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Helicobacter pylori and Peptic Ulcer Disease
The Key to Cure
- What is H. pylori?
- How common is H. pylori?
- What illness does H. pylori cause?
- What are the symptoms of ulcers?
- Who should be tested and treated for H. pylori?
- How is H. pylori infection diagnosed?
- What are the treatment regimes used for H. pylori?
- FDA-Approved Treatment Options
- Are there any long-term consequences of H. pylori infection?
- How do people get infected with H. pylori?
- What can people do to prevent H. pylori infection?
- What is the CDC doing to prevent H. pylori infection?
- How can I get more information about H. pylori
Helicobacter pylori (H. pylori) is a spiral-shaped bacterium that is found in the gastric mucous layer or adherent to the epithelial lining of the stomach. H. pylori causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers. Before 1982, when this bacterium was discovered, spicy food, acid, stress, and lifestyle were considered the major causes of ulcers. The majority of patients were given long-term medications, such as H2 blockers, and more recently, proton pump inhibitors, without a chance for permanent cure. These medications relieve ulcer-related symptoms, heal gastric mucosal inflammation, and may heal the ulcer, but they do NOT treat the infection. When acid suppression is removed, the majority of ulcers, particularly those caused by H. pylori, recur. Since we now know that most ulcers are caused by H. pylori, appropriate antibiotic regimens can successfully eradicate the infection in most patients, with complete resolution of mucosal inflammation and a minimal chance for recurrence of ulcers.
Approximately two-thirds of the world's population is infected with H. pylori. In the United States, H. pylori is more prevalent among older adults, African Americans, Hispanics, and lower socioeconomic groups.
Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children. Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. The role of H. pylori in non-ulcer dyspepsia remains unclear.
Approximately 25 million Americans suffer from peptic ulcer disease at some point in their lifetime. Each year there are 500,000 to 850,000 new cases of peptic ulcer disease and more than one million ulcer-related hospitalizations. The most common ulcer symptom is gnawing or burning pain in the epigastrium. This pain typically occurs when the stomach is empty, between meals and in the early morning hours, but it can also occur at other times. It may last from minutes to hours and may be relieved by eating or by taking antacids. Less common ulcer symptoms include nausea, vomiting, and loss of appetite. Bleeding can also occur; prolonged bleeding may cause anemia leading to weakness and fatigue. If bleeding is heavy, hematemesis, hematochezia, or melena may occur.
Persons with active gastric or duodenal ulcers or documented history of ulcers should be tested for H. pylori, and if found to be infected, they should be treated. To date, there has been no conclusive evidence that treatment of H. pylori infection in patients with non-ulcer dyspepsia is warranted. Testing for and treatment of H. pylori infection are recommended following resection of early gastric cancer and for low-grade gastric MALT lymphoma. Retesting after treatment may be prudent for patients with bleeding or otherwise complicated peptic ulcer disease. Treatment recommendations for children have not been formulated. Pediatric patients who require extensive diagnostic work-ups for abdominal symptoms should be evaluated by a specialist.
Several methods may be used to diagnose H. pylori infection. Serological tests that measure specific H. pylori IgG antibodies can determine if a person has been infected. The sensitivity and specificity of these assays range from 80% to 95% depending upon the assay used. Another diagnostic method is the breath test. In this test, the patient is given either 13C- or 14C-labeled urea to drink. H. pylori metabolizes the urea rapidly, and the labeled carbon is absorbed. This labeled carbon can then be measured as CO2 in the patient's expired breath to determine whether H. pylori is present. The sensitivity and specificity of the breath test ranges from 94% to 98%. Upper esophagogastroduodenal endoscopy is considered the reference method of diagnosis. During endoscopy, biopsy specimens of the stomach and duodenum are obtained and the diagnosis of H. pylori can be made by several methods: The biopsy urease test - a colorimetric test based on the ability of H. pylori to produce urease; it provides rapid testing at the time of biopsy. Histologic identification of organisms - considered the gold standard of diagnostic tests. Culture of biopsy specimens for H. pylori, which requires an experienced laboratory and is necessary when antimicrobial susceptibility testing is desired.
Therapy for H. pylori infection consists of 10 days to 2 weeks of one or two effective antibiotics, such as amoxicillin, tetracycline (not to be used for children <12 yrs.), metronidazole, or clarithromycin, plus either ranitidine bismuth citrate, bismuth subsalicylate, or a proton pump inhibitor. Acid suppression by the H2 blocker or proton pump inhibitor in conjunction with the antibiotics helps alleviate ulcer-related symptoms (i.e., abdominal pain, nausea), helps heal gastric mucosal inflammation, and may enhance efficacy of the antibiotics against H. pylori at the gastric mucosal surface. Currently, eight H. pylori treatment regimens are approved by the Food and Drug Administration (FDA) (Table 1); however, several other combinations have been used successfully. Antibiotic resistance and patient noncompliance are the two major reasons for treatment failure. Eradication rates of the eight FDA-approved regimens range from 61% to 94% depending on the regimen used. Overall, triple therapy regimens have shown better eradication rates than dual therapy. Longer length of treatment (14 days versus 10 days) results in better eradication rates.
FDA-approved treatment options
Omeprazole 40 mg QD + clarithromycin 500 mg TID x 2 wks, then omeprazole 20 mg QD x 2 wks
Ranitidine bismuth citrate (RBC) 400 mg BID + clarithromycin 500 mg TID x 2 wks, then RBC 400 mg BID x 2 wks
Bismuth subsalicylate (Pepto Bismol®) 525 mg QID + metronidazole 250 mg QID + tetracycline 500 mg QID* x 2 wks + H2 receptor antagonist therapy as directed x 4 wks
Lansoprazole 30 mg BID + amoxicillin 1 g BID + clarithromycin 500 mg TID x 10 days
Lansoprazole 30 mg TID + amoxicillin 1 g TID x 2 wks**
Rantidine bismuth citrate 400 mg BID + clarithromycin 500 mg BID x 2 wks, then RBC 400 mg BID x 2 wks
Omeprazole 20 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days
Lansoprazole 30 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days
*Although not FDA approved, amoxicillin has been substituted for tetracycline for patients for whom tetracycline is not recommended.
**This dual therapy regimen has restrictive labeling. It is indicated for patients who are either allergic or intolerant to clarithromycin or for infections with known or suspected resistance to clarithromycin.
Recent studies have shown an association between long-term infection with H. pylori and the development of gastric cancer. Gastric cancer is the second most common cancer worldwide; it is most common in countries such as Colombia and China, where H. pylori infects over half the population in early childhood. In the United States, where H. pylori is less common in young people, gastric cancer rates have decreased since the 1930s.
It is not known how H. pylori is transmitted or why some patients become symptomatic while others do not. The bacteria are most likely spread from person to person through fecal-oral or oral-oral routes. Possible environmental reservoirs include contaminated water sources. Iatrogenic spread through contaminated endoscopes has been documented but can be prevented by proper cleaning of equipment.
Since the source of H. pylori is not yet known, recommendations for avoiding infection have not been made. In general, it is always wise for persons to wash hands thoroughly, to eat food that has been properly prepared, and to drink water from a safe, clean source.
CDC, with partners in other government agencies, academic institutions, and industry, is conducting a national education campaign to inform health care providers and consumers of the link between H. pylori and stomach and duodenal ulcers. CDC is also working with partners to study routes of transmission and possible prevention measures, and to establish an antimicrobial resistance surveillance system to monitor the changes in resistance among H. pylori strains in the United States.
- NIH Consensus Development Conference. Helicobacter pylori in peptic ulcer disease. JAMA 272:65-69, 1994.
- Soll, AH. Medical treatment of peptic ulcer disease. Practice guidelines. [Review]. JAMA 275:622-629, 1996. [published erratum appears in JAMA 1996 May 1;275:1314].
- Hunt, RH. Helicobacter pylori: from theory to practice. Proceedings of a symposium. Am J Med 1996; 100 (5A) supplement.
- The American Gastroenterological Association, American Digestive Health Foundation, 7910 Woodmont Avenue, 7th floor, Bethesda, MD 20814, (301) 654-2055 telephone, (301) 654-5920 fax.
- The National Digestive Diseases Information Clearinghouse, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 2 Information Way, Bethesda, MD 20892-3570, (301) 654-3810 telephone.
- Hunt RH, Thompson ABR. Canadian Helicobacter pylori Consensus Conference. Can J. Gastroenterol 1998, 12(1):31-41.
- European Helicobacter pylori Study Group. Current European concepts in the management of H. pylori information. The Maastricht Consensus. Gut 1997; 41, 8-13.
For further information, contact:Health Communications Activity
Division of Bacterial and Mycotic Diseases
Coordinating Center for Infectious Diseases
Centers for Disease Control and Prevention
1600 Clifton Road, MS-A49
Atlanta, GA 30333