**2. Pathophysiology of peptic ulcer and** *H. pylori* **infection**

The pathophysiology of the gastric ulcers is characterized by the reduction of acid secretion, chronic gastritis, duodenogastric reflux of bile and pancreatic juice; on the other hand, in the duodenal ulcers there are elevation of gastric acid secretion, increase of parietal cell mass, and duodenal acid/pepsin charge. The identification of *H. pylori* infection as leading cause of peptic ulcer has completely changed the knowledge of the disease. Briefly we can believe that in the general population, the prevalence of the *H. pylori* infection as cause of peptic ulcer is very high, over 90% of patients with duodenal ulcer and 75% circa of patients with gastric ulcer. Furthermore, the *H. pylori* can be found in the gastroduodenal tract without disease. Usually the *H. pylori* is present in the patients with chronic gastritis that can develop in atrophic gastritis. The treatment therapies of *H. pylori* infection have been currently performed in the last decades and have shown effective, high recovery rate in peptic ulcer disease [9]. The usual way of the diagnosis is by endoscopic examination, and the medical therapy is currently effective. The complications of peptic ulcers, as bleeding, perforation, outflow obstruction usually require the endoscopic or radiological interventions or in some cases surgical procedures. The *H. pylori* causes damage, injury within the gastroduodenal mucosa followed by inflammatory response with mucosal ulceration. The *H. pylori*, in the gastric lumen, develops defense mechanism with production of urease enzyme, conversion of urea into ammonia and carbon dioxide, gastric acid tamponade, decreasing adverse gastric acidity. The alkalinization of the gastric setting causes decrease of somatostatine production, reduction of gastrin secretion, restriction. In summary, the disruption of secretory balance of gastrin is followed by parietal cell hyperplasia and rise of gastrinemia and gastric acidity [10]. The non-steroidal anti-inflammatory drugs (NSAIDs) and acetylsalicilic acid (ASA) accomplish peptic ulcers by local and systemic actions. These drugs, as acid, develop on gastroduodenal mucosal cells, cytotoxic action, and damage cell proliferation. The systemic action of NSAIDs develops by prevention of gastric prostaglandin output and its protective action versus mucosal damage of acydity by increase of mucus and bicarbonate production and increment of mucosal blood perfusion [11].

### **2.1 Briefly clinical appearance of uncomplicated peptic ulcer**

Most evident symptom is the epigastric pain. This symptom can show a characteristic temporal cadency: the pain becomes worse in gastric ulcer after eating, but, on the contrary, it decreases over a period of time in duodenal ulcer after taking some meal. This traditional symptomatological distinction between gastric and duodenal ulcer is no longer the evident clinical data. Often the epigastric pain can be radiated to the back and linked to dyspepsia with the symptoms such as nausea, gastroduodenal reflux, heartburn, belching, etc. The diagnostic program for uncomplicated peptic ulcer encompasses gastroduodenal endoscopy as first step. In the gastric ulcer it is necessary to complete the examination with biopsy of the lesion for the risk of malignancy; endoscopy will be repeated, also with biopsy if it needs, to check for healing after the therapy. In the duodenal ulcer biopsies and further endoscopies are less required. In the diagnosed or suspected peptic ulcer, the test for *H. pylori* is routinely performed as mucosal biopsy for histological and microbiological control or with urease test [12].
