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Epidemiology and etiology of peptic ulcer disease

Section Editor
Mark Feldman, MD, MACP, AGAF, FACG
Deputy Editor
Shilpa Grover, MD, MPH


Peptic ulcers are defects in the gastrointestinal mucosa that extend through the muscularis mucosae (picture 1). They persist as a function of the acid or peptic activity in gastric juice. Peptic ulcer disease (PUD) is an important cause of morbidity and health care costs; estimates of expenditures related to work loss, hospitalization, and outpatient care (excluding medication costs) are $5.65 billion per year in the United States [1].

The natural history of peptic ulcer ranges from resolution without intervention to the development of complications with the potential for significant morbidity and mortality, such as bleeding and perforation. (See "Overview of the complications of peptic ulcer disease".)


The time trends in the epidemiology of peptic ulcer disease (PUD) reflect complex, multifactorial etiologies. Peptic ulcers were rare before the 1800s. The pathology of gastric ulcers (GUs) was first described in 1835 [2]; during the late 1800s the prominent form was GUs in young women. Duodenal ulcers (DUs) were rare until about 1900 and then became a prevalent condition during the first half of the 20th century. However, in developed countries the mortality from peptic ulcer disease has fallen dramatically for birth cohorts born after the turn of the 20th century [3].

As noted above, it is now evident that the epidemiology of peptic ulcer disease largely reflects environmental factors, primarily Helicobacter pylori infection, nonsteroidal anti-inflammatory drug (NSAID) use, and smoking. However, these environmental factors do not tell the whole story of the time trends and the birth-cohort effect for peptic ulcer disease. In particular, H. pylori was a prevalent human infection well before the late 1800s, so that this infection per se cannot explain the rise in ulcer prevalence and shift from GUs to DUs [4].

The influence of environmental factors on the pattern of gastritis may be a key variable in these birth-cohort effects. At the end of the 19th century (and currently in many developing countries) H. pylori infection was characterized by pangastritis involving the gastric antrum and body and leading to acid hyposecretion, which predisposed to gastric cancer and GUs [4-7]. In contrast, DUs are associated with antral-predominant gastritis that spares the acid-secreting body, but is negatively associated with more or severe body gastritis and with gastric cancer [8]. The reason is that DUs require acid secretion to be preserved, which cannot be achieved in the face of moderate body gastritis, whereas gastric cancer is associated with hypochlorhydria.


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Literature review current through: Apr 2016. | This topic last updated: Apr 22, 2014.
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