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Nonsteroidal anti-inflammatory drugs (nsaid) are widely used for treatment of people and animals. Their use is limited by frequent side effects commonly involving the gastrointestinal tract, most important of which is development of ulcerating lesions principally in the stomach. Unfortunately, presence of such lesions is often unsuspected because clinical signs may be overlooked until a complication develops. We reported that such damage can be detected by measuring the increase in gastric permeability that is a hallmark of this condition. Sucrose is a novel probe molecule for determination of site-specific gastric permeability. As a disaccharide, it is large enough to be effectively excluded by the intact gastric epithelium, and because it is rapidly digested within the small intestine, absorption of the intact molecule implies damage proximal to this site. Recently, we found that increased sucrose permeability is useful in predicting presence of endoscopically relevant gastric damage in people. We extended these results to the detection of nsaid-induced gastropathy in dogs. Dogs treated with aspirin developed nsaid-induced gastropathy (including gastric ulceration), and the degree of endoscopically detectable damage correlated well with sucrose permeability. Furthermore, healing of these lesions could also be monitored by sequential measurements of sucrose permeability. Sucrose permeability decreased more rapidly than the disappearance of gastric ulcers, suggesting that this technique is more sensitive to generalized mucosal damage than is the presence of discrete, endoscopically visible ulceration. This was confirmed by creating artificial ulcers in the antrum and observing that sucrose permeability was not increased in this setting. We conclude that determination of increased sucrose permeability is a useful, noninvasive means of predicting presence of gastric damage in dogs treated with nsaid.

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in American Journal of Veterinary Research


Objective—To evaluate the use of sucrose permeability testing to detect ulcers in the gastric squamous mucosa of horses.

Animals—13 adult horses ranging from 5 to 19 years of age.

Procedure—Following induction of gastric ulcers by intermittent feed deprivation, horses underwent sucrose permeability testing (administration of sucrose by nasogastric intubation followed by collection of urine at 2 and 4 hours after intubation) and gastric endoscopy. Squamous ulcers were assigned a severity score (range, 0 to 3) by use of an established scoring system. Horses were subsequently administered omeprazole for 21 days, and sucrose testing and endoscopy were repeated. Pair-wise comparisons of urine sucrose concentration were made between horses with induced ulcers before and after omeprazole treatment. Urine sucrose concentrations also were compared on the basis of ulcer severity score.

Results—Urine sucrose concentrations and ulcer severity scores were significantly higher in horses with induced ulcers before omeprazole treatment than after treatment. Urine sucrose concentrations were significantly higher for horses with ulcer severity scores > 1. Use of a cut-point value of 0.7 mg/mL revealed that the apparent sensitivity and specificity of sucrose permeability testing to detect ulcers with severity scores > 1 was 83% and 90%, respectively. Results were similar after adjusting sucrose concentrations for urine osmolality.

Conclusions and Clinical Relevance—Urine sucrose concentration appears to be a reliable but imperfect indicator of gastric squamous ulcers in horses. Sucrose permeability testing may provide a simple, noninvasive test to detect and monitor gastric ulcers in horses. ( Am J Vet Res 2004;65:31–39)

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in American Journal of Veterinary Research