Much controversy surrounds the interaction of Helicobacter pylori infection and the use of Aspirin (ASA) or non-aspirin nonsteroidal anti-inflammatory drugs (NANSAIDs). The issue is comprised of many components, best dealt with singly. In summary, the severity of drug-associated gastritis, but not its incidence or prevalence, is influenced by infection prior to ASA or NANSAID therapy. Furthermore, the severity of dyspeptic symptoms appears worse in infected drug users. Both Chemical and Helicobacter gastritis, by increasing neutrophils in the tissue, lead to ulcers, although the induction of prostaglandin synthesis by inflammation in some circumstances may also be mildly protective. More ulcers are found in Hp+ve than Hp-ve users of NSAIDS, but ulcers in the stomach may heal more easily with acid suppressive therapy in infected patients. Eradication of infection is beneficial in aspirin users and in those beginning NANSAID therapy. Adaptation to aspirin is confined to Hp-ve cases. However, in long-term users of NANSAIDs, H. pylori eradication does not appear to speed ulcer healing, reduce recurrence, or prevent complications. These are best achieved by long-term maintenance therapy with a proton-pump inhibitor drug.