Complicated peptic ulcer disease represents a considerable health burden worldwide. Perforation occurs in a minority of ulcers, but is associated with considerable morbidity and mortality. Demographic changes in populations have caused a shift in location, type and outcomes for perforated peptic ulcers. Unlike the intense investigations into ulcerogenic factors in general, including the role of Helicobacter pylori and increasingly low-dose aspirin drugs, little is known about factors contributing to perforation per se. The balance between acidity and protective and restorative factors is disturbed and modified by drugs, medications, smoking, alcohol, bacteria and fungi. Host genetics may play a role as well as variation in bacterial strains but also hitherto unknown factors that need warrants further investigative efforts. A lack of better understanding of perforation mechanisms needs to be remedied by revitalized research in emergency surgery. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. (C) 2016 Lippincott Williams & Wilkins, Inc.
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