Effects of Helicobacter pylori and Non-Steroidal Anti-Inflammatory Drugs on Peptic Ulcer

Abstract

Peptic ulcer (PU) was a local gastrointestinal lesion due to gastric fluid, gastric acid and pepsin insult. The lesion may involve in mucosal layer, submucosal or even muscle and plasma layer in duodenum and stomach. It was characterized as not only easy to relapse but also hard to prevent (Wang et al., 1998). Its etiology and mechanism was very sophisticated due to the imbalance between offensive factors (gastric acid, pepsin, H. pylori and NSAIDs) and defensive factors (gastric mucus, bicarbonates and blood flow of gastric mucosa) ( Hoogerwerf & Pasricha, 2006). There were at least 3 defensive barriers in the gastric wall to resist gastric acid and pepsin: the mucus-bicarbonates barrier that includes mucus and the bicarbonates grade in the mucus, the mucosa barrier that is the tight conjunction structure among gastric epithelial cells, and the blood flow in mucosa that provides oxygen and nutrition to mucosa and support the turnover of gastric epithelium and mucus. H. pylori and NSAIDs were gastric mucosa’s offensive factors (Tytgat, 2000). Although they cause peptic ulcer by destroying the gastric barrier function, the mechanism was not clear. There were arguments for their simultaneous effects on peptic ulcer (Fendrick et al., 2001). Therefore, it is important to clarify the relationship between H. pylori and NSAIDs, especially when both cause simultaneously the damage to gastric mucosa.