An in-depth report on the causes, diagnosis, treatment, and prevention of stomach and gastrointestinal (GI) ulcers.
Duodenal ulcers; Gastric ulcers; Helicobacter pylori; H. pylori
Most people with severe ulcers experience significant pain and sleeplessness, which can have a dramatic and adverse impact on their quality of life.
Peptic ulcers caused by H. pylori or NSAIDs can be very serious if they cause hemorrhage or perforate the stomach or duodenum. Up to 15% of people with ulcers experience some degree of bleeding, which can be life-threatening. Ulcers that form where the small intestine joins the stomach can swell and scar, resulting in a narrowing or closing of the intestinal opening. In such cases, the patient will vomit the entire contents of the stomach, and emergency treatment is necessary.
Complications of peptic ulcers cause an estimated 6,500 deaths each year. These figures, however, do not reflect the high number of deaths associated with NSAID use. Ulcers caused by NSAIDs are more likely to bleed than those caused by H. pylori.
Because there are often no GI symptoms from NSAID ulcers until bleeding begins, doctors cannot predict which patients taking these drugs will develop bleeding. The risk for a poor outcome is highest in people who have had long-term bleeding from NSAIDs, blood clotting disorders, low systolic blood pressure, mental instability, or another serious and unstable medical condition. Populations at greatest risk are the elderly and those with other serious conditions, such as heart problems.
H. pylori is strongly associated with certain cancers. Some studies have also linked it to a number of non-gastrointestinal illnesses, although the evidence is inconsistent.
Stomach Cancers. Stomach cancer, also called gastric cancer, is the second most common type of cancer worldwide. In developing countries where the rate of H. pylori is very high, the risk of stomach cancer is six times higher than in the U.S. Evidence now suggests that H. pylori may be as carcinogenic to the stomach as cigarette smoke is to the lungs.
Eradication of H. pylori may reduce the risk of stomach cancer, but not eliminate it. The patient's risk depends on how much damage the mucus membranes sustained before H. pylori treatment was started. The damage can be measured during an endoscopy.
Infection with H. pylori promotes a precancerous condition called atrophic gastritis. The process most likely starts in childhood. It may lead to cancer through the following steps:
When H. pylori infection starts in adulthood it poses a lower risk for cancer, because it takes years for atrophic gastritis to develop, and an adult is likely to die of other causes first. Other factors, such as specific strains of H. pylori and diet, might also influence the risk for stomach cancer. For example, a diet high in salt and low in fresh fruits and vegetables has been associated with a greater risk. Some evidence suggests that the H. pylori strain that carries the cytotoxin-associated gene A (CagA) may also be a particular risk factor for precancerous changes.
People with duodenal ulcers caused by H. pylori appear to have a lower risk of stomach cancer, although scientists do not know why. It may be that different H. pylori strains affect the duodenum and the stomach. Or, the high levels of acid found in the duodenum may help prevent the spread of the bacteria to critical areas of the stomach.
Other Diseases. H. pylori has also been weakly associated with other nonintestinal disorders, including migraine headache, Raynaud's disease (which causes cold extremities), and skin disorders such as chronic hives.
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.
© 2011 University of Maryland Medical Center (UMMC). All rights reserved.
UMMC is a member of the University of Maryland Medical System,
22 S. Greene Street, Baltimore, MD 21201. TDD: 1-800-735-2258 or 1.866.408.6885