Asymptomatic damage to the upper gastrointestinal tract is a common problem that may present with life-threatening sequelae such as bleeding. This scenario is especially prevalent in the population that ingest nonsteroidal anti-inflammatory agents (NSAIDs). Currently, there exists no means to screen these patients for the presence or absence of gastroduodenal damage prior to clinical presentation. Endoscopy, which remains the "gold standard" for the detection of upper gastrointestinal damage, is a time consuming technique that requires special expertise and may not be generally available. As such, it is an inappropriate technique for the widespread screening of large populations. It is now recognized that intestinal damage can be detected by determining that intestinal permeability is increased in diseases in that affect the small intestine, such as celiac or Crohn's disease. These methods are relatively simple: The patient ingests nondigestible sugar probes that cross damage mucosa and can be detected in the urine in increased amounts. Over the last several years, we have adapted these concepts for the simple noninvasive detection of gastroduodenal damage and have demonstrated that sucrose is an interesting probe molecule that specifically reports damage from the extreme proximal end of the gastrointestinal tract. In this article we review the data that support this contention and demonstrate the clinical usefulness of this approach for the detection of gastric damage in man.