SUMMARYThere is general agreement thatHelicobacter pylorieradication is indicated in all infected patients with duodenal ulcer disease and is probably indicated in all infected patients with gastric ulcer disease. However, translation of treatment recommendations into practice leads to some difficult clinical decisions. Three of the more perplexing questions are whether or not all patients with dyspepsia andH. pylorishould be treated, whether or not a definitive diagnosis of ulcer should be established by an invasive method, and whetherH. pylorieradication is sufficient to prevent recurrence of bleeding ulcers, especially in patient groups that have a high frequency of nonsteroidal anti‐inflammatory drug (NSAID) use. Another common problem is the question of whether or not to establish the success of an eradication regimen in an individual patient and the choice of method to obtain this information. There is also an obvious need to develop better antimicrobial regimens aimed specifically atHelicobacter pylori.At the basic level, almost nothing is known about the mechanisms by whichH. pyloriproduces peptic ulcer in 10–20% of infected patients while producing gastritis in all infected subjects. There is good evidence that host factors, including intrinsic rate of acid secretion, family history and smoking are independent additive risk factors for ulcer. Ingestion of NSAIDs appears to be an independent and separate risk factor. There is evidence that strains ofH. pylorithat lack certain genetic markers may have a reduced likelihood of causing ulcers, but the‘ulcer’ marker is present in the majority of infected subjects without ulcer. One goal of research inH. pylori‐infected subjects should be to identify those without ulcer who are at high risk of developing ulce