2001, 15: 413–31.
12. De Francesco V, Ierardi E, Hassan C, Zullo A. Helicobacter pylori therapy: Present and future. World J Gastrointest Pharmacol Ther, 2012, 3(4): 68-73.
13. Erah PO, Goddard AF, Barrett DA, Shaw PN, Spiller RC. The stability of amoxycillin, clarithromycin and metronidazole in gastric juice: relevance to the treatment of Helicobacter pylori infection. J Antimicrob Chemother, 1997, 39(1): 5-12.
14. Maev IV, Andreev DN, Kucheryavyi YuA, Dicheva DT. Host factors influencing the eradication rate of Helicobacter pylori. World Applied Sci J, 2014, 30: 134-140.
15. Maev IV, Andreev DN. Molecular-genetic predictors of anti-Helicobacter therapy resistance. Terapevticheskiy Arkhiv, 2017, 89 (8): 5-12.
16. Li-Wan-Po A, Girard T, Farndon P, Cooley C, Lithgow J. Pharmacogenetics of CYP2C19: functional and clinical implications of a new variant CYP2C19*17. Br J Clin Pharmacol, 2010, 69(3): 222-30.
17. Padol S, Yuan Y, Thabane M, Padol IT, Hunt RH. The effect of CYP2C19 polymorphisms on H. pylori eradication rate in dual and triple first-line PPI therapies: a meta-analysis. Am J Gastroenterol, 2006, 101(7): 1467-75.
18. Tang HL, Li Y, Hu YF, Xie HG, Zhai SD. Effects of CYP2C19 loss-of-function variants on the eradication of H. pylori infection in patients treated with proton pump inhibitor-based triple therapy regimens: a meta-analysis of randomized clinical trials. PLoS One, 2013, 8:e62162.
19. Vallve M, Vergara M, Gisbert JP, et al. Single vs. double dose of a proton pump inhibitor in triple therapy for Helicobacter pylori eradication: a meta-analysis. Aliment Pharmacol Ther, 2002, 16: 1149–56.
20. Villoria A, Garcia P, Calvet X, et al. Meta-analysis: high-dose proton pump inhibitors vs. standard dose in triple therapy for Helicobacter pylori eradication. Aliment Pharmacol Ther, 2008, 28: 868–77.
21. Andreev DN, Dicheva DT, Maev IV. Possibilities for optimization of Helicobacter pylori infection eradication therapy in modern clinical practice. Terapevticheskiy Arkhiv, 2017, 2: 76-83.
22. McNicholl AG, Linares PM, Nyssen OP, Calvet X, Gisbert JP. Meta-analysis: esomeprazole or rabeprazole vs. first-generation pump inhibitors in the treatment of Helicobacter pylori infection. Aliment Pharmacol Ther, 2012, 36(5): 414–425.
23. Desta ZX, Shin JG, Flockhart DA. Clinical significance of the cytochrome P450 2C19 genetic polymorphism. Clin. Pharmacokinet., 2002, 41(12): 913–958.
24. Asaki S, Kimpara T, Iijima K, Ohara S. Continuous intragastric pH monitoring. Nihon Rinsho, 1997, 55(2): 95-8.
25. Katz PO. Ambulatory intragastric pH monitoring: clinical laboratory to clinical practice. Rev Gastroenterol Disord, 2003, 3(4): S3-9.
26. Maev IV, Lebedeva EG, Dicheva DT, et al. The rationale for the daily monitoring of intragastric acidity with pharmacological tests. In collected works: Topical issues of gastroenterology. M., 2012: 94-100.
27. Uotani T, Miftahussurur M, Yamaoka Y. Effect of bacterial and host factors on Helicobacter pylori eradication therapy. Expert Opin Ther Targets, 2015, 19(12): 1637-50.
28. Sychev DA, Denisenko NP, Sizova ZM, Grachev AV, Velikolug KA. The frequency of CYP2C19 genetic polymorphisms in Russian patients with peptic ulcers treated with proton pump inhibitors. Pharmgenomics Pers Med, 2015, 8: 111-4.
Review
For citations:
Yurenev GL, Partsvania-Vinogradova EV, Andreev DN, Dicheva DT, Maev IV. State of acid-producing function of the stomach in patients with helicobacter pylori-associated gastroduodenal ulcer disease and no response to eradication therapy. Meditsinskiy sovet = Medical Council. 2018;(6):174-179. (In Russ.) https://doi.org/10.21518/2079-701X-2018-6-174-179