Western countries have seen a progressive decline of H. pylori prevalence as well as an increasing Selleckchem Ibrutinib use of NSAIDs and aspirin, the latter mainly prescribed for cardiovascular protection [2,3]. In addition, a novel entity – so-called idiopathic ulcer – has emerged, where PUD does not appear to be related with either H. pylori or NSAIDs [4]. Worldwide reported prevalence of idiopathic PUD ranges from 4% to 40%, with relatively high rates in American and Asian studies [5,6], and a low prevalence in Europe [7,8]. A UK study of 3923 cases of uncomplicated PUD found that

the prevalence of idiopathic PUD had increased over time from 5% in 1997 to 12% in 2005, while the proportion of H. pylori-positive cases decreased from 35% to 29% [9]. However, it should be noted that H. pylori status was not assessed in over 60% of patients in this study, casting some doubt on the reliability of these results [9]. In an endoscopic study in the US, PUD was diagnosed in 14 (5.6%) of 251 patients, and H. pylori infection was detected in only one patient, while six patients were NSAID users, giving a prevalence of idiopathic PUD of 50% (7 of 14) [10]. However, as many as 44.6% of the enrolled patients was taking either a proton pump inhibitor (PPI) or a H2-blocker at the time of endoscopy,

which could have confounded detection of both ulcers and H. pylori [10]. In India, H. pylori infection was not detected in 52 (40.6%) of 128 PUD patients without NSAID use [11]. In contrast, Metabolism inhibitor in an Italian study [12], only 4% of 300 consecutive patients with PUD were both H. pylori and NSAIDs use negative, while H. pylori was the only factor in 62.3% of cases, NSAIDs in 22%, and both factors were present in the remaining 11.7% of cases. The reasons for such

geographic discrepancy remain unclear, but varying prevalence of H. pylori infection in the general population may play a role, as well as possible surreptitious use of NSAIDs Metalloexopeptidase and aspirin. Also, the diagnostic procedures used (histology, rapid urease test, etc.) for H. pylori assessment and adequate interruption (for at least 2 weeks) of PPI therapy before testing could have played a role [13]. Irrespective of etiology, both incidence and prevalence of PUD have been dramatically decreasing in developed countries in the last decades. In a systematic review including studies that collected data up to early 2000 [14], the annual incidence of PUD was estimated to range from 0.15% to 0.40% according to physician administrative data, and from 0.04% to 0.17% according to hospitalization data. Similarly, the annual prevalence of PUD ranged from 0.12% to 1.50% and from 0.10% to 0.19%, on physician- and hospitalization-based data, respectively. Moreover, all studies consistently registered a decrease in both incidence and prevalence of PUD over time [14].