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Peptic ulcers - Introduction

Description

An in-depth report on the causes, diagnosis, treatment, and prevention of stomach and gastrointestinal (GI) ulcers.

Alternative Names

Duodenal ulcers; Gastric ulcers; Helicobacter pylori; H. pylori

Introduction:

A peptic ulcer is an open sore or raw area that tends to develop in one of two places:

The lining of the stomach (gastric ulcer)
The upper part of the small intestine -- the duodenum (duodenal ulcer)

In the U.S., duodenal ulcers are three times more common than gastric ulcers.

A peptic ulcer is an open sore or raw area in the lining of the stomach (gastric) or the upper part of the small intestine (duodenal).

Ulcers average between one-quarter and one-half inch in diameter. They develop when digestive juices produced in the stomach, intestines, and digestive glands damage the lining of the stomach or duodenum.

The two important components of digestive juices are hydrochloric acid and the enzyme pepsin. Both substances are critical in the breakdown and digestion of starches, fats, and proteins in food. They play different roles in ulcers:

Hydrochloric acid. A common misperception is that excess hydrochloric acid, which is secreted in the stomach, is solely responsible for producing ulcers. Patients with duodenal ulcers do tend to have higher-than-normal levels of hydrochloric acid, but most patients with gastric ulcers have normal or lower-than-normal acid levels. Some stomach acid is important for protecting against H. pylori, the bacteria that causes most peptic ulcers. [Note: An exception is ulcers that occur in Zollinger-Ellison syndrome. This is a rare genetic condition in which very high levels of gastrin, a hormone that stimulates the release of hydrochloric acid, are secreted by tumors in the pancreas or duodenum.]
Pepsin. Pepsin is an enzyme that breaks down proteins in food. Because the stomach and duodenum are also composed of protein, they are susceptible to the actions of pepsin. Pepsin is, therefore, also an important factor in the formation of ulcers.

Click the icon to see an image of the stomach.

Fortunately, the body has a defense system to protect the stomach and intestine against these two powerful substances:

The mucus layer, which coats the stomach and duodenum, forms the first line of defense.
Bicarbonate, which the mucus layer secretes, neutralizes the digestive acids.
Hormone-like substances called prostaglandins help dilate the blood vessels in the stomach, to ensure good blood flow and protect against injury. Prostaglandins are also believed to stimulate bicarbonate and mucus production.

Disrupting any of these defense mechanisms makes the lining of the stomach and intestine susceptible to the actions of acid and pepsin, increasing the risk for ulcers.

Resources

http://digestive.niddk.nih.gov -- National Digestive Diseases Information Clearinghouse
www.gastro.org -- American Gastroenterological Association
www.acg.gi.org -- American College of Gastroenterology

References

Bertleff M, Helm JA, Bemelman WA, van der Ham AC, van der Harst E, Oei HI, et al. Randomized clinical trial of laparoscopic versus open repair of the perforated peptic ulcer: The LAMA Trial. World J Surg. 2009;33(7):1368-1373.

Chey WD, Wong BC. Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102(8):1808-1825.

Grainek IM, Barkun AN, Bardou M. Management of acute bleeding from a peptic ulcer. N Engl J Med. 2008;359(9):928-937.

Kim JI, Cheung DY, Cho SH, et al. Oral proton pump inhibitors are as effective as endoscopic treatment for bleeding peptic ulcer: a prospective, randomized, controlled trial. Dig Dis Sci. 2007;52(12):3371-3376.

Lanza FL, Chan FK, Quigley EM. Practice Parameters Committee of the American College of Gastroenterology. Guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol. 2009;104(3):728-738.

Luo J, Nordenvall C, Nyren O, et al. The risk of pancreatic cancer in patients with gastric or duodenal ulcer disease. Int J Cancer. 2007;120(2):368-372.

Malagelada J-R, KuipersMartin EJ, Blaser J. Acid Peptic Disease: Clinical manifestations, Diagnosis, Treatment, and Prognosis. In: Goldman: Cecil Medicine, 23rd ed. Philadelphia, PA: WB Saunders, 2007.

Mercer DW, Robinson EK. Stomach. In: Townsend: Sabiston Textbook of Surgery, 18th ed. Philadelphia, PA: WB Saunders, 2007.

Pietroiusti A, Forlini A, Magrini A, et al. Shift work increases the frequency of duodenal ulcer in H. pylori infected workers. Occup Environ Med. 2006;63(11):773-775.

Ramakrishnan K, Salinas RC. Peptic ulcer disease. Am Fam Physician. 2007;76(7):1005-1012.

Saif MW, Elfiky A, Salem RR. Gastrointestinal perforation due to bevacizumab in colorectal cancer. Ann Surg Oncol. 2007;14(6):1860-1869.

Taha AS, McCloakwy C, Prasad R, Bezlyak V. Famotidine for the prevention of peptic ulcers and oesophagitis in patients taking low-dose aspirin (FAMOUS): A phase III, randomized, double-blind, placebo-controlled trial. Lancet. 2009:doi: 10.1016/S0140-6736(09)61246-0.

Take S, Mizuno M, Ishiki K, et al. Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer disease. J Gastroenterol. 2007;42(suppl 17):21-27.

Reviewed last on: 7/17/2009
Reviewed by: Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

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