Epidemiology And Etiology

Approximately, 25 million Americans are affected by PUD, with the lifetime prevalence estimated to be 12% in men and 10% in women. Annual direct and indirect costs associated with PUD in the United States are estimated to be more than $9 billion. Despite the widespread use of conventional anti-ulcer therapy that effectively reduces gastric acid secretion, ulcers frequently recur, with 1-year recurrence rates (after ulcer initial healing) estimated to range from 60% to 100%.1

H. pylori infection and NSAID use account for most cases of PUD. The relatively high incidence of PUD in the elderly may be due to higher NSAID use. Although hospitalizations related to PUD have decreased over the past two decades, the incidence of PUD-related complications such as bleeding and perforation remain unchanged.

In general, ulcers related to H. pylori infection more commonly affect the duodenum whereas ulcers related to NSAIDs more frequently affect the stomach (Fig. 18—1). However, ulcers may be found in either location from either cause. GU tend to occur much later in life than DU, with the peak incidence of GU occurring in patients over 60 years of age. Malignancy is more commonly found with GU than DU.

FIGURE 18-1. Anatomic structure of the stomach and duodenum and most common locations of gastric and duodenal ulcers. (From Ref. 37.)

Helicobacter pylori

Since its discovery nearly 25 years ago, the role of H. pylori in PUD has been increasingly recognized, and it is now one of the most common causes of PUD.3 While H. pylori causes gastritis in all infected patients, only a small proportion (less than 20%) of patients actually develop symptomatic PUD.

H. pylori normally resides in the human stomach and is transmitted via the fecal-oral route or through ingestion of fecal-contaminated water or food. Infection with H. pylori is more common in developing countries because of crowded conditions and the presence of contaminated food and water. H. pylori colonization does not necessarily reflect an active infection since the organism can attach itself to the gastric epithelium without invading cells. Cellular invasion by H. pylori is necessary for an active infection, which is usually asymptomatic and leads to chronic active gastritis.


Duodenal ulcer

FIGURE 18-1. Anatomic structure of the stomach and duodenum and most common locations of gastric and duodenal ulcers. (From Ref. 37.)

esophageal spnincter

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