**1. Introduction**

In the past decades, after the widespread therapeutic use of antisecretive drugs (cimetidine, ranitidine, and proton pump inhibitors), the incidence of peptic ulcer disease showed a real and significant decrease. The treatment of the *Helicobacter pylori* infections contributed to these results, demonstrated by the reduced prevalence of these infections [1]. However, the expected reduction in ulcer disease complications did not clearly occur [2, 3]. It is possible to hypothesize a role in the widespread use, also as self-medication, of drugs with gastric injurious side effect such as acetylsalicylic acid (ASA) or nonsteroidal anti-inflammatory drugs (NSAIDs) and besides a role of inaccurate therapy for *H. pylori* infection [4]. Some research studies have shown the role of independent risk factors and a synergic action performed by the use of NSAIDs and the presence of *H. pylori* infection on the evolution of gastroduodenal mucosal impairment/ulceration, ulcer bleeding, and perforation [5]. There are also other significant risk factors of gastroduodenal ulcer occurrence and their complications, such as alcohol consumption, nicotine use, stress life conditions, immunosuppressor therapies, gastric acid hypersecretion states with hypergastrinemia, hyperhistaminemia, etc. [6–8]. In the gastroduodenal site, the mucosal transitional zones are the areas of major risk of development of peptic ulcer because of being exposed to damaging effects of pepsin, gastric acid secretion, bile, and pancreatic juice. The gastric ulcers are usually located along the lesser curvature, in continuousness with the fundus, site of the gastric acid production by the parietal cells. The duodenal ulcers habitually occur in the duodenal bulb and in the prepyloric area.
