Helicobacter pylori is a Gram-negative bacterium that chronically infects the stomach of more than 50% of the human population, and represents the major cause of gastric cancer, gastric lymphoma, gastric autoimmunity and peptic ulcer diseases [1–4]. The International Agency for Research on Cancer classifies H. pylori as a human carcinogen for distal gastric cancer. Eradicating the bacterium, in high-risk populations, reduces the incidence of gastric cancer [5]. Likewise, antibiotic treatment leads to the regression of gastric MALT lymphoma [2]. H. pylori also contributes to other conditions, such as vitamin B12 and iron deficiencies, idiopathic thrombocytic purpura, and growth retardation in children [6].

Current guidelines indicate that the eradication of H. pylori infection is considered mandatory in patients with peptic ulcer and gastric malignancies, such as gastric adenocarcinoma and MALT lymphoma [6, 7]. Furthermore, it is recommended in patients with non-ulcer dyspepsia, especially in those with the evidence of macroscopic or microscopic mucosal abnormalities (erosions, intestinal metaplasia, atrophy), naïve non-steroidal anti-inflammatory drugs (NSAIDs) users, chronic NSAIDs users, first-degree relatives of gastric cancer patients as well as in unexplained iron deficiency anaemia, and idiopathic thrombocytopenic purpura. Low-dose aspirin (ASA) therapy is widely used in primary care because of the proved efficacy in both primary and secondary prevention of cardiovascular events [8]. A synergistic interaction between H. pylori infection and NSAIDs has been extensively documented although the benefits of H. pylori eradication in NSAIDs users are conflicting [6, 9–11]. H. pylori has been shown to increase, by almost seven times, the risk of upper gastrointestinal complications in chronic NSAIDs users [12, 13]. The relationship between H. pylori infection and NSAIDs in gastroduodenal pathology is complex. Since both NSAIDs and H. pylori can cause peptic ulcers, H. pylori eradication can only be expected to prevent the recurrence of H. pylori ulcers, and while it may also reduce the incidence of ulcers among those with both H. pylori and NSAID use, the effects will vary depending on the proportion with real H. pylori ulcers in the population studied [6].

Zullo et al. [14] designed a very interesting study (reported in the current issue) to assess the management of H. pylori infection in a very large cohort of chronic NSAID users in primary care clinical settings. H. pylori was being used only in a minority (less than 20%) of primary care patients receiving chronic NSAID therapy. H. pylori was eventually cured in two-third of the infected cases. The low alertness towards such H. pylori infection in these patients suggests a need for prompt implementation of current guidelines. Furthermore, the results obtained by Zullo et al. [14], other large meta-analysis studies, strongly support the concept that patients requiring long-term NSAIDs/ASA therapy should be tested and cured of the infection [9, 14, 15] because the cure of H. pylori infection contributes to the reduction of potential life-threatening gastrointestinal critical events (such as gastroduodenal bleeding) in primary care unstable patients.