[Peptic ulcer and Helicobacter pyrlori. Results and consequences of its eradication]

Helicobacter pylori (Hp) a known pathogen of peptic ulcer disease (PUD), causes more than 90% of them when non steroidal anti-inflammatory agents (NSAID) are excluded. Prevalence of Hp is greater than 70% within some underdeveloped societies, but yet less than 1% suffer PUD. Such selectivity has been attributed to pathogenic differences of diverse Hp strains, their relative proportion in a given patient, but also to genetic host factors that favors colonization and different immunologic responses that end up in PUD in some, while gastritis is the only consequence in others. Other pathophysiologic factors, independent of Hp such as acid hypersecretion or duodenal bicarbonate hyposecretion may interplay with Hp to provoke PUD. Pepsinogen I levels are better predictors of PUD than Hp is in a given individual. PUD recurrence is less than 2% per year, although some controversies prevail whether Hp should be eradicated in patients requiring NSAID, since eradication does not prevent PUD, does not improves healing of existing ulcers nor decreases risk of bleeding. Even though, bleeding recurrence is less frequent when Hp has been treated. Prevalence of Hp is quite similar in bleeding PUD to that of general population of a given geographic area, Hp it is not a risk factor for this complication. Hp eradication in PUD causes reflux esophagitis in 25% of patients, and reflux medical control is far more difficult. Even worse hypergastrinemia produced by antisecretory agents is further increased under Hp infection, and their use over 1 year is accompanied by ECL hyperplasia in 30% of them. Thus Hp interplay and consequences are diverse and complex. Their knowledge is needed for proper selection of patients that need eradication.