H. pylori gastritis and gastric acid closely interact. In H. pylori-positive patients, profound acid suppressive therapy induces a corpus-predominant pangastritis, which is associated with accelerated corpus gland loss and development of atrophic gastritis. Both corpus-predominant and atrophic gastritis have been associated with an increased risk of development of gastric cancer. H. pylori eradication leads to resolution of gastritis and may induce partial regression of pre-existent gland loss. H. pylori eradication does not aggravate GERD nor does it impair the efficacy of proton pump inhibitor maintenance therapy for this condition. This is the background of the advise within the European guidelines for the management of H. pylori infection to offer an H. pylori test and treat policy to patients who require proton pump inhibitor maintenance therapy for GERD. As such a policy fully reverses H. pylori pangastritis even in patients who have been treated for years with proton pump inhibitors, there is no need to eradicate H. pylori before the start of proton pump inhibitors. In fact, the somewhat slower initial response of H. pylori-negative GERD patients to proton pump inhibitor therapy and the fact that many GERD patients will only require short-term therapy suggests to first start the proton pump inhibitor, and only test and treat when maintenance therapy needs to be prescribed. Such considerations prevent the persistent presence of active corpus-predominant gastritis in proton pump inhibitor-treated reflux patients without impairing the clinical efficacy of treatment.A decade ago, the role of Helicobacter pylori in chronic gastritis and peptic ulcer disease had become recognized, and further research had revealed that chronic H. pylori gastritis predisposed to atrophic gastritis and gastric cancer. This led to the recognition by the WHO that H. pylori was a class I carcinogen, i.e. a carcinogen beyond doubt (International Agency for Research on Cancer 1994). This classification strongly stimulated further research into the interaction between H. pylori and its host, among others into factors which modulate the severity of H. pylori gastritis and the risk of long-term complications. This research focused in subsequent years on three topics, respectively related to bacterial virulence factors, host genetics, and gastric acid secretion. The message for all three factors was similar, i.e. patients with more severe gastritis had a higher risk of developing long-term complications. This message was well accepted in relation to bacterial virulence factors and host genetics, but it evoked much controversy and debate in relation to acid secretion. The main reason for this was that gastric acid secretion can in contrast to host genetics and bacterial virulence be influenced, and thus the discussion involved acid suppressive therapy. A reduction of gastric Author for correspondence: Ernst J. Kuipers, Department of Gastroenterology and Hepatology, Erasmus University Medical Center, P.O. Box 2040, 3000 CA Rotterd...