#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Proton-pump inhibitors – up to date


Authors: J. Martínek 1;  M. Lukáš 2,3
Authors place of work: Interní klinika 1. LF UK a ÚVN Praha 1;  Klinické a výzkumné centrum pro střevní záněty, ISCARE Lighthouse a. s. a 1. LF UK v Praze 2;  Ústav klinické biochemie a laboratorní diagnostiky, 1. LF UK v Praze 3
Published in the journal: Gastroent Hepatol 2011; 65(6): 331-342
Category: Klinická a experimentální gastroenterologie: přehledová práce

Summary

To date, five proton pump inhibitors (PPIs) are available: The first generation of PPIs includes omeprazole, lansoprazole and pantoprazole; the second generation is represented by rabeprazole and esomeprazole which have several advantages over the older agents, particularly in terms of rapid action and profound and consistent acid inhibition. The older PPIs, mainly omeprazole and lansoprazole are predominantly metabolised by CYP2C19, whereas pantoprazole and esomeprazole are metabolized also by other metabolic pathways and only to a lesser extent by CYP2C19. The PPIs have been developed and licensed in different dosages; omeprazole 20 mg, esomeprazole 40 mg, lansoprazole 30 mg, pantoprazole 40 mg and rabeprazole 20 mg. First generation of PPIs have comparable antisecretion efficacy which is influenced by enzymatic activity of CYP2C19. Currently, PPis are used in several indication of acid-related diseases. They have significant role in therapy of gastric and duodenal ulcers; gastro-oesophageal reflux disease; therapy and prophylaxis of NSAIDs gastropathy; co-therapy in eradication of Helicobacter pylori infection; therapy of functional dyspepsia and treatment and prophylaxis of recurrent non-variceal upper GI bleeding. The safety profile of PPIs seems to be favourable, both in short-term and long-term use.

Key words:
proton pump inhibitors – omeprazole – lansoprazole – pantoprazole – esomeprazole – rabeprazole – Helicobacter pylori – gastroesophageal reflux disease


Zdroje

1. Sachs G, Prinz C, Persey SJ. Acid related disorders. Sushu Publishing Inc. 1995.

2. Bonnevie O, Nielsen AM, Matzen P et al. Gastric acid secretion and duodenal ulcer healing during treatment with omeprazole. Scand J Gastroenterol 1984; 19(7): 882–884.

3. Kromer W, Kruger U, Huber R et al. Differences in pH-dependent activation rates of substituted benzimidazoles and bio­logical in vitro correlates. Pharmacology 1998; 56(2): 57–70.

4. Pantoflickova D, Dorta G, Jornod P et al. Acid inhibition on the first day of dosing: comparison of four proton pump inhibitors. Aliment Pharmacol Ther 2003; 17(12): 1507–1514.

5. Miner P, Katz P, Sostek M. Gastric acid control with esomeprazole, lansoprazole, omeprazole, pantoprazole, and rabeprazole: a five-way crossover study. Am J Gastro­enterol 2003; 98(12): 2616–2620.

6. Martinek J, Blum AL, Stolte M et al. Effects of Pumaprazole (BY841), a novel reversible proton pump antagonist, and of Omeprazole on intragastric acidity before and after cure of Helicobacter pylori infection. Aliment Pharmacol Ther 1999; 13(1): 27–34.

7. Vigneri S, Termini R, Leandro G et al. A comparison of five maintenance therapies for reflux esophagitis.N Engl J Med 1995; 333(17): 1106–1110.

8. Pipkin GA, Mills JG. Onset of action of antisecretory drugs: beneficial effects of a rapid increase in intragastric pH in acid reflux disease. Scand J Gastroenterol Suppl 1999; 230: 3–8.

9. Kalaitzakis E, Björnsson E. A review of esomeprazole in the treatment of gastro­esophageal reflux disease. Ther Clin Risk management 2007; 3(4): 653–663.

10. Edwards SJ, Lind T, Lundell L. Systematic review of proton pump inhibitors for the acute treatment of reflux esophagitis. Aliment Pharmacol Ther 2001; 15(11): 1729–1736.

11. Slaughter JC, Goutte M, Kymer JA et al. Caution about overinterpretation of symptom indexes in reflux monitoring for refractory gastroesophageal reflux disease. Clin Gastroenterol Hepatol 2011; 9(10): 868–874.

12. Wolfe M, Sachs G. Acid suppression: Optimizing therapy for gastroduodenal ulcer healing, gastroesophageal reflux disease, and stress related erosive syndrome. Gastro­enterology 2000; 118 (2 Suppl 1): S9–S31.

13. Chuah SK, Tsay FW, Hsu PI et al. A new look at anti-Helicobacter pylori therapy. World J Gastroenterol 2011; 17(35): 3971–3975.

14. Hsu PI, Lai KH, Lin CK et al. A prospective randomized trial of esomeprazole versus pantoprazole based triple therapy for Helicobacter pylori eradication. Am J Gastro­enterol 2005; 100(11): 2387–2392.

15. Wallace JL, Syer S, Denou E et al. Proton pump inhibitors exacerbate NSAID-induced small intestinal injury by inducing dysbiosis. Gastroenterology 2011; 141(4): 1314–1322.

16. Blum AL, Talley NJ, O´Morrain C et al. Lack of effect of treating Helicobacter pylori infection in patients with nonulcer dyspepsia. Omeprazole plus Clarithromycin and Amoxicillin Effect One Year after Treatment (OCAY) Study Group. N Engl J Med 1998; 339(26): 1875–1881.

17. Bultas J. Význam kombinace klopidogrelu s inhibitory protonové pumpy. Čes a Slov Gastroent a Hepatol 2010; 64(4): 25–31.

18. Kwok CS, Loke YK. Meta-analysis: the effects of proton pump inhibitors on cardio­vascular events and mortality in patients receiving clopidogrel. Aliment Pharmacol Ther 2010; 31(8): 810–823.

19. Hulot JS, Collet JP, Silvain J et al. Cardiovascular risk in clopidogrel-treated patients according to cytochrome P450 2C19*2 lossof-function allele or proton pump inhibitor coadministration: a systematic meta-analysis. J Am Coll Cardiol 2010; 56(2): 134–143.

20. Hsu PI, Lai KH, Liu CP et al. Esomeprazole with clopidogrel reduces peptic ulcer recurrence, compared with clopidogrel alone, in patients with atherosclerosis. Gastroenterology 2011; 140(3): 791–798.

21. Bavishi C, DuPont HL. Systemic review: the use of proton pump inhibitors and increased susceptibility to enteric infection. Aliment Pharmacol Ther 2011; 34(11–12): 1269–1981.

22. Solcia E, Fiocca R, Villani L et al. Hyper­plastic, dysplastic, and neoplastic ECL-like proliferation of the gastric mucosa. Am J Surg Pathol 1995; 19 (Suppl 1): S1–S7.

23. Joelson S, Joelson IB, Lundborg P et al. Safety experience from long term treatment with omeprazole. Digestion 1992; 51  (Suppl 1): 93–101.

24. Penman ID, El-Omar E, Ardill JES et al. Plasma gastrin concentration are normal in patients with colorectal neoplasia and unaltered following tumor resection. Gastro­enterology 1994; 106(5): 1263–1270.

25. Kuipers EJ, Lundell L, Klinkenberg-Knol E et al. Atrophic gastritis and H. pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Engl J Med 1996; 334(16): 1018–1022.

26. Lundell L, Miettinen P, Myrvold HE et al. Lack of effect of acid suppression therapy on gastric atrophy. Gastroenterology 1999; 117(2): 319–326.

27. Genta RM, Rindi G, Fiocca R et al. Effect of 6-12 months of esomeprazole treatment on gastric mucosa. Am J Gastro­enterol 2003; 98(6): 1257–1265.

28. Corley DA, Kubo Ai, Zhao W et al. Proton Pump Inhibitors and Histamine-2 Receptor Antagonists are Associated with Hip Fractures among At-Risk Patients. Gastro­enterology 2010; 139(1): 93–101.

Štítky
Detská gastroenterológia Gastroenterológia a hepatológia Chirurgia všeobecná

Článok vyšiel v časopise

Gastroenterologie a hepatologie

Číslo 6

2011 Číslo 6
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Kurzy

Zvýšte si kvalifikáciu online z pohodlia domova

Aktuální možnosti diagnostiky a léčby litiáz
nový kurz
Autori: MUDr. Tomáš Ürge, PhD.

Všetky kurzy
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#