Noninvasive detection of nonsteroidal anti-inflammatory drug-induced gastropathy in dogs

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.