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GASTRITIS & PEPTIC ULCER DISEASE RESOURCE CENTER

  Gastritis includes a myriad of disorders that involve inflammatory changes in the gastric mucosa, including erosive gastritis caused by a noxious irritant, reflux gastritis from exposure to bile and pancreatic fluids, hemorrhagic gastritis, infectious gastritis, and gastric mucosal atrophy. Peptic ulcer disease (PUD) refers to a discrete mucosal defect in the portions of the gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin secretion.
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Gastritis, Chronic Gastroenterology
  Chronic gastritis, by definition, is a histopathological entity characterized by chronic inflammation of the stomach mucosa. Gastritises can be classified based on the underlying etiologic agent (eg, Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity, allergic response) and the histopathological pattern, which may suggest the etiologic agent and clinical course (eg, H pylori–associated multifocal atrophic gastritis). Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis). Although minimal inflammation is observed in some gastropathies, such as those associated with NSAID intake, these entities are discussed in this article because they are frequently included in the differential diagnosis of chronic gastritis.
 
Peptic Ulcer Disease Gastroenterology
  Peptic ulcer disease (PUD) is a common disorder that affects millions of individuals in the United States each year, with a major impact on health care costs. In the last two decades, major advances have been made in the understanding of the pathophysiology of PUD, particularly regarding the role of Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs). This has led to important changes in diagnostic and treatment strategies, with the potential for improving the clinical outcome and decreasing health care costs.
 
Peptic Ulcer Disease Pediatrics
  The lesion of peptic ulcer disease (PUD) is a disruption in the mucosal layer of the stomach or duodenum. An ulcer is distinguished from an erosion by its penetration of the muscularis mucosa or the muscular coating of the gastric or duodenal wall. PUD represents the imbalance between defensive factors that protect the mucosa and offensive or aggressive factors that disrupt this important barrier. Some mucosal protective factors include the water-insoluble mucous gel layer, local production of bicarbonate, regulation of gastric acid secretion, and adequate mucosal blood flow. Aggressive factors include the acid-pepsin environment, infection with Helicobacter pylori, and mucosal ischemia.
 
   
 
  Gebert B, Fischer W, Haas R. The Helicobacter pylori vacuolating cytotoxin: from cellular vacuolation to immunosuppressive activities. Rev Physiol Biochem Pharmacol. 2004 Dec;152(1):205-220. Epub 2004 Jul 27.
  El Mouzan MI, Abdullah AM. Peptic ulcer disease in children and adolescents. J Trop Pediatr. 2004 Dec;50(6):328-30.
  Ohara T, Morishita T, Suzuki H, Masaoka T, Nagata H, Hibi T. Pathophysiological role of human beta-defensins 2 in gastric mucosa. Int J Mol Med. 2004 Dec;14(6):1023-1027.
  Ford A, Delaney B, Forman D, Moayyedi P. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database Syst Rev.. 2004 Oct 18;(4):CD003840.
  Cryer B. COX-2-specific inhibitor or proton pump inhibitor plus traditional NSAID: is either approach sufficient for patients at highest risk of NSAID-induced ulcers? Gastroenterology. 2004 Oct;127(4):1256-8.
  Chan FK, Hung LC, Suen BY, Wong VW, Hui AJ, Wu JC, Leung WK, Lee YT, To KF, Chung SC, Sung JJ. Celecoxib versus diclofenac plus omeprazole in high-risk arthritis patients: results of a randomized double-blind trial. Gastroenterology. 2004 Oct;127(4):1038-43.



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