Evaluation of lansoprazole (an H+/K+-ATPase inhibitor) and azithromycin (an antibiotic) for control of gastric ulceration in swine during periods of feed deprivation

Citation
S. Melnichouk et al., Evaluation of lansoprazole (an H+/K+-ATPase inhibitor) and azithromycin (an antibiotic) for control of gastric ulceration in swine during periods of feed deprivation, CAN J VET R, 63(4), 1999, pp. 248-252
Citations number
33
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
CANADIAN JOURNAL OF VETERINARY RESEARCH-REVUE CANADIENNE DE RECHERCHE VETERINAIRE
ISSN journal
08309000 → ACNP
Volume
63
Issue
4
Year of publication
1999
Pages
248 - 252
Database
ISI
SICI code
0830-9000(199910)63:4<248:EOL(HI>2.0.ZU;2-K
Abstract
Helicobacter-like organisms as well as fermentative bacteria have been impl icated in gastric ulcer production in swine. Irregular feeding schedules ar e also considered a major risk factor. A research trial was conducted to de termine whether medication with an acid secretion inhibitor (lansoprazole), either alone or in combination with an antibiotic (azithromycin), would pr otect pigs from gastric ulceration if the animals were subjected to a 48 h period of fasting. In a 2 x 3 factorial design, 48 pigs were fasted, while an equal number were fed ad libitum. Within these 2 study groups, pigs were randomly assigned to 1 of 3 treatments: control, 30 mg lansoprazole s.i.d. for 7 d, or lansoprazole (30 mg s.i.d. for 7 d) and azithromycin (500 mg s .i.d. for 3 d). Overall, fasted pigs were 1.9 times more likely to develop erosive or ulcerative lesions of the pars esophagea (chi(2) = 9.89, P < 0.0 02). Treatment with an acid secretion inhibitor alone or in combination wit h an antibiotic did not protect pigs from developing gastric lesions. Helic obacter-like organisms were not detected in any of the stomachs. Possibly, the lansoprazole dose of 30 mg given once per day was insufficient to preve nt pH levels from becoming low enough to cause damage to epithelial tissue. Alternatively other substances such as bile acids may have caused the ulce rative lesions, even though stomach acid production was suppressed.