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      Serum Concentrations of Gastrin after Famotidine and Omeprazole Administration to Dogs

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          Abstract

          Background

          The duration of antacid‐induced hypergastrinemia after cessation of administration of omeprazole and famotidine apparently has not been determined in dogs.

          Hypothesis

          That serum gastrin will return to basal concentrations by 7 days after cessation of famotidine or omeprazole administration.

          Animals

          Nine healthy, adult, male, research colony dogs.

          Methods

          Randomized, cross‐over design. Serum gastrin was determined daily for 7 days to establish baseline concentrations. Famotidine (1.0 mg/kg q24h) or omeprazole (1.0 mg/kg q24h) was administered PO for 7 days followed by a 14‐day washout. Serum concentrations of gastrin were determined daily during 7 days of administration and daily for 7 days after cessation of administration. Each drug was evaluated in 8 of the 9 dogs.

          Results

          Omeprazole caused a significant increase in serum gastrin concentration (37.2 ± 7.3 to 71.3 ± 19.0 ng/L; P = .006). Famotidine induced a transient increase in serum gastrin (37.2 ± 7.3 to 65.5 ± 38.5 ng/L; P = .02) that peaked at administration day 3 and declined thereafter. By day 7 after cessation of both drugs, there was no difference in serum gastrin concentrations compared to those before administration (famotidine P = .99; omeprazole P = .99). During or after administration, gastrin concentrations above 3 times the upper reference range were rare (12 of 224 samples).

          Conclusions and Clinical Importance

          A 7‐day withdrawal from short‐term administration of famotidine or omeprazole is sufficient for serum gastrin to return to baseline concentrations. Withholding famotidine or omeprazole for longer before investigating pathologic causes of hypergastrinemia is unnecessary.

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          Most cited references17

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          Primary peptic ulcerations of the jejunum associated with islet cell tumors of the pancreas.

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            Effects of ranitidine, famotidine, pantoprazole, and omeprazole on intragastric pH in dogs.

            To identify the normal gastric acid secretion profile in dogs and determine the degree of gastric acid suppression associated with 4 gastric acid suppressants. 12 healthy Beagles. Intragastric pH was measured continuously for 24-hour periods with a digital recording system placed via a gastrostomy tube. Baseline measurements were obtained when food was withheld and when dogs were fed a standard diet. Dogs were then treated with ranitidine (2 mg/kg, IV, q 12 h), famotidine (0.5 mg/kg, IV, q 12 h), pantoprazole (1 mg/kg, IV, q 24 h), omeprazole (1 mg/kg, PO, q 24 h), or saline solution for 7 days; intragastric pH was recorded on days 0, 2, and 6. Subsequently, the effects of administering famotidine (0.5 mg/kg, IV, q 8 h; 6 dogs) and omeprazole as a suspension (1 mg/kg, PO, q 12 h; 6 dogs) were evaluated. Median 24-hour intragastric pH, percentage of time pH was > or = 3, and percentage of time pH was > or = 4 were determined. Median pH, percentage of time pH was > or = 3, and percentage of time pH was > or = 4 were all significantly higher when food was withheld than when dogs were fed. Famotidine, pantoprazole, and omeprazole significantly suppressed gastric acid secretion, compared with saline solution, as determined on the basis of median 24-hour pH and percentages of time pH was > or = 3 or > or = 4. However, ranitidine did not. Omeprazole suspension suppressed gastric acid secretion. Results suggest that in healthy dogs, famotidine, pantoprazole, and omeprazole significantly suppress gastric acid secretion. Twice daily administration of a suspension of omeprazole, was the only regimen tested that approached the potential therapeutic efficacy for acid-related disease when assessed by criteria used for human patients.
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              Efficacy of oral famotidine and 2 omeprazole formulations for the control of intragastric pH in dogs.

              Little is known about the efficacy of commonly used acid suppressants on intragastric pH in dogs. To compare the effect of oral famotidine, 2 formulations of omeprazole, and placebo on intragastric pH in dogs with a catheter-free, continuous pH monitoring system. Six healthy adult mixed-breed colony dogs. Utilizing a randomized, 4-way cross over, open-label study, dogs were administered famotidine PO (1.0-1.3 mg/kg q12h), omeprazole tablet (1.5-2.6 mg/kg q24h), omeprazole reformulated paste (RP) (Gastrogard, 1.5-2.6 mg/kg q24h), and placebo for 7 days followed by a 10-day washout period. Radiotelemetric pH capsules were placed with gastroscopy assistance to continuously record intragastric pH for 4 days (days 4-7 of dosing). The percentage of time that intragastric pH was ≥3 and ≥4 was compared among treatment groups using repeated measures of analysis of variance. Tukey's Studentized range test was used to determine which groups were different with α= 0.05. Mean ± SD percent time intragastric pH was ≥3 and ≥4 was 22 ± 8% and 14 ± 6% for famotidine, 63 ± 14% and 52 ± 17% for omeprazole tablet, 54 ± 17% and 44 ± 18% for omeprazole RP, and 6 ± 6% and 5 ± 5% for placebo. Both omeprazole formulations significantly increased intragastric pH compared with famotidine and placebo, but omeprazole tablet and RP was not significantly different from each other. Oral omeprazole tablet and RP provide superior gastric acid suppression to famotidine, and should therefore be considered more effective for the treatment of acid related disorders in dogs. Copyright © 2010 by the American College of Veterinary Internal Medicine.
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                Author and article information

                Journal
                J Vet Intern Med
                J. Vet. Intern. Med
                10.1111/(ISSN)1939-1676
                JVIM
                Journal of Veterinary Internal Medicine
                John Wiley and Sons Inc. (Hoboken )
                0891-6640
                1939-1676
                23 July 2014
                Sep-Oct 2014
                : 28
                : 5 ( doiID: 10.1111/jvim.2014.28.issue-5 )
                : 1465-1470
                Affiliations
                [ 1 ] Department of Small Animal Clinical SciencesMichigan State University College of Veterinary Medicine East Lansing MI
                [ 2 ] Department of Pathology and Diagnostic InvestigationMichigan State University College of Veterinary Medicine East Lansing MI
                Author notes
                [*] [* ]Corresponding author: C.A. Johnson, D205 Veterinary Medical Center, Michigan State University, East Lansing, MI 48824‐1314; e‐mail: cajohnson@ 123456cvm.msu.edu .
                Article
                JVIM12408
                10.1111/jvim.12408
                4895597
                25056694
                86a4ce2f-3c92-4606-83c4-5ff3748e4b4a
                Copyright © 2014 by the American College of Veterinary Internal Medicine
                History
                : 26 February 2014
                : 14 May 2014
                : 11 June 2014
                Page count
                Pages: 6
                Funding
                Funded by: internal funding
                Categories
                Standard Article
                Standard Articles
                Custom metadata
                2.0
                jvim12408
                September/October 2014
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.8.9 mode:remove_FC converted:06.05.2016

                Veterinary medicine
                antacid,gastrinoma,hypergastrinemia,ulcer,vomiting
                Veterinary medicine
                antacid, gastrinoma, hypergastrinemia, ulcer, vomiting

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