Prevacid
Assessment of patient satisfaction with a formulary switch from omeprazole to lansoprazole in gastroesophageal reflux disease maintenance therapy.

Condra LJ, Morreale AP, Stolley SN, Marcus D.

Department of Pharmacy, Veteran Affairs San Diego Healthcare System, CA 92161, USA. condraljc aol.com

OBJECTIVE: To determine if patients perceived a difference in the efficacy, side effects, and value of omeprazole versus lansoprazole for gastroesophageal reflux disease (GERD) maintenance therapy after a formulary conversion, and to evaluate the costs of the conversion. STUDY DESIGN: An unblinded questionnaire was mailed to patients who were currently receiving GERD maintenance therapy with lansoprazole from the Veterans Affairs San Diego Healthcare System. PATIENTS AND METHODS: Three hundred patients who had been on omeprazole for a minimum of 2 months prior to the formulary conversion and on lansoprazole for a minimum of 2 months after the formulary conversion were surveyed. Patients were asked to rate the severity and frequency of their symptoms (pain, heartburn, and regurgitation) on a scale from 0 to 9 for each medication. Questions regarding side effects, medication preference, and satisfaction with the formulary conversion process were also addressed. RESULTS: Fifty-two percent of the surveys were returned. There was no statistically significant difference between median total symptom scores for omeprazole and lansoprazole (1.33 vs. 1.34, respectively). More patients reported side effects to lansoprazole (P < 0.001) than to omeprazole. Sixty-four percent of patients preferred omeprazole (P < 0.005). The formulary conversion was estimated to save $29,000 per year. CONCLUSIONS: Omeprazole was the medication preferred by patients for GERD maintenance therapy. Patients were willing to pay an additional fee for their preferred agent. Fewer adverse events were reported with omeprazole. The potential cost savings of the formulary conversion may have been at the expense of patient satisfaction.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10537869&dopt=Abstract lansoprazole Prevacid



Prevacid
Acid-independent gastroprotective effects of lansoprazole in experimental mucosal injury.

Blandizzi C, Natale G, Gherardi G, Lazzeri G, Marveggio C, Colucci R, Carignani D, Del Tacca M.

Department of Oncology, University of Pisa, Italy.

The protective effects of the proton pump inhibitor lansoprazole on gastric mucosal damage induced by ethanol-HCl or hemorrhagic shock were investigated in the present study. The morphometric analysis of gastric histological sections revealed that lansoprazole dose-dependently reduced mucosal injury evoked by ethanol-HCl (ED50 = 24.3 micromol/kg) or hemorrhagic shock (ED50 = 38.9 micromol/kg), these effects being associated with marked increments of Alcian blue recovery from gastric bound mucus (ED50 = 31.4 micromol/kg and 27.6 micromol/kg, respectively). In addition, lansoprazole inhibited gastric acid secretion from pylorus-ligated rats (ED50 = 9.8 micromol/kg). Further experiments, performed on rats with ethanol-HCl-induced gastric injury, indicated that the protective effects of lansoprazole were not modified by L-365,260, suramin, N(G)-nitro-L-arginine, or systemic ablation of capsaicin-sensitive sensory nerves, whereas they were partly blocked by indomethacin and fully prevented by N-ethyl-maleimide. In addition, lansoprazole did not modify somatostatin concentrations in gastric mucosa. The present results provide evidence that lansoprazole prevents the necrotic damage of gastric mucosa induced by ethanol-HCl or hemorrhagic shock. According to the rank order of ED50 values, these effects appear to depend mainly on the enhancement of the gastric mucus barrier rather than on the reduction of acid secretion. It is also proposed that an increased production of prostaglandins, as well as an increased availability of sulfhydryl compounds at level of gastric mucosa may account for the gastroprotective effects of lansoprazole.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10548356&dopt=Abstract lansoprazole Prevacid



Prevacid
Prevalence of potential proton-pump inhibitor drug interactions: a retrospective review of prescriptions in community pharmacies.

Saltiel E, Fask A.

Cedars-Sinai Medical Center, Los Angeles, California 90035, USA.

Drug interactions are a major cause of drug-related problems. This study assessed the comparative frequency of potential drug-drug interactions in patients receiving either omeprazole or lansoprazole. We reviewed prescription data from 144 community pharmacies in 25 states for the period of October 12, 1996, through October 20, 1997, from which the rates at which patients received either proton-pump inhibitor concurrently with > or =1 potentially interacting drugs were determined. A total of 7306 patients received only omeprazole, and 2486 received only lansoprazole. In this sample, 722 patients (9.9%) who received omeprazole also received a potentially interacting medication at the same time, compared with 8 patients (0.3%) who received lansoprazole (P<0.001). These data suggest that clinicians should be conscientious when selecting or dispensing drugs for patients taking omeprazole, given the relatively high prevalence of potential drug interactions in clinical practice.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10566575&dopt=Abstract lansoprazole Prevacid



Prevacid
Minor effects of Helicobacter pylori on gastric secretion and dose of lansoprazole during long-term treatment in ZE and non-ZE acid hypersecretors.

Hirschowitz BI, Simmons J, Mohnen J.

Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, UAB Station, Birmingham, AL 35294-0007, USA. bhirschowitz gihep.uab.edu

BACKGROUND: Helicobacter pylori infection may increase or decrease acid secretion and may augment proton pump inhibitor efficacy. Pepsin effects have not been reported. In Zollinger-Ellison syndrome (ZE) specifically, H. pylori has been reported to decrease acid. AIM: To examine H. pylori effects on secretion and dose of medication in hypersecretors (basal acid output > 15 mmol/h) undergoing long-term treatment with individually optimized lansoprazole doses. METHODS: Sixty-five patients (47 ZE and 18 non-ZE), treated for > 3 months to 10 years, were tested every 6 months with endoscopy, gastric analysis and serum gastrin. RESULTS: Forty-three per cent were H. pylori-positive. Acid, pepsin and gastrin were not different between H. pylori-positive and H. pylori-negative patients before or during long-term lansoprazole treatment. Initially, H. pylori-positive patients required less lansoprazole than H. pylori-negative patients (68 +/- 6 vs. 96 +/- 8 mg/day), but after 3 years the doses converged (83 vs. 86 mg/day). The disappearance of H. pylori in 15 patients caused no significant changes in acid, pepsin, gastrin or lansoprazole dose in the following 4 years. CONCLUSIONS: H. pylori had no significant initial or long-term physiological or potential clinical effects on acid or pepsin secretion or gastrin in these acid hypersecretors.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11860414&dopt=Abstract lansoprazole Prevacid



Prevacid
The gastric H,K-ATPase blocker lansoprazole is an inhibitor of chloride channels.

Schmarda A, Dinkhauser P, Gschwentner M, Ritter M, Furst J, Scandella E, Woll E, Laich A, Rossmann H, Seidler U, Lang F, Paulmichl M.

Department of Physiology, University of Innsbruck, Austria.

1. It was postulated that swelling dependent chloride channels are involved in the proton secretion of parietal cells. Since omeprazole, lansoprazole and its acid activated sulphenamide form AG2000 are structurally related to phenol derivatives known to block swelling dependent chloride channels, we set out to test, whether these substances--which are known to block the H,K-ATPase--could also lead to an inhibition of swelling-dependent chloride channels. Swelling-dependent chloride channels--characterized in many different cell types--show highly conserved biophysical and pharmacological features, therefore we investigated the effect of omeprazole, lansoprazole and its acid activated sulphenamide form AG2000 on swelling-dependent chloride channels elicited in fibroblasts, after the reduction of the extracellular osmolarity. 2. Omeprazole, lansoprazole and its acid activated sulphenamide form AG2000 are able to block swelling-dependent chloride channels (IClswell). 3. Lansoprazole and its protonated metabolite AG2000 act on at least two different sites of the IClswell protein: on an extracellular site which seems to be in a functional proximity to the nucleotide binding site, and on an intracellular site which allows the formation of disulfide-bridges. 4. The inhibition of the proton pump and the simultaneous blocking of chloride channels by omeprazole, lansoprazole and its acid activated sulphenamide form AG2000, as described here could be an effective mode to restrict proton secretion in parietal cells.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10711360&dopt=Abstract lansoprazole Prevacid