Fig. 15.13 ) are also responsible for PUD. In the United States, NSAID use is becoming the most common cause of gastric ulcers as H. pylori infection rates are falling and low-dose aspirin use in the aging population is increasing. PUD may occur in any portion of the gastrointestinal tract exposed to acidic gastric juices but is most common in the gastric antrum and first portion of the duodenum. Peptic (acid-induced) injury may occur in the esophagus as a result of acid reflux (GERD) or acid secretion by ectopic gastric mucosa. Peptic injury in the small intestine may also be associated with gastric heterotopia, including that within a Meckel diverticulum.
PUD is common and is a frequent cause of physician visits worldwide. It leads to treatment of over 3 million individuals, 190,000 hospitalizations, and 5000 deaths in the United States each year. The lifetime risk for developing an ulcer is approximately 10% for males and 4% for females.
H. pylori infection and NSAID use are the primary underlying causes of PUD. More than 70% of PUD cases are associated with H. pylori infection and in these individuals PUD generally develops on a background of chronic gastritis. Because only 5% to 10% of H. pylori–infected individuals develop ulcers, it is probable that host factors as well as variation among H. pylori strains also contribute to the pathogenesis.
Gastric acid is fundamental to the pathogenesis of PUD. Hyperacidity may be caused by H. pylori infection, parietal cell hyperplasia, and excessive secretory responses. Insufficient inhibition of stimulatory mechanisms such as gastrin release may also contribute. For example, Zollinger-Ellison syndrome, characterized by multiple peptic ulcerations in the stomach, duodenum, and even jejunum, is caused by uncontrolled release of gastrin by a tumor and the resulting massive acid production.
Cofactors in peptic ulcerogenesis include chronic NSAID use, as noted; cigarette smoking, which impairs mucosal blood flow and healing; and high-dose corticosteroids, which suppress prostaglandin synthesis and impair healing. Peptic ulcers are more frequent in individuals with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism. In the latter two conditions, hypercalcemia stimulates gastrin production and thereby increases acid secretion.
MORPHOLOGYPepticulcersarefourtimesmorecommonintheproximalduodenumthaninthestomach.Duodenalulcersusuallyoccurwithinafewcentimetersofthepyloricvalveandinvolvetheanteriorduodenalwall.Gastricpepticulcersarepredominantlylocatedneartheinterfaceofthebodyandantrum.
Pepticulcersaresolitaryinmorethan80%ofpatients.Lesionslessthan0.3cmindiametertendtobeshallow,whereasthoseover0.6cmarelikelytobedeeper.Theclassicpepticulcerisaroundtooval,sharply punched-out defect (
Fig.15.15A ).Thebaseofpepticulcersissmoothandcleanasaresultofpepticdigestionofexudateandonhistologicexaminationiscomposedofrichlyvasculargranulationtissue(
Fig.15.15C ).Ongoingbleedingwithintheulcerbasemaycauselife-threateninghemorrhage.Perforation isacomplicationthatdemandsemergentsurgicalintervention.