The Choice of Proton Pump Inhibitor: Does it matter?
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C Basic & Clinical Pharmacology & Toxicology 2004, 94, 106–111. Printed in Denmark . All rights reserved Copyright C ISSN 1742-7835 MiniReview The Choice of Proton Pump Inhibitor: Does it matter? Per M. Hellström1 and Sigurd Vitols2 Units of Gastroenterology and Hepatology, and 2Clinical Pharmacology, Department of Medicine, 1 Karolinska Hospital, Stockholm, Sweden (Received September 22, 2003; Accepted January 13, 2004) Abstract: Proton pump inhibitors are used at different dosages for the treatment of acid-related gastrointestinal disorders, such as gastro-oesophageal reflux and peptic ulcer disease. Comparisons of four different proton pump inhibitors: lansop- razole, omeprazole, pantoprazole, and rabeprazole show that they all have similar potency and efficacy. Rabeprazole, however, displays a slightly more rapid onset of acid inhibition than the others; the clinical advantage of this seems limited. The S-isomer of omeprazole, esomeprazole, exhibits a somewhat higher potency than the other proton pump inhibitors. Reports supporting a clinical advantage of this property are not convincing. To conclude, all inhibitors seem comparable as regards inhibition of gastric acid secretion. In 1988 the first proton pump inhibitor, omeprazole was scanned reviewed scientific articles from the PubMed li- launched. Since then the use of these inhibitors has in- brary of officially recognized medical journals. creased steadily and we can now choose between several inhibitors of different molecular structures. The patent pro- The drug target: The enzyme Hπ,Kπ-ATPase tection of omeprazole expired in 2003 and we are already seeing a number of generics on the market. The indications Proton pump inhibitors are substituted benzimidazoles with for proton pump inhibitors have been broadened through alkaline properties, which act as precursors of thiophilic the discovery of Helicobacter pylori as the infectious agent sulphenamides. The transformation is pH-dependent and causing peptic ulcer disease. Today eradication of the bac- occurs within the parietal cell. The sulphenamide is cova- terium is the mainstay of treatment. Due to the high preva- lently bound to hydrogen sulphide residues of the Hπ,Kπ- lence of gastro-oesophageal reflux disease in the population ATPase molecule on the luminal side of the canaliculi in the this is now the most important indication for treatment parietal cell (fig. 1). This binding takes place at a high velo- with a proton pump inhibitor. city at pH 1 (Sachs et al. 1995). The inhibitory effect of The first proton pump inhibitor was omeprazole and the omeprazole on the Hπ,Kπ-ATPase is similar for the S- and latest proton pump inhibitor is esomeprazole (S-omeprazo- R-isomers. Both isomers are activated in a pH-dependent le). Omeprazole is a racemate of two optical forms, the R- fashion and transformed to a cyclic sulphenamide, which isomer and the S-isomer. The isomers are metabolized in effect is independent of its optical form (Erlandsson et al. the liver along two separate metabolic pathways; the S-iso- 1990). The higher the pKa of the precursor, the more rapid mer having a less efficient metabolism resulting in higher is the conversion from inactive to active molecule: the sul- plasma levels in vivo. Nonetheless (and illogically) the rec- phenamide. ommended dose of the S-isomer is 40 mg daily; the recom- The mechanism of action is similar for all proton pump mended daily dose of omeprazole is 20 mg (Thitiphuree & inhibitors. They bind to a common distinct site on the a- Talley 2000). The question to be raised is: Do the various subunit of the proton pump, namely cysteine 813 on the proton pump inhibitors differ in potency and pharmaco- luminal loop between transmembrane domains 5 and 6. logical characteristics, and if so, are these differences of Pantoprazole also binds to the adjacent cysteine 822, and clinical importance? And, finally, what dosage would be ap- omeprazole to cysteine 892. Lansoprazole and rabeprazole propriate for treatment of acid-related disorders in the clin- bind to additional sites at cysteine 892 and cysteine 321 ical setting? In order to answer these questions we have (Besancon et al. 1997). All proton pump inhibitors form active sulphenamides at a similar rate at pH 1. Hence, their maximal antisecretory capacity and potency in vivo are similar provided that the Author for correspondence: Per M. Hellström, Unit of Gastro- enterology and Hepatology, Department of Medicine, Karolinska pharmacokinetic properties of the molecules are compar- Hospital, SE-171 76 Stockholm, Sweden (fax π46 8 51772058, able. The antisecretory capacity of omeprazole is similar to e-mail Per.Hellstrom/medks.ki.se). that of pantoprazole in animal experiments (Kromer et al.
MiniReview CHOICE OF PROTON PUMP INHIBITOR FOR ACID INHIBITION 107 Antisecretory potency in man The intra- and inter-experiment variability in acid inhibi- tory effect of the various proton pump inhibitors is con- siderable. Thus, results from different studies have to be examined and evaluated with caution. It seems that even a double dosage of proton pump inhibitors will not always lead to statistically significant differences in acid inhibition. Fig. 1. Schematic drawing of the molecular structure of the enzyme Such data support the view that the proton pump inhibitors Hπ,Kπ-ATPase. The enzyme consists of 1034 amino acid residues localized to two subunits. Upon secretion of Hπ-ions one phos- are utilized within the upper shallow range of the dose-re- phate group is transferred from ATP in the cytoplasm to aspartic sponse curve, where an increased dosage only leads to a acid in the active centre of the enzyme, which leads to the formation marginally increased effect. of a phosphorous intermediate. This intermediate releases Hπ-ions Studies in vitro exhibit a similar acid inhibitory effect of at the luminal side of the enzyme. The catalytic a-subunit, driving the exchange between Hπ- and Kπ-ions, is a large protein with 10 omeprazole, lansoprazole, pantoprazole and rabeprazole domains crossing the cell membrane. The proton pump inhibitors (Bastaki et al. 2000). Dose-response studies comparing (PPIs) bind to the part of the enzyme that is located on the outer, omeprazole, lansoprazole and pantoprazole in man have luminal membrane of the canaliculi, and inhibits phosphorylation shown a similar pH-raising effect of the drugs on a milli- and exchange of Hπ- and Kπ-ions. The b-subunit crosses the cell gram basis (Ashida et al. 1995; Langtry & Wilde 1997). This membrane only at one point. The extracellular domain of the b- subunit is heavily glucosylated adjacent to the a-subunit. The func- has been confirmed by investigations in animals (Kromer et tion of the b-subunit is yet to be defined. al. 1990). Lansoprazole and omeprazole also produce a similar increment of intragastric pH (Yasuda et al. 1994), albeit with a somewhat more rapid onset of action for lan- 1990). Although pantoprazole (pKa 3.96) and rabeprazole soprazole (Brummer et al. 1997). Comparisons between 40 (pKa 4.9) differ greatly in terms of pKa, and activation rate, mg omeprazole daily and 40 mg pantoprazole daily show they induce the same degree of gastric acid inhibition with similar increments of intragastric pH during 24 hr (Hannan similar ID50-values, which also holds true for lansoprazole et al. 1992). Omeprazole and pantoprazole, both at doses (pKa 4.01), as well as omeprazole and esomeprazole (pKa of 20 and 40 mg, also lead to comparable results for the 3.97) (Kromer et al. 1998) (fig. 2). The activation of proton healing of gastroesophageal reflux disease (Plein et al. pump inhibitors is considered to have a doubling-time of 1998), as well as duodenal and gastric peptic ulcers (Kromer 1–5 min., which should be compared to a half-life in the et al. 1999) (fig. 3). In accordance with this observation, circulation of about 60 min. (Yasuda et al. 1994). The po- studies of omeprazole and rabeprazole, both at 20 mg dos- tency of anyone of these drugs depends on the amount of age, reveal similar clinical effects for healing of gastro- free precursor, plasma AUC (‘‘area under curve’’), and the oesophageal reflux disease (Dekkers et al. 1999), duodenal activation time at pH 1. Since all proton pump inhibitors and gastric ulcers (Müller et al. 1992). Thus, data speak for are available in plasma for binding to the Hπ,Kπ-ATPase a similar potency of the proton pump inhibitors. for a considerably longer time span than needed for inhi- Studies of the pharmacokinetics of esomeprazole and bition of the enzyme, minor differences in time lag for the omeprazole at a dose of 20 mg (five days treatment) show activation of the proton pump inhibitors in an acidic milieu higher plasma concentrations of esomeprazole (almost are therefore negligible. twice greater AUC) than of omeprazole (Lind et al. 2000). At a dose of 40 mg, esomeprazole causes considerably higher plasma concentrations (about 5 times greater AUC) than with 20 mg omeprazole (Lind et al. 2000). With 20 mg, esomeprazole maintains intragastric pH⬎4 for more Fig. 2. Intravenous dosage of proton pump inhibitors to achieve Fig. 3. Duration of intragastric pH⬎4 during 24 hr in subjects half-maximal inhibition (ID50; average∫95% confidence interval) of treated with omeprazole and pantoprazole, both at 40 mg daily pentagastrin-stimulated acid secretion in the chronic gastric fistula doses in comparable studies, study A (Koop et al. 1994) and study rat. One mmol of each drug equals 0.37 mg lansoprazole; 0.35 mg B (Brunner et al. 1997). The results illustrate the variability in re- omeprazole; 0.38 mg pantoprazole; 0.36 mg rabeprazole (Kromer sults between different studies. Comparisons between different et al. 1990). studies should therefore be made with caution (Kromer et al. 1999).
108 PER M. HELLSTRÖM AND SIGURD VITOLS MiniReview than 12 hr in 54% of individuals compared to 44% for ome- There are reports of comparative studies of different pro- prazole. At 40 mg, the corresponding value for esomeprazo- ton pump inhibitors revealing a strong effect of some agents le is 92%. Accordingly, intragastric pH⬎4 is maintained for already at a low dose, suggesting a high potency. We found 16 hr in 24%, 14% and 54% of the individuals, respectively two studies where a significantly better effect was seen with (Lind et al. 2000). This difference in acid inhibition is mir- rabeprazole than with omeprazole at 20 mg daily. In one rored by differences in intragastric pH. Esomeprazole at a of these studies, the 24 hr intragastric pH was measured daily dose of 40 mg generates an intragastric pH of 4.9 (on (Williams et al. 1998), revealing a more rapid pH increment the average), while 20 mg generates pH 4.1, which should with rabeprazole than with omeprazole during an 8-day be compared to pH 3.6 after omeprazole 20 mg (Lind et al. treatment of healthy individuals. In another study of gastric 2000). Esomeprazole 40 mg daily has been found to be ulcer (Dekkers et al. 1998), 20 mg rabeprazole was found more effective in raising intragastric pH than lansoprazole to be more effective than 20 mg omeprazole as regards 30 mg, pantoprazole 40 mg or rabeprazole 20 mg, as well symptom relief, but equally effective as regards ulcer heal- as omeprazole at doses of 20 and 40 mg (Röhss et al. 2000a) ing. The published findings have to be evaluated against the (fig. 4). The conclusion of these findings is that, for any variability of the effects of the proton pump inhibitors; so given proton pump inhibitor an increased AUC will cause far, true differences concerning their effectiveness or useful- a greater acid inhibition. It remains to show that such dif- ness have not been disclosed. We have found two studies ferences in acid inhibition are of clinical importance. that claim a stronger effect of a lower dose of a specific proton pump inhibitor in relation to a higher dose of an- other (Florent & Forestier 1997). One of these studies did Dose-response relationships not demonstrate any difference between lansoprazole 30 mg Basically, the acid inhibitory effect of proton pump inhibi- daily and pantoprazole 40 mg as regards endoscopic or tors displays rectilinear dose-response relationships up to a symptomatic remission in gastro-oesophageal reflux disease near-maximal effect. Doses currently used in clinical prac- (Florent & Forestier 1997), whereas the results of the other tice seem to induce acid inhibition in the 60–90% range, study indicate that treatment with lansoprazole 30 mg gives which means that the values often fall on the rectilinear part a better result than treatment with pantoprazole 40 mg in of the dose-response curve. In studies of gastro-oesophageal the maintenance treatment of reflux oesophagitis (Jaspersen reflux disease, lansoprazole displays increased healing rates et al. 1998). when the dose is increased from 15 to 30 mg daily but with Several clinical studies have shown esomeprazole 40 mg no further improvement at 60 mg (Earnest et al. 1998). In to be marginally more effective than omeprazole 20 mg in the same way, pantoprazole shows increased healing rates the treatment of gastro-oesophageal reflux disease and ero- with doses from 10 to 40 mg. The dose-response relation- sive oesophagitis. Studies on erosive oesophagitis during an ships that are applicable for omeprazole and pantoprazole 8-week period demonstrated that esomeprazole at doses of in the treatment of gastro-oesophageal reflux disease and 20 and 40 mg gave healing rates of 89.9% and 94.1%, re- duodenal, as well as gastric peptic ulcer disease have been spectively, compared to omeprazole 20 mg with a healing analyzed by Kromer et al. (1999), who showed higher heal- rate of 86.9% (Kahrilas et al. 2000). Moreover, esomeprazo- ing rates with 40 than with 20 mg. Since a clear relationship le 40 mg gave better symptom relief and more complete between acid inhibition and healing of duodenal ulcer dis- healing of oesophagitis than lansoprazole 30 mg (Castell et ease exists, as shown by Savarino et al. (1994), it is reason- al. 2002). Other studies, however, show that pantoprazole able to assume that the healing of duodenal ulcers reflects 40 mg causes the same oesophageal pH-increment (Simon the inhibition of acid secretion. et al. 2001) and symptom relief as esomeprazole 40 mg in the treatment of moderate to severe oesophagitis (Scholten et al. 2002). In patients with gastro-oesophageal reflux dis- ease esomeprazole at doses of 40 mg or 20 mg gives a simi- lar symptom relief during 4–8 weeks of treatment (Nexium (package insert), Wilmington 2001). Optimal dosage of proton pump inhibitors in acute and maintenance treatment of acid-related disorders Many studies of gastro-oesophageal reflux disease demon- strate that treatment with 40 mg omeprazole gives a better healing rate than 20 mg. Compared to omeprazole 20 mg, esomeprazole 40 mg causes about 15% higher healing rates in gastro-oesophageal reflux disease (Kahrilas et al. 2000). Fig. 4. Duration of intragastric pH⬎4 during 24 hr in 114 patients Dose-dependent healing rates in gastro-oesophageal reflux under treatment with esomeprazole or omeprazole, both at 40 mg disease also seem valid for pantoprazole as shown in studies daily, on the fifth day of treatment (Röhss et al. 2000b). of 10, 20 and 40 mg daily (Bochenek et al. 1998). Lansopra-
MiniReview CHOICE OF PROTON PUMP INHIBITOR FOR ACID INHIBITION 109 tenance treatment with a sustained healing of 93.2% during a 6-month period (Johnson et al. 2001). Data from studies of pantoprazole show similar results with 20 and 40 mg (Plein et al. 1998). Taken together, 20 mg daily seems to be an adequate dose of esomeprazole, omeprazole and panto- prazole, while a 15-mg dose of lansoprazole seems to be sufficient in the maintenance treatment of gastro-oeso- phageal reflux disease. Conclusion Proton pump inhibitors are used in various standard dos- ages for inhibition of acid secretion in acute and mainten- ance treatment of acid-related disorders. Comparisons be- tween different proton pump inhibitors show that the four compounds lansoprazole, omeprazole, pantoprazole and Fig. 5. Different proton pump inhibitors compared with omeprazo- rabeprazole have a similar anti-secretory potency on a milli- le 20 mg daily. Odds ratio with 95% confidence interval for healing gram basis. Rabeprazole seems to produce a slightly more of gastro-oesophageal reflux disease with various proton pump in- rapid onset of acid inhibition than the others. Esomeprazo- hibitors. Comparison with omeprazole 20 mg daily (odds ratio 1.0), 8-week treatment period (Corinaldesi et al. 1995; Mossner et al. le displays a somewhat greater acid inhibitory potency than 1995; Castell et al. 1996; Mee & Rowley 1996; Mulder et al. 1996; other proton pump inhibitors. The clinical gain of these Bochenek et al. 1998; Dekkers et al. 1999; Delchier et al. 2000). The findings seems marginal and studies demonstrating clinical healing ratio shows the relative difference in healing rates between importance are lacking. The inhibition of Hπ,Kπ-ATPase omeprazole and other proton pump inhibitors, where 1.0 represents with a daily dosage of 40 mg of the proton pump inhibitors an equal treatment result with 95% confidence interval. falls in the top range of the dose-response curve, which means that differences in acid inhibitory effect between the different inhibitors tend to be minor and difficult to estab- lish. zole displays comparative dose-response relationships as re- From available data the dosage 30–40 mg of proton gards efficiency of 15 and 30 mg (Earnest et al. 1998). To pump inhibitors appears to be optimal for the treatment of summarize, available data indicate that the optimal dosage active ulcer disease as well as moderate to severe gastro- of any proton pump inhibitor for the treatment of gastro- oesophageal reflux disease. For the eradication of Helicob- oesophageal reflux disease is 30–40 mg daily (fig. 5). acter pylori a two-dose regimen of proton pump inhibitor In the treatment of peptic ulcer disease it seems that the in combination with antibiotics is required. In mild sympto- optimal dosage for prompt symptom relief and increased matic gastro-oesophageal reflux disease, or in maintenance healing rate is 40 mg daily with omeprazole as well as treatment after the healing of erosive oesophagitis 15–20 mg pantoprazole. Lansoprazole has not been investigated at daily seems sufficient. These ‘‘standard dosages’’ of proton this dosage, but a dosage of 60 mg seems more effective pump inhibitors accord with current knowledge as regards than lower dosages as judged from studies of intragastric potency and efficacy of the different proton pump inhibi- 24-hr pH measurements (Seensalu et al. 1995). In other tors, and do not solely mirror the relative potency of the words, the pharmacodynamic profile of lansoprazole does drugs on a milligram basis. The conclusion would be that not seem to differ from those of other proton pump inhibi- all proton pump inhibitors display similar potency. tors. Rabeprazole 20 mg inhibits acid secretion as effec- In a global perspective patented proton pump inhibitors tively as omeprazole 20 mg, both as regards peptic ulcer are now competing with generics. A consequence of the and reflux disease (Dekkers et al. 1999). A specific feature competition for market shares will be reduced pricing. of rabeprazole seems to be that the onset of acid inhibition From a clinical point of view the most important goal must occurs more rapidly than with omeprazole and can be be to establish criteria for the selection of the proper drug noted already on the first day of treatment (Williams & and the appropriate dose. In the clinical setting, all proton Pounder 1999). This effect may reflect the high pKa of ra- pump inhibitors have a similar potency and the same in- beprazole. herent capacity to inhibit acid secretion. The clinician has In terms of maintenance treatment of gastro-oesophageal to decide what degree of acid inhibition he aims for in the reflux disease, 15 mg lansoprazole, alternatively 20 mg ome- individual patient, based on his knowledge of the nature prazole or pantoprazole, is considered sufficient, even and severity of the disease. The desired result will be ob- though there are studies showing that a dose of 10 mg may tained with any one of the proton pump inhibitors after be as effective (Laursen et al. 1995). As regards esomeprazo- selecting the proper dosage of the drug to be used in that le it seems that a daily dose of 20 mg gives a reliable main- particular patient.
110 PER M. HELLSTRÖM AND SIGURD VITOLS MiniReview References Johnson, D. A., S. B. Benjamin, N. B. Vakil, J. L. Goldstein, M. Lamet, J. Whipple, D. Damico & B. Hamelin: Esomeprazole once Ashida, K., M. Sakaguchi, M. Tanaka, H. Takiuchi, Y. Egashira & daily for 6 months is effective therapy for maintaining healed K.-I. Katsu: Clinical study on the pathophysiology and treatment erosive esophagitis and for controlling gastroesophageal reflux of PPI-resistant ulcers. J. Clin. Gastroenterol. 1995, 20 (suppl. 2), disease symptoms: a randomized, double-blind, placebo-con- 67–71. trolled study of efficacy and safety. Amer. J. Gastroenterol. 2001, Bastaki, S. M., I. Chandranath & A. Garner: Comparison of five 96, 27–34. antisecretory agents acting via gastric Hπ/Kπ-ATPase. J. Kahrilas, P. J., G. W. Falk, D. A. Johnson, C. Schmitt, D. W. Col- Physiol. Paris 2000, 94, 19–23. lins, J. Whipple, D. D’Amico, B. Hamelin & B. Joelsson: Esomep- Besancon, M., A. Simon, G. Sachs & J. Shin: Sites of reaction of razole improves healing and symptom resolution as compared the gastric H, K-ATPase with extracytoplasmic thiol reagents. J. with omeprazole in reflux oesophagitis patients: a randomized Biol. Chem. 1997, 272, 22438–22446. controlled trial. The Esomeprazole Study Investigators. Aliment. Bochenek, W., D. Miska & M. Beg: Efficacy of pantoprazole in Pharmacol. Therap. 2000, 14, 1249–1258. reflux erosive esophagitis (EE) is dose related. Digestion 1998, 59 Koop, H., S. Kuly, M. Flüg, A. Scneider & K. Rose: Comparison (suppl. 3), 601. of 24-h intragastric pH and gastrin profiles during therapy with Brummer, R. J. M., B. J. Geerling & R. W. Stockbrügger: Initial and the proton pump inhibitors pantoprazole and omeprazole. Gut chronic gastric acid inhibition by lansoprazole and omeprazole in 1994, 35 (suppl. 4), A79. relation to meal administration. Dig. Dis. Sci. 1997, 42, 2132– Kromer, W., S. Horbach & R. Lühmann: Relative efficacies of gas- 2137. trin proton pump imhibitors: Their clinical and pharmacological Brunner, G., H. Danz-Neeff, C. Athmann & N. Samayoa: Com- basis. Pharmacology 1999, 59, 57–77. parison of pantoprazole (40 mg sid) versus omeprazole (40 mg Kromer, W., U. Krüger, R. Huber, M. Hartmann & V. W. Steinijans: sid) on intragastric pH and serum gastrin in healthy volunteers. Differences in pH-dependent activation rates of substituted Can. J. Gastroenterol. 1997, 11 (suppl. A), S2. benzimidazoles and biological in vitro correlates. Pharmacology Castell, D., P. Kahrilas, J. Richter, N. Vakil, D. Johnson, S. Zucker- 1998, 56, 57–70. man, W. Skammer & J. Levine: Esomeprazole (40 mg) compared Kromer, W., S. Postius, R. Riedel, W. Simon, G. Hanauer, U. with lansoprazole (30 mg) in the treatment of erosive esophagitis. Brand, S. Gönne & M. Parsons: BY 1023/SK&F 96022 INN Amer. J. Gastroenterol. 2002, 97, 575–583. pantoprazole, a novel gastric pump inhibitor, potently inhibits Castell, D., J. Richter, M. Robinson, S. Sontag & M. Haber: Effi- acid secretion but lacks relevant cytochrome P450 interactions. cacy and safety of lansoprazole in the tratment of erosive reflux J. Pharmacol. Exp. Therap. 1990, 254, 129–135. esophagitis. The Lansoprazole Group. Amer. J. Gastroenterol. Langtry, H. D. & M. I. Wilde: Lansoprazole. An update of its phar- 1996, 91, 1749–1757. macological properties and clinical efficacy in the management Corinaldesi, R., M. Valentini, J. Belaiche, R. Colin, H. Geldof & C. of acid-related disorders. Drugs 1997, 54, 473–500. Maier: Pantoprazole and omeprazole in the treatment of reflux Laursen, S., T. Havelund, S. Bondesen, J. Hansen, G. Sanchez, E. oesophagitis: a European multicentre study. Aliment. Pharmacol. Sebelin, C. Fenger & K. Lauritzen: Omeprazole in the long-term Therap. 1995, 9, 667–671. treatment of gastro-oesophageal reflux disease. A double-blind Dekkers, C. P. M., J. A. Beker, B. Thjodleifsson, A. Gabryelewicz, randomized dose-finding study. Scand. J. Gastroenterol. 1995, 30, N. Bell, T. J. Humphries & E. R. S. Group: Comparison of rabep- 839–846. razole 20 mg vs. omeprazole 20 mg in the treatment of active Lind, T., L. Rydberg, A. Kylebäck, A. Jonsson, T. Andersson, G. gastric ulcer: A European multicentre study. Aliment. Pharmacol. Hasselgren, J. Holmberg & K. Röhss: Esomeprazole provides im- Therap. 1998, 12, 789–795. proved acid control vs. omeprazole In patients with symptoms of Dekkers, C. P. M., J. A. Beker, B. Thjodleifsson, A. Gabryelewicz, gastro-oesophageal reflux disease. Aliment. Pharmacol. Therap. N. E. Bell, T. J. Humphries & E. R. S. Group: Double-blind, placebo-controlled comparison of rabeprazole 20 mg vs. omepra- 2000, 14, 861–867. zole 20 mg in the treatment of erosive or ulcerative gastro-oseso- Mee, A. & J. Rowley: Rapid symptom relief in reflux oesophagitis: fageal reflux disease. Aliment. Pharmacol. Therap. 1999, 13, 49– A comparison of lansoprazole and omeprazole. Aliment. Pharm- 57. acol. Therap. 1996, 10, 757–763. Delchier, J., Cohen G & T. Humphries: Rabeprazole, 20 mg once Mossner, J., A. Holscher, R. Herz & A. Schneider: A double-blind daily or 10 mg twice dialy, is equivalent to omeprazole, 20 mg study of pantoprazole and omeprazole in the treatment of reflux once daily, in the healing of erosive gastrooesophageal reflux dis- oesophagitis: A multicenter trial. Aliment. Pharmacol. Therap. ease. Scand. J. Gastroenterol. 2000, 35, 1245–1250. 1995, 9, 321–326. Earnest, D. L., E. Dorsch, J. Jones, D. E. Jennings & P. A. Greski- Mulder, C., W. Dekker & M. Gerretsen: Lansoprazole 30 mg versus Rose: A placebo-controlled dose-ranging study of lansoprazole omeprazole 40 mg in the treatment of reflux oesophagitis grade in the management of reflux esophagitis. Amer. J. Gastroenterol. II, III and IVa (a Dutch multicentre trial): Dutch Study Group. 1998, 93, 238–243. Eur. J. Gastroenterol. Hepatol. 1996, 8, 1101–1106. Erlandsson, P., R. Isaksson, P. Lorentzon & P. Lindberg: Resolution Müller, P., B. Simon, H. Khalil, R. Lühmann, U. Leucht & A. of the enantiomers of omeprazole and some of its analogues by Schneider: Dose-range finding study with the proton pump in- liquid chromatography on a trisphenylcarbamoylcellulose-based hibitor pantoprazole in acute duodenal ulcer patients. Z. Gastro- stationary phase. The effect of the enantiomers of omeprazole enterol. 1992, 30, 771–775. on gastric glands. J. Chromatogr. 1990, 532, 305–319. Nexium (package insert). Astrazeneca Wilmington, D. A. L.: 2001. Florent, C. & S. Forestier: Twenty-four-hour monitoring of intra- Plein, K., J. Hotz, H. Wurzer, I. Fumagalli, H. Tenor & A. Schneid- gastric acidity: Comparison between lansoprazole 30 mg and er: Prevention of relapse in gastro-esophageal reflux disease pantoprazole 40 mg. Eur. J. Gastroenterol. Hepatol. 1997, 9, 195– (GERD). A randomized, double blind, long-term, multi-centre 200. study using 20 mg or 40 mg pantoprazole. Digestion 1998, 59 Hannan, A., J. Weil, C. Broom & R. P. Walt: Effects of oral panto- (suppl. 3), 600. prazole on 24-hour intragastric acidity and plasma gastrin pro- Röhss, K., C. Claar-Nilsson, H. Rydholm & L. Nyman: Esomepra- files. Aliment. Pharmacol. Therap. 1992, 6, 373–380. zole 40 mg provides more effective acid control than lansoprazole Jaspersen, D., K. L. Diehl, H. Schoeppner, P. Geyer & E. Martens: 30 mg. Gastroenterology 2000a, 118, A20. A comparison of omeprazole, lansoprazole and pantoprazole in Röhss, K., C. Lundin, H. Rydholm & L. Nyman: Esomeprazole 40 the maintenance treatment of severe reflux oesophagitis. Aliment. mg provides more effective acid control than omeprazol 40 mg. Pharmacol. Therap. 1998, 12, 49–52. Amer. J. Gastroenterol. 2000b, 95, 2432–2433.
MiniReview CHOICE OF PROTON PUMP INHIBITOR FOR ACID INHIBITION 111 Sachs, G., J. Shin, C. Briving, B. Wallmark & S. Hersey: The phar- esophageal pH in patients with symptomatic GERD. Amer. J. macology of the gastric acid pump: the Hπ,Kπ ATPase. Annu. Gastroenterol. 2001, 96 (suppl.), 108. Rev. Pharmacol. Toxicol. 1995, 35, 277–305. Thitiphuree, S. & N. J. Talley: Esomeprazole, a new proton pump Savarino, V., G. S. Mela, P. Zentilin, P. Cutela, M. R. Mele, S. Vig- inhibitor: pharmacological characteristics and clinical efficacy. neri & G. Celle: Variability in individual response to various Int. J. Clin. Pract. 2000, 54, 537–541. doses of omeprazole. Implications for antiulcer therapy. Dig. Dis. Williams, M. P. & R. E. Pounder: The pharmacology of rabeprazo- Sci. 1994, 39, 161–168. le. Aliment. Pharmacol. Therap. 1999, 13 (suppl. 3), 3–10. Scholten, T., U. Hole & G. Gatz: Similar reduction of symptom Williams, M. P., J. Secombe, M. I. Hamilton & R. E. Pounder: A load within 4 weeks of treatment with pantoprazole 40 mg or placebo-controlled trial to assess the effects of 8 days of dosing esomeprazole 40 mg in patients with moderate to severe GERD. with rabeprazole versus omeprazole on 24-h intragastric acidity Can. J. Gastroenterol. 2002, 16 (suppl. A), 138. and plasma gastrin concentrations in young healthy male sub- Seensalu, R., M. Iwarzon, I. Janczewska, B. Hammarlund, A. Ok- jects. Aliment. Pharmacol. Therap. 1998, 12, 1079–1089. sanen & M. Sagar: Dose-response comparison of lansoprazole Yasuda, S., A. Ohnishi, T. Ogawa, Y. Tomono, J. Hasegawa, H. and omeprazole on 24-hour gastric acidity and plasma gastrin in Nakai, Y. Shimamura & N. Morishita: Pharmacokinetic prop- healthy volunteers. Gastroenterology 1995, 108 (suppl.), A215. erties of E3810, a new proton pump inhibitor, in healthy male Simon, B., P. Mueller, G. Gatz & P. Sander: Equivalent effect of volunteers. Int. J. Clin. Pharmacol. Therap. 1994, 32, 466–473. pantoprazole 40 mg o.d. and esomeprazole 40 mg o.d. on intra-
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