Since the first description of H. pylori infection of the gastric mucosa by Warren and Marshall [1], the bacterium has progressively gained importance and, nowadays, it is recognized as the main pathogenetic factor in chronic gastritis, ulcer disease and gastric neoplasms. In recent years, there is increasing evidence of an association of H. pylori gastric infection with various extragastric diseases. H. pylori infection induces changes in the physiology of the upper gastrointestinal tract. Its effects on exocrine pancreatic physiology, as well as on the onset and clinical course of exocrine pancreatic diseases, have been poorly investigated up to now. However, they are possible since the bacterium induces changes in the gastrointestinal physiology and because the exocrine pancreas interacts strictly with the stomach and the duodenum.