Gastric ulcer is an inflammatory disease and develops due to the imbalance between aggressive and protective factors in the gastrointestinal (GI) tract. Available evidence suggests that use of non-steroidal anti-inflammatory drugs (NSAIDs) is one of the major causative factors in the pathogenesis of human gastric mucosal injury, which may even lead to gastric cancer. The NSAIDs are one of the most widely prescribed drugs in the world, and are extensively used to alleviate pain and inflammation. They have also been more recently used for cardiac patients, and as antineoplastic agents. Due to this use, and their easy availability, the use of NSAIDs is expected to grow exponentially, which is likely to significantly increase NSAID-associated gastric complications, and cause a ‘silent epidemic’ in the near future. NSAID-related gastroduodenal damage is very frequent, and the most serious  complication of any drug therapy (Wallace, 2011). The problem has assumed alarming proportions according to reports of the US Food and Drug Administration (FDA) and other world health regulatory agencies (Roth, 2005). The NSAIDs mainly cause upper GI complications, ranging from dyspeptic symptoms in up to 40%, to peptic ulceration in 20e30% of the chronic NSAID users, and even duodenal ulcers. Evidence reveals that NSAIDs can also induce small intestinal injury via complex mechanisms, the pathogenesis of which is still unclear (Wallace, 2011). Currently, the use of NSAIDs accounts for approximately 25% of gastric ulcer cases, with an upward trend (Halter et al., 2001; Dhikav et al., 2003).