TY - JOUR
AU - Laine, Loren
AB - ObjectiveTo develop practical guidelines for the treatment of patients with suspected and documented Helicobacter pylori–related gastroduodenal diseases.MethodsA panel of physicians with expertise in H pylorireviewed, critically appraised, and synthesized the literature on assigned topics and presented their overviews to the panel. Consensus was obtained in controversial areas through discussion.Results and ConclusionsThe panel recommended testing for H pyloriin patients with active ulcers, a history of ulcers, or gastric mucosa-associated lymphoid tissue lymphomas. Young, otherwise healthy patients with ulcerlike dyspepsia and those with a family history or fear of gastric cancer may also undergo H pyloritesting. Nonendoscopic methods are preferred for H pyloridiagnosis. Dual medication regimens should not be used for therapy; twice-daily triple therapy with a proton pump inhibitor or ranitidine bismuth citrate, clarithromycin, and amoxicillin for 10 to 14 days is an appropriate therapy. Posttreatment assessment of H pyloristatus using urea breath testing should be considered in patients with a documented history of ulcer disease or with persistent symptoms.AN ESTIMATED 30% to 40% of the US population is infected with Helicobacter pylori.Infection with this spiral, urease-producing organism causes histological gastritis in all those infected, is the major cause of peptic ulcer disease, and is an important risk factor for the development of gastric adenocarcinoma and lymphoma.Helicobacter pylorigastritis is found in up to 95% of patients with duodenal ulcers and 80% of patients with gastric ulcers in some parts of the world.In the United States, the percentage is closer to 75%, perhaps reflecting a larger role for nonsteroidal anti-inflammatory drug–induced ulcer disease.In individuals with H pyloriinfection, the estimated lifetime risk for peptic ulcer disease is approximately 15%.Infection with H pyloriincreases the risk for gastric adenocarcinoma up to 9-fold as determined by a meta-analysis of 3 nested case-control studies.Given these findings, the International Agency for Research on Cancerclassified H pylorias a group 1 (a definite cause of cancer in humans) carcinogen.Helicobacter pylori–related peptic ulcer disease significantly impacts patient quality of life and functional status. In a 1989 National Health Interview Surveyof 41,457 individuals, up to 25% of those with a recent ulcer reported being in poor health, incapable of major activity, restricted in daily activity, unable to perform work, or confined to bed for more than 7 days during the previous 12 months.The overall economic impact of H pyloriinfection is staggering. It is estimated that the direct costs of treating H pylori–related diseases and associated complications and lost productivity is $3.0 to $5.6 billion annually.Studieshave documented that cure of H pyloriinfection in patients with peptic ulcers is associated with a reduction in ulcer recurrence and, in many patients, obviation of maintenance antisecretory therapy. In addition, cure of H pyloriinfection may produce regression or resolution of low-grade gastric mucosa-associated lymphoid tissue lymphomas.Given the potential benefits of eradication of H pylori, a group of gastroenterologists and primary care physicians met to critically appraise and synthesize the current literature on H pyloriinfection to develop practical guidelines for diagnosis and treatment of patients with H pylori–related diseases.WHO SHOULD BE TESTED FOR H PYLORI?Tests designed to detect H pylorishould be performed only if the result will affect patient treatment. Specifically, H pyloridiagnostic testing should be ordered only if a decision has been made to treat patients who have a positive result.The clinical superiority and cost benefits of H pyloritesting of patients with newly diagnosed (by endoscopy or radiography) gastric or duodenal ulcer has been well studied.Given the strong association between H pyloriinfection and ulcer disease, patients with a history of ulcer disease who are currently receiving maintenance antisecretory therapy should also be tested for H pyloriinfection.In addition, decision and cost-benefit analyses support nonendoscopic diagnostic testing of young, otherwise healthy patients with symptoms of ulcerlike dyspepsia.Finally, patients with mucosa-associated lymphoid tissue lymphoma should be tested and treated.The role of testing for H pyloriinfection in individuals receiving nonsteroidal anti-inflammatory agents is controversial.Decision analysessuggest that screening for H pylorito prevent gastric cancer may also be cost-effective. In a study by Parsonnet and colleagues,if H pylorieradication prevented only 30% of attributable cancers, screening the entire US population at age 50 years would cost $1 billion—an amount similar to the estimated costs of colorectal screening—and provide a cost-benefit ratio of $25,000 per year of life saved. If screening were performed in high-risk populations such as Japanese Americans, H pyloricure would only have to reduce the risk of gastric cancer by 5% to be cost-effective at the benchmark of $50,000 per year of life saved. Although these data are compelling, no controlled clinical trials have been performed and no study has documented that eradication of H pyloriwill decrease the risk of developing gastric cancer.Therefore, routine population-based screening for H pyloricannot be recommended at this time. On the other hand, it is rational clinical behavior to screen individuals who come to a physician with a fear or strong family history of gastric adenocarcinoma.METHODS OF H PYLORIDETECTIONMethods used to detect H pyloriare typically referred to as endoscopic and nonendoscopic, with each having its advantages and disadvantages based on a patient's clinical history and current presentation.Endoscopic methods involve assessing several gastric biopsy samples for the presence of H pyloriby histological examination, urease activity, or culture.Of these assessment methods, histological examination is considered the reference standard. Use of special stains such as Giemsa or "Genta" stain may make identification of the organism easier on histological examination.Assessment of the biopsy sample for urease activity (rapid urease test) is a highly sensitive (approximately 90%) and specific (approaching 100%) method of H pyloridetection.A limitation to the use of urease testing is in patients receiving proton pump inhibitors (PPIs) or high-dose histamine2receptor antagonists (H2RAs), which might decrease H pyloridensity and consequently urease activity, thereby producing a false-negative result.Culturing of H pyloriis generally not used in establishing a primary diagnosis because of the potential for false-negative results due to errors in specimen acquisition, storage, or transportation and its time-consuming nature (ie, requires up to 2 weeks for growth to occur).The performance of culture is useful for the determination of antibiotic resistance, especially in patients who continue to be positive for H pyloriafter an initial treatment regimen.Helicobacter pyloridetection by nonendoscopic methods such as blood antibody detection tests, urea breath tests (UBTs), and the recently approved assay for the detection of H pyloriantigen in stool specimensis indicated in clinical situations in which endoscopy is not indicated. Unlike blood antibody detection methods, UBT and fecal antigen detection denote active H pyloriinfection.Antibody tests to detect IgG antibodies to H pyloriare less expensive and more convenient to use than UBTs but are somewhat less accurate.Antibody tests can now be done in the office setting on fingerstick whole blood specimens, with results obtained within 10 minutes. Antibody testing is commonly used in the evaluation of dyspeptic patients before or in place of endoscopy. Because antibody titers often take many months to decrease after successful treatment and remain positive in many patients for years, blood antibody testing (eg, serologic testing) is less useful for the monitoring of posttreatment H pyloristatus.The UBT is a measure of current H pyloriinfection, relying on H pyloriurease to hydrolyze urea labeled with radioactive carbon (13C or 14C) and produce isotopically labeled carbon dioxide in the breath. As with biopsy-based rapid urease tests, there is the potential for false-negative UBT test results in individuals receiving antisecretory agents such as PPIs or high-dose H2RAs, antimicrobial agents, or bismuth-containing compounds, which reduce H pyloridensity.Therefore, UBT should be avoided in those who have received bismuth or antibiotic drugs within the previous 4 weeks or antisecretory agents within the previous 2 weeks.Stool antigen testing has emerged as a rapid, nonendoscopic method of H pyloridetection. A recently published studyfound that stool antigen testing is highly sensitive and specific in the detection of H pyloriin patients with dyspepsia and in those who have completed an H pylorieradication regimen. In the diagnosis of H pyloriinfection, the stool antigen detection method was highly sensitive (80%-100%) and comparable to that of the UBT (84%-100%). Stool antigen detection performed 4 weeks after completion of an H pylorieradication regimen had a sensitivity of 90%, a specificity of 95%, and a negative predictive value of 98%, rates that were comparable to those obtained with 13C UBT.Although the high rates of sensitivity and specificity with the stool antigen test in patients enrolled in the study by Vaira et alare promising, several other investigators found a high rate of false-positive results in patients tested 4 weeks after completion of anti–H pyloritreatment.CHOICE OF H PYLORIDETECTION METHOD BY CLINICAL SITUATIONNew-Onset Peptic UlcerPatients with a newly established diagnosis of ulcer disease made by endoscopy or radiography should have as their initial diagnostic test a rapid urease test or a serum antibody test, respectively. If the results are positive, the patient should be treated with an effective H pylorieradication regimen (ie, antimicrobial agents plus an antisecretory agent). If the initial test results are negative, H pyloristatus should be confirmed by another test given the importance this knowledge will have on future therapy. In the case of an endoscopically documented ulcer, this confirmation could be by histological examination, blood antibody detection, UBT, or stool antigen test. In patients whose ulcer is found by radiographic means, a UBT or stool antigen test should be done to confirm the patient's H pyloristatus. In either scenario, if the confirmatory test result is also negative, the patient's ulcer should be treated in standard fashion (eg, with a PPI or H2RA) and other causes for ulcer disease should be considered. If the confirmatory test result is positive, suggesting that the initial test was falsely negative, the patient should be treated with an effective anti–H pyloriregimen.History of Peptic Ulcer DiseaseAll patients who are currently receiving antisecretory agents, who have a history of uncomplicated ulcer disease documented by endoscopy or radiography, or who have a self-reported history of ulcer disease should be tested for H pyloriinfection using nonendoscopic detection methods. If the results are negative, use of the maintenance antisecretory drug can be discontinued if the sole indication for its use was history of peptic ulcer disease. Negative H pyloristatus can be confirmed by a UBT at least 2 weeks after cessation of therapy or by stool antigen detection at least 4 weeks after therapy cessation in objectively diagnosed patients and on symptom recurrence in clinically diagnosed patients. The rationale for the difference in approach relates to a greater probability that patients with objectively diagnosed disease will be infected than will patients without such documentation.DyspepsiaPatients with new-onset dyspepsia who are 50 years and younger and who have no alarm symptoms suggestive of underlying malignancy (eg, bleeding, weight loss, anemia, or early satiety) should undergo H pyloriantibody testing. Alternatively, these patients may be tested using the UBT or stool antigen detection. Patients undergoing H pyloritesting by UBT should not have ingested PPIs or high-dose H2RAs within the previous 2 weeks or antimicrobial agents within the previous 4 weeks. If the test results are positive, these patients should be offered H pylorieradication therapy, the rationale being that some of these individuals will have active ulcer disease and benefit from therapy. A proportion of those who do not have an ulcer (ie, functional dyspepsia) may also benefit from eradication of H pyloriand should also be at lower risk for development of gastric adenocarcinoma.Patients with new-onset dyspepsia who are older than 50 years or those of any age who have alarm symptoms should undergo upper endoscopy. If objective disease is found (ie, malignancy or ulcer disease) during endoscopy, H pyloriinfection should be detected by rapid urease testing of biopsy specimens. Patients who are positive for H pylorishould have their infection treated within the context of the clinical diagnosis. If the rapid urease test results are negative, H pyloristatus can be confirmed using antibody testing or histological examination. Alternatively, a UBT can be used to confirm H pyloristatus.TREATMENT OF H PYLORIINFECTIONNumerous regimens designed to cure H pyloriinfection have been evaluated and reported in the literature. Most regimens combine 1, 2, or 3 antibiotic agents (including bismuth compounds) with an antisecretory agent. Use of antisecretory agents combined with antimicrobial drugs increases the H pylorieradication rate (probably because an increase in the pH of the stomach increases the efficacy of some antimicrobial agents).In addition, PPIs have been foundto have intrinsic in vitro inhibitory activity against H pylori. The use of antisecretory therapy also seems to hasten relief of ulcer symptoms.No therapy is 100% effective for H pyloriinfection. However, several regimens have been devised that attain cure rates between 80% and 90%. These regimens consist of twice-daily triple therapy with a PPI or ranitidine bismuth citrate along with 2 antimicrobial agents such as clarithromycin and either amoxicillin or metronidazole.Classic bismuth-based triple therapy (bismuth subsalicylate, metronidazole, and tetracycline all given 4 times a day) achieves eradication rates of approximately 80% in the United States; the eradication rate potentially can be increased by addition of a PPI.The major concern regarding bismuth-based triple therapy relates to patient compliance because of the complexity of the regimen. Currently available dual therapies are not recommended for treatment of H pyloriinfection.Factors that significantly affect H pyloricure rate are patient compliance with the regimen, duration of therapy, and presence of antimicrobial resistance. Regardless of the regimen selected to treat H pyloriinfection, patients should be advised that full treatment compliance is necessary to maximize their potential for infection cure. Despite the results of numerous European studiesthat suggest that 7 days of triple therapy is sufficient, clinical trialsperformed in the United States have found that the highest rates of cure are associated with treatment durations of 10 to 14 days. Therefore, we recommend that PPI or ranitidine bismuth citrate–based triple therapy be administered for 10 to 14 days.Primary resistance to metronidazole therapy is common, 28% to 39% in the United States.The rate of clarithromycin-resistant strains of H pyloriis approximately 11%, and amoxicillin- or tetracycline-resistant strains have been reported only rarely.However, after failed treatment with metronidazole or clarithromycin, resistance to these agents must be assumed if susceptibility testing is not available.FOLLOW-UP OF H PYLORITHERAPYEvaluation of patients after completion of H pyloritherapy is helpful in determining the patient's future clinical course. Duodenal ulcers recurred in 6% of patients cured of infection compared with 67% of those who remained positive for H pylori.Similar findingswere noted in patients with gastric ulcers: ulcer recurrence after treatment occurred in 4% of cured patients and 59% of those who continued to harbor H pylori.Patient symptoms after H pyloritherapy do not always correlate with eradication success or failure. Relief of dyspepsia does not always suggest H pyloricure, although 2 studiesfound that persistence of certain ulcer-related symptoms (ie, nausea, epigastric discomfort, and ulcer pain) were predictive of continued infection. In one study,symptoms or their absence were highly sensitive and specific for confirming eradication 6 months after treatment. However, the authors caution that symptom-based assessment should not be used to assess treatment outcome in high-risk patients. Conversely, continued symptoms do not always denote treatment failure. Therefore, follow-up and confirmatory testing might be useful in determining a patient's response to treatment and risk of ulcer recurrence.Nonendoscopic methods (eg, UBT) are recommended for confirming H pylorieradication after completion of therapy if such confirmation is deemed necessary.A UBT should be performed no sooner than 4 to 6 weeks after completion of H pyloritherapy. Use of PPIs or high-dose H2RAs should be discontinued for at least 2 weeks before administration of the UBT.A recent studyfound stool antigen detection to be a reliable method of confirmatory testing when performed 4 weeks after treatment. However, some studieshave found a high rate of false-positive results using stool antigen detection 4 weeks after treatment.Antibody testing is less useful in the immediate evaluation of posttreatment response because high levels of antibodies to H pyloriremain for variable and extended periods.However, for an individual more than a year after therapy, seroconversion is a reliable indicator of successful eradication.If endoscopy is clinically indicated (ie, to confirm ulcer healing) after treatment, the clinician should obtain multiple biopsy specimens from the gastric body and antrum for histological examination and urease testing to exclude persistent infection.Findings of a recent studysuggest that patients have a desire to know their H pyloristatus after completion of an H pylorieradication regimen. However, economic factors might limit the utility of performing confirmatory testing in all patients. Follow-up testing to confirm eradication should be performed routinely in all patients with a confirmed diagnosis of new ulcer disease or a documented history of complicated ulcer disease. Patients with a reported history of uncomplicated ulcer disease not documented by endoscopy or radiography and those with a history of dyspepsia should have follow-up testing if symptoms recur. Confirmatory testing may also be performed in patients in whom their unknown H pyloristatus is causing excess worrying or loss of sleep.MANAGEMENT OF PERSISTENT H PYLORIINFECTION AFTER TREATMENTPatients who remain positive for H pyloriafter completion of an effective anti–H pyloriregimen should be assessed with regard to treatment compliance. However, many patients may continue to experience symptoms or remain positive for H pyloridespite full treatment compliance.ALTERNATIVE REGIMENS IN PATIENTS FAILING INITIAL H PYLORITHERAPYThe choice of an alternative regimen should be based on the initial treatment regimen. For example, if triple therapy consisting of a PPI or ranitidine bismuth citrate, clarithromycin, and amoxicillin was used as first-line treatment, the second treatment course should consist of a PPI, metronidazole, bismuth subsalicylate, and tetracycline.Alternatively, patients who do not respond to the initial treatment course may be referred to a gastroenterologist for further workup.It is recommended that patients who do not respond to an initial and a secondary course of anti–H pyloritherapy be referred to a gastroenterologist. These patients often require endoscopy with biopsy and culture for the determination of antibiotic resistance. Further therapy would then be based on the resistance patterns detected.SUMMARY AND RECOMMENDATIONSHelicobacter pyloriis a ubiquitous organism that is associated with histological gastritis, peptic ulcer disease, gastric mucosa-associated lymphoid tissue lymphoma, and an increased risk of gastric adenocarcinoma. Studies have documented that cure of the infection is associated with ulcer healing, symptom resolution, and cure of the H pylori–related ulcer disease. Cure of H pyloriinfection reduces the morbidity associated with ulcer disease, conserves health care resources, and frequently eliminates the need for maintenance antisecretory drug therapy. Figure 1, Figure 2, and Figure 3are proposed to aid physicians in caring for patients with a newly diagnosed ulcer, a previous history of peptic ulcer disease, and dyspepsia, respectively.Figure 1.Patients with a diagnosis of new ulcer. The diagnosis of Helicobacter pyloriinfection should be made using the rapid urease test in those undergoing endoscopy and blood antibody testing in those undergoing an upper gastrointestinal tract series. Negative H pyloritest results should be confirmed using nonendoscopic methods. Patients with positive H pyloritest results should be treated with 10 to 14 days of a twice-daily regimen that includes a proton pump inhibitor (PPI) or ranitidine bismuth citrate (RBC), clarithromycin, and amoxicillin or metronidazole. Patients with ulcer who are negative for H pylorishould be treated with 4 to 6 weeks of a PPI or a histamine2receptor antagonist (H2RA). *, Nonendoscopic methods for active infection include urea breath test (UBT) and stool antigen detection. The UBT should be performed only after use of antisecretory agents has been discontinued for at least 2 weeks and use of antimicrobial agents and bismuth has been discontinued for at least 4 weeks. Stool detection should be performed at least 4 weeks after H pylorieradiction therapy. Clinicians should keep in mind the potential for false-positive results with this test in patients who have completed a course of anti–H pyloritreatment. †, Patients who do not respond to a first course of therapy with a PPI or RBC, clarithromycin, and amoxicillin should be retreated with a PPI, metronidazole, bismuth subsalicylate, and tetracycline. Those who continue to have positiveH pyloritest results after 2 courses of anti–H pyloritreatment should be referred to a gastroenterologist. ‡, Patients with complicated ulcer disease who are positive for H pylori(by blood antibody testing or rapid urease test) should be treated for their infection followed by 6 weeks of antisecretory drug therapy. Cure of the infection should be assessed using the UBT 2 weeks after completion of the antisecretory agent therapy or by stool antigen testing.Figure 2.Patients with previous uncomplicated ulcer disease currently receiving maintenance antisecretory agents. Determination of Helicobacter pyloristatus in these patients should be made using blood antibody testing. Patients who are positive for H pylorishould be treated with 10 to 14 days of a twice-daily regimen that includes a proton pump inhibitor (PPI) or ranitidine bismuth citrate (RBC), clarithromycin, and amoxicillin or metronidazole. Patients who are negative for H pylorican stop taking maintenance antisecretory agents provided that a history of uncomplicated peptic ulcer disease was the sole reason for its use. Items listed with an asterisk and dagger are explained in the legend to Figure 1.Figure 3.Patients with dyspepsia. These patients should be treated according to their age and presenting symptoms. Those older than 50 years and those of any age with alarm symptoms should undergo endoscopy. Patients 50 years or younger and without alarm symptoms should be evaluated for Helicobacter pyloriinfection using blood antibody testing. Patients who are positive for H pylorishould be treated with 10 to 14 days of a twice-daily regimen that includes a proton pump inhibitor (PPI) or ranitidine bismuth citrate (RBC), clarithromycin, and amoxicillin or metronidazole. Items listed with an asterisk and dagger are explained in the legend to Figure 1. GERD indicates gastroesophageal reflux disease.Patients with confirmed ulcer disease should be evaluated for H pyloriinfection. Nonendoscopic testing for H pyloriinfection is also recommended for individuals 50 years and younger with symptoms suggestive of ulcer disease and without alarm symptoms suggestive of malignancy. Other subgroups of individuals might also warrant H pylorievaluation. The method of H pyloridetection depends on the patient's clinical presentation. Regardless of how or why they were diagnosed, patients who are positive for H pylorishould be offered treatment with an effective anti–H pyloriregimen. After treatment, patients with documented ulcer disease warrant follow-up evaluation of their posttreatment H pyloristatus.JParsonnetHelicobacter pyloriand gastric cancer.Gastroenterol Clin North Am.1993;22:89-104.National Institutes of HealthHelicobacter pyloriin peptic ulcer disease.NIH Consens Statement.1994;12:1-23.BJMarshallJRWarrenUnidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration.Lancet.1984;1:1311-1315.EJKuipersJCThijsHPMFestenThe prevalence of Helicobacter pyloriin peptic ulcer disease.Aliment Pharmacol Ther.1995;9(suppl 2):59-69.ILaineRJHopkinsLSGirardiHas the impact of Helicobacter pyloritherapy on ulcer recurrence in the United States been overstated? a meta-analysis of rigorously designed trials.Am J Gastroenterol.1998;93:1409-1415.JValleMKekkiPSipponenTIhamakiMSiuralaLong-term course and consequences of Helicobacter pylorigastritis.Scand J Gastroenterol.1996;31:546-550.DFormanPWebbJParsonnettHelicobacter pyloriand gastric cancer.Lancet.1994;343:243-244.JParsonnetGDFriedmanDPVandersteenHelicobacter pyloriinfection and the risk of gastric carcinoma.N Engl J Med.1991;325:1127-1131.ANomuraGNStemmermannPChyouHelicobacter pyloriinfection and gastric carcinoma among Japanese Americans in Hawaii.N Engl J Med.1991;325:1132-1136.Not AvailableInfection with Helicobacter pylori.In: IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, Schistosomes, Liver Flukes andHelicobacter pylori: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans.Vol 61. Lyon, France: International Agency for Research on Cancer; 1994:177-240.ASonnenbergJEEverhartHealth impact of peptic ulcer in the United States.Am J Gastroenterol.1997;92:614-620.TFImperialeTSperoffRDCebulAJMcCulloughA cost analysis of alternative treatments for duodenal ulcer.Ann Intern Med.1995;123:665-672.NVakilBFennertyThe economics of eradicating Helicobacter pyloriinfection in duodenal ulcer disease.Am J Med.1996;100(suppl 5A):60-63.GNJTytgatIANoachEAJRauwsHelicobacter pyloriinfection and duodenal ulcer disease.Gastroenterol Clin North Am.1993;22:127-140.LLaineHelicobacter pyloriand complicated ulcer disease.Am J Med.1996;100(suppl):52S-59S.EBayerdorfferANeubauerBRudolphRegression of primary gastric lymphoma of mucosa-associated lymphoid tissue type after cure of Helicobacter pyloriinfection.Lancet.1995;345:1591-1594.ASonnebergWFTownsendCosts of duodenal ulcer therapy with antibiotics.Arch Intern Med.1995;155:922-928.BO'BrienRGoereeHMohamedRHuntCost-effectiveness of Helicobacter pylorieradication for the long-term management of duodenal ulcer in Canada.Arch Intern Med.1995;155:1958-1964.PUngeBJonssonN-OStalhammarThe cost-effectiveness of Helicobacter pylorieradication versus maintenance and episodic treatment in duodenal ulcer patients in Sweden.Pharmacoeconomics.1995;8:410-427.AMFendrickJTMcCortMEChernewRAHirthCPatelBSBloomImmediate eradication of Helicobacter pyloriin patients with previously documented peptic ulcer disease: clinical and economic effects.Am J Gastroenterol.1997;11:2017-2024.JJOfmanJEtchasonSFullertonKLKahnAHSollManagement strategies for Helicobacter pylori–seropositive patients with dyspepsia: clinical and economic consequences.Ann Intern Med.1997;126:280-291.MDSilversteinTPettersonNTalleyInitial endoscopy or empirical therapy with or without testing for Helicobacter pylorifor dyspepsia: a decision analysis.Gastroenterology.1996;110:72-83.AMFendrickMEChernewRAHirthBSBloomAlternative management strategies for patients with suspected peptic ulcer disease.Ann Intern Med.1995;123:260-268.GSteinbachRFordGGloberAntibiotic treatment of gastric lymphoma of mucosa-associated lymphoid tissue: an uncontrolled trial.Ann Intern Med.1999;131:88-95.ACWotherspoonCDoglioniTCDissRegression of primary low-grade B-cell gastric lymphoma of mucosa-associated lymphoid tissue type after eradication of Helicobacter pylori.Lancet.1993;342:575-577.DMWeberMADimopoulosDPAnanduWCPughGSteinbachRegression of gastric lymphoma of mucosa-associated lymphoid tissue with antibiotic therapy for Helicobacter pylori.Gastroenterology.1994;107:1835-1838.ERoggeroEZuccaGPinottiEradication of Helicobacter pyloriinfection in primary low-grade gastric lymphoma of mucosa-associated lymphoid tissue.Ann Intern Med.1995;122:767-769.UBleckerTWMcKeithanJHartBSKirschnerResolution of Helicobacter pylori–associated gastric lymphoproliferative disease in a child.Gastroenterology.1995;109:973-977.CMontalbanAManzanalDBoixedaHelicobacter pylorieradication for the treatment of low-grade gastric MALT lymphoma: follow-up together with sequential molecular studies.Ann Oncol.1997;8(suppl 2):37-39.ANeubauerCThiedeAMorgnerCure of Helicobacter pyloriinfection and duration of remission of low-grade gastric mucosa-associated lymphoid tissue lymphoma.J Natl Cancer Inst.1997;89:1350-1355.JParsonnetRAHarrisHMHackDKOwensModeling cost-effectiveness of Helicobacter pyloriscreening to prevent gastric cancer: a mandate for clinical trials.Lancet.1996;348:150-154.AMFendrickMEChernewRAHirthBSBloomRRBandekarJMScheimanClinical and economic effects of H. pyloriscreening to prevent gastric cancer.Arch Intern Med.1999;159:142-148.RMGentaDYGrahamComparison of biopsy sites for the histopathological diagnosis of Helicobacter pylori: a topographic study of H. pyloridensity and distribution.Gastrointest Endosc.1994;40:342-345.RMGentaGORobasonDYGrahamSimultaneous visualization of Helicobacter pyloriand gastric morphology: a new stain.Hum Pathol.1994;25:221-226.LLaineDNLewinWNaritokuREstradaHCohenProspective comparison of commercially available rapid urease tests for the diagnosis of Helicobacter pylori.Gastrointest Endosc.1996;44:523-526.DYGrahamRGentaDGEvansHelicobacter pyloridoes not migrate from the antrum to the corpus in response to omeprazole.Am J Gastroenterol.1996;91:2120-2124.LLaineREstradaMTrujilloKKniggeMBFennertyEffect of proton-pump inhibitor therapy on diagnostic testing for Helicobacter pylori.Ann Intern Med.1998;129:547-550.WDCheyMWoodsJMScheimanTTNostrantJDelValleLansoprazole and ranitidine affect the accuracy of the 14C-urea breath test by a pH-dependent mechanism.Am J Gastroenterol.1997;92:446-450.WDCheyMSpybrookSCarpenterTTNostrantGHEltaJMScheimanProlonged effect of omeprazole on the 14C-urea breath test.Am J Gastroenterol.1996;91:89-92.CCMcGowanTLCoverMJBlaserThe proton pump inhibitor omeprazole inhibits acid survival of Helicobacter pyloriby a urease-independent mechanism.Gastroenterology.1994;107:1573-1578.HCohenLLaineEndoscopic methods for the diagnosis of H. pylori.Aliment Pharmacol Ther.1997;11(suppl 1):3-9.DVairaPMalfertheinerFMegraudDiagnosis of Helicobacter pyloriinfection with a new non-invasive antigen-based assay: multicentre study.Lancet.1999;354:30-33.JEOrmandJFTalleyHACarpenterC-urea breath test for diagnosis of Helicobacter pylori.Dig Dis Sci.1990;35:879-884.AFCutlerSHavstadCKMaMJBlaserGIPerez-PerezTTSchubertAccuracy of invasive and noninvasive tests to diagnose Helicobacter pyloriinfection.Gastroenterology.1995;109:136-141.PAMarchildonLMCiotaFZZamaniyanJSPeacockDYGrahamEvaluation of three commercial enzyme immunoassays compared with the C urea breath test for detection of Helicobacter pyloriinfection.J Clin Microbiol.1996;34:1147-1152.FPerriBMaesBGeypensThe influence of isolated doses of drugs, feeding and colonic bacterial ureolysis on urea breath test results.Aliment Pharmacol Ther.1995;9:705-709.VSavarinoGBissoMPivariEffect of omeprazole and ranitidine on the accuracy of 13C-urea breath test (UBT) [abstract].Gut.1998;43(suppl 2):A51.AMakristathisEPaschingKSchutzeDetection of Helicobacter pyloriin stool specimens by PCR and antigen enzyme immunoassay.J Clin Microbiol.1998;36:2772-2774.LTrevisaniSSartoriFGalvaniEvaluation of a new enzyme immunoassay for detecting Helicobacter pyloriin feces: a prospective pilot study.Am J Gastroenterol.1999;94:1830-1833.XCalvetFFeuMForneThe evaluation of a new immunoenzyme analysis for the detection of Helicobacter pyloriinfection in stool samples.Gastroenterol Hepatol.1999;22:270-272.AFGoddardRCSpillerThe effect of omeprazole on gastric juice viscosity, pH, and bacterial counts.Aliment Pharmacol Ther.1996;10:105-109.PUngeAGadHGnarpeJOlssonDoes omeprazole improve antimicrobial therapy directed towards Campylobacter pyloriin patients with antral gastritis?Scand J Gastroenterol.1989;167:49-54.SWHoskingTKWLingSCSChungDuodenal ulcer healing by eradication of Helicobacter pyloriwithout anti-acid treatment: randomized controlled trial.Lancet.1994;343:508-510.SKLamCKChingKCLaiDoes treatment of Helicobacter pylori(Hp) with antibiotics alone heal duodenal ulcer (DU)? a randomized double-blind placebo controlled study.Gut.1997;41:43-48.LLaineREstradaMTrujilloKFukanagaGNeilRandomized comparison of differing periods of twice-a-day triple therapy for the eradication of Helicobacter pylori.Aliment Pharmacol Ther.1996;10:1029-1033.MMYousfiHMTEl-ZimaityMTAl-AssiRAColeRMGentaDYGrahamMetronidazole, omeprazole, and clarithromycin: an effective combination therapy for Helicobacter pyloriinfection.Aliment Pharmacol Ther.1995;9:209-212.LLaineREstradaMTrujilloSEmamiRandomized comparison of ranitidine bismuth citrate–based triple therapies for Helicobacter pylori.Am J Gastroenterol.1997;92:2213-2215.AHSollfor the Practice Parameters Committee of the American College of GastroenterologyMedical treatment of peptic ulcer disease: practice guidelines.JAMA.1996;275:622-629.RWMVan der HulstJJKellerEAJRauwsGNJTytgatTreatment of Helicobacter pyloriinfection: a review of the world literature.Helicobacter.1996;1:6-19.DAPeuraThe report of the Digestive Health Initiative International Update Conference on Helicobacter pylori.Gastroenterology.1997;113(suppl):S4-S8.Not AvailableHelidac [package insert].Norwich, NY: Procter & Gamble.WAde BoerWMMDriessenARJanszEffect of acid suppression on efficacy of treatment for Helicobacter pyloriinfection.Lancet.1995;345:817-820.TJBorodyPAndrewsGFracchiaOmeprazole enhances efficacy of triple therapy in eradicating Helicobacter pylori.Gut.1995;37:477-481.TLindSJOVeldhuyzen van ZantenPUngeEradication of Helicobacter pyloriusing one-week triple therapies combining omeprazole with two antimicrobials: the MACH-1 Study.Helicobacter.1996;1:138-144.JJMisiewiczAWHarrisKDBardhamOne week triple therapy for Helicobacter pylori: a multicentre comparative study.Gut.1997;41:735-739.LLaineTMaloneWBoechenekWWangCurrent US rates of H. pyloriantibiotic resistance and factors predicting resistance: results from ongoing trials at 77 sites [abstract].Gastroenterology.1999;116:A228.DSRiffSKiddPRoseMHaberSiepman NWeissfeldTriple therapy with lansoprazole, clarithromycin, and amoxicillin for the cure of Helicobacter pyloriinfection: a short report.Helicobacter.1996;1:238-242.HLamouliatteRCaylaFZerbibPTalbiFMegraudAde MascarelTriple therapy with PPI-amoxicillin-clarithromycin for H. pylorieradication: the optimal regimen in 1996 [abstract].Gastroenterology.1996;110:A171.ASWeissfeldDESimmonsPHVanceETrevinoSKiddPGreski-RoseIn vitro susceptibility of pre-treatment isolates of Helicobacter pylorifrom two multicenter United States clinical trials.Gastroenterology.1996;110:A295.RJHopkinsLSGirardiEATurneyRelationship between Helicobacter pylorieradication and reduced duodenal and gastric ulcer recurrence: a review.Gastroenterology.1996;110:1244-1252.NVakilBHahnDMcSorleyRecurrent symptoms and gastro-esophageal reflux disease in patients with duodenal ulcer treated for Helicobacter pyloriinfection.Aliment Pharmacol Ther.2000;14:45-51.PSPhullDHallidayABPriceMRJacynaAbsence of dyspeptic symptoms as a test for Helicobacter pylorieradication.BMJ.1996;312:349-350.PDKleinDYGrahamMinimum analysis requirements for the detection of Helicobacter pyloriinfection by the 13C-urea breath test.Am J Gastroenterol.1993;88:1865-1969.BAMVan de WouwWAde BoerHWEMHermsenJGMValkenburgLMGeuskensGNJTytgatUsefulness of the 14C-urea breath test as a semi-quantitative monitoring instrument after therapy for Helicobacter pyloriinfection.Scand J Gastroenterol.1997;32:112-117.TUKousunenKSeppalaSSarnaPSipponenDiagnostic value of decreasing IgG, IgA, and IgM antibody titres after eradication of Helicobacter pylori.Lancet.1992;339:893-895.MFeldmanBCryerELeeWLPetersonRole of seroconversion in confirming cure of Helicobacter pyloriinfection.JAMA.1998;280:363-365.AMFendrickWDCheyNMagaretJPalaniappanMBFennertySymptom status and the desire for Helicobacter pyloriconfirmatory testing after eradication therapy in patients with peptic ulcer disease.Am J Med.1999;107:133-136.The European Helicobacter pylori Study Group (EHPSG)Current European concepts in the management of Helicobacter pyloriinfection: the Maastricht Consensus Report.Gut.1997;41:8-13.NChibaRHHuntBismuth, metronidazole and tetracycline (BMT) acid suppression in H. pylorieradication: a meta-analysis [abstract].Gut.1996;39(suppl 2):A36.WAde BoerHow to achieve a near 100% cure rate for H pyloriinfection in peptic ulcer patients: a personal viewpoint.J Clin Gastroenterol.1996;22:313-316.Accepted for publication September 15, 1999.This work was supported by an unrestricted educational grant from TAP Pharmaceuticals Inc, Deerfield, Ill.Corresponding author: Walter L. Peterson, MD, Veterans Affairs Medical Center (111 B-1), 4500 S Lancaster Rd, Dallas, TX 75216.
TI - Helicobacter pylori–Related Disease
JO - JAMA Internal Medicine
DO - 10.1001/archinte.160.9.1285
DA - 2000-05-08
UR - https://www.deepdyve.com/lp/american-medical-association/helicobacter-pylori-related-disease-0vAcWgT6nf
SP - 1285
EP - 1291
VL - 160
IS - 9
DP - DeepDyve
ER -