GASTROENTEROLOGY ARTICLE OF THE WEEK
January 28, 2010
Malfertheiner P, Chan FK, McColl KE. Peptic ulcer disease. Lancet 2009;374:1449-61
1. Pathophysiology leading to peptic ulceration in H. pylori infection include:
a. Induction of gastric metaplasia in the duodenum as a pre-requisite for
duodenal ulcer formation
b. Inhibition of somatostatin production by antral D cells leading to
hypergastrenemia and acidity
c. Inflammation of the proximal stomach leading to increased parietal cell mass
and hyperacidity
d. Resolution of duodenal gastric metaplasia after H. pylori eradication
e. Expression of the Vac-A gene in H. pylori increases risk of ulceration
True or False
2. Patients with H. pylori and duodenal ulcer tend to have the heaviest H. pylori infestation in the gastric antrum
3. Among persons with H. pylori infection, 35% to 40% will develop peptic ulceration
4. Low dose aspirin therapy does increase the risk of ulcers significantly
5. Proton-pump inhibitor therapy increases the severity of proximal gastric inflammation caused by H. Pylori
6. After eradication of H. pylori in a patient with gastric ulcers, PPI therapy should continue for 4-8 weeks.
7. Concomitant use of aspirin negates the “protective” effects of selective Cox-2 inhibitor therapy in reducing adverse GI events
8. Low dose aspirin may be less ulcerogenic than NSAID’s but increases risk for GI bleeding / GI blood loss
9. The use of corticosteroids alone increase the risk of ulcer disease
10. At the end of eradication therapy for H. pylori in a patient with DU, PPI therapy may be discontinued
11. Patients with one or two risk factor ulcer disease who need NSAID can receive either and NSAID + PPI or a Cox-2
12. Patients with cardiovascular contraindication to selective Cox-2 inhibitors who need NSAID’s, naproxen + PPI is the recommended therapy