H pylori infection is associated with development of which malignancy
Ref Harrison 17/e p1858; Robbins 8/e p316,9/e p329 H. pylori infection and NSAID use are the primary underlying causes of PUD. The imbalances of mucosal defenses and damaging forces that cause chronic gastritis (Fig. 14-13) are also responsible for PUD. Thus, PUD generally develops on a background of chronic gastritis. Although more than 70% of PUD cases are associated with H. pylori infection, only 5% to 10% of H. pylori-infected persons develop ulcers. It is probable that host factors as well as variation among H. pylori strains determine the clinical outcomes. Gastric hyperacidity is fundamental to the pathogenesis of PUD. The acidity that drives PUD may be caused by H. pylori infection, parietal cell hyperplasia, excessive secretory responses, or impaired inhibition of stimulatory mechanisms such as gastrin release. For example, Zollinger-Ellison syn- drome, characterized by multiple peptic ulcerations in the stomach, duodenum, and even jejunum, is caused by uncon- trolled 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 cor- ticosteroids, which suppress prostaglandin synthesis and impair healing. Peptic ulcers are more frequent in persons with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism. In the latter two conditions, hypercalcemia stimulates gastrin pro- duction and therefore increases acid secretion. Finally, psy- chologic stress may increase gastric acid production and exacerbate PUD. H. pylori gastritis typically affects the antrum and is associ- ated with increased gastric acid production. The induced mucosa-associated lymphoid tissue (MALT) can transform into lymphoma.
MALTomas
Atherosclerosis
Sarcoma
Gastrointestinal stromal tumors
General anatomy