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The aging stomach: implications for NSAID gastropathy
  1. Department of Medicine, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, Texas 78284–7878, USA
  2. Department of Medicine, University of Texas Southwestern Medical Center and Veterans Affairs Medical Center, Dallas, Texas 75216, USA
  1. Dr Lee.

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Over 30 million people worldwide use non-steroidal anti-inflammatory drugs (NSAIDs) daily, and nearly 50% of these NSAID users are elderly.1 ,2 Numerous human studies have shown that the use of NSAIDs is associated with various gastroduodenal mucosal lesions,2-4 sometimes collectively referred to as NSAID gastropathy,4 and that NSAID gastropathy and its life-threatening complications occur primarily in elderly patients.5 ,6 Overall, the use of NSAIDs increases the risk of peptic ulcer disease, ulcer complications (haemorrhage and/or perforation), and death from ulcer by a factor of between 2 and 4.3 ,5 ,7 In the United States alone, medical costs attributable to NSAID gastropathy and its complications exceed $4 (£2.4) billion a year.2 Although increased NSAID use among the elderly is an obvious risk factor, epidemiological data suggest that aging is an independent risk factor for the development of NSAID gastropathy and its complications.5 ,6 ,8 The aim of this article is to review recent developments in the area of age related changes in gastric physiology that may predispose the elderly to NSAID gastropathy. A better understanding of the age related changes in gastric mucosal functions will help us to develop novel interventions for the treatment and prevention of NSAID induced gastrointestinal injury in susceptible elderly people.

Mechanisms of NSAID induced gastric mucosal injury

The mechanisms by which aspirin and other NSAIDs produce acute and chronic gastroduodenal mucosal injury are incompletely understood. In general, gastric mucosal injury is thought to result when aggressive luminal factors (such as acid and pepsin) overwhelm local mucosal protective factors (such as mucus and bicarbonate).8 ,9Results from animal studies suggest that the production of mucosal lesions by aspirin is a result of two independent mechanisms: …

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