Maastricht iv/ Florence Consensus Report
Yüklə 0,54 Mb. Pdf görüntüsü
|
|
1a B H pylori eradication to prevent gastric cancer should be undertaken in populations at high risk 1c A Preneoplastic high-risk conditions require endoscopic follow- up. Prospective studies are needed to determine the correct timing of follow-up 2c A
657 Guidelines tests to identify subjects at high risk for gastric cancer. Subjects with severe gastric atrophy, in whom H pylori has disappeared and who are therefore serologically negative for H pylori, are at a particularly high risk. The combination of H pylori infection and atrophic gastritis determined by serological examination is suitable for the identi fication of subjects with a high risk of gastric cancer. Statement 15: Risk stratification of patients with premalignant gastric conditions is useful and should be based on the severity and distribution of lesions. Evidence level: 2b Grade of recommendation: B Patients with preneoplastic changes of the gastric mucosa are at an increased risk of developing gastric cancer. 274 H pylori
eradication treatment has the potential to prevent gastric cancer. However, recent reports after long-term follow-up have suggested that H pylori eradication does not prevent gastric cancer development in all infected patients, especially in those who have preneoplastic changes of the gastric mucosa before eradication treatment is given. 45 Therefore, risk strati fication of patients with premalignant gastric conditions is useful and should be based on the severity and distribution of lesions. The gastritis OLGA-staging conveys useful information on the potential clinicopathological outcome of the gastritisdin particular, the likelihood of progression to gastric cancer. The adoption of this system is therefore useful for patient manage- ment. According to OLGA-staging and H pylori status, patients with gastritis can be con fidently stratified and managed according to their cancer risk. This has been shown for separate populations with different gastric cancer risk. 290e292 More
recently the OLGIM histological staging has been shown to be of similar value. In this histological system IM is used as the preneoplastic marker instead of atrophy. 293
Statement 16: H pylori eradication to prevent gastric cancer should be considered in the following: first-degree relatives of family members with a diagnosis of gastric cancer; patients with previous gastric neoplasia already treated by endoscopic or subtotal gastric resection; patients with a risk of gastritis: severe pan-gastritis, corpus-predominant gastritis, severe atrophy; patients with chronic gastric acid inhibition for more than 1 year; patients with strong environmental risk factors for gastric cancer (heavy smoking, high exposure to dust, coal, quartz, cement and/or work in quarries); H pylori-positive patients with a fear of gastric cancer. Evidence level: 1a to 4 Grade of recommendation: A H pylori eradication to prevent gastric cancer should be undertaken in patients at high risk. A first-degree relative of a family member with a diagnosis of gastric cancer is at high risk.
294 First- degree relatives have a two to three times increased risk of developing gastric cancer. 295e300
If more than one first-
degree relative has contracted gastric cancer the risk for others is increased by a factor of 10. Patients with the CDH-1 mutation should be offered genetic consultation and prophylactic gastrectomy. 301e307 There is an absolute indication for eradication treatment in patients at high risk, but they also require follow-up. Patients who have had a previous gastric operation, prior gastric neoplasia (MALT lymphoma, adenoma, cancer), pan-gastritis, corpus-dominant gastritis and in conjunction with IM and atrophy are all at high risk. 308e311
Patients who have been receiving acid inhibition for >1 year
and those who will be given long-term acid inhibition for >1 year are at increased risk. 312 Patients exposed to one or more strong environmental risk factors for gastric cancer such as heavy smoking, a high exposure to dust, coal, quartz, cement and/or work in quarries and those who live in a geographical area with a high incidence of gastric cancer should undergo eradication treatment. 172 313 314 Finally, H pylori-positive patients with fear of gastric cancer should receive eradication treatment. Statement 17: H pylori eradication to prevent gastric cancer should be undertaken in populations at high risk. Evidence level: 1c Grade of recommendation: A H pylori infection is a necessary but not sufficient cause for gastric cancer. Recent H pylori guidelines recommend population screening and treatment for H pylori in high-risk regions. 172
This strategy would be cost-effective where gastric cancer rates are high and most effective before the development of gastric atrophy. H pylori eradication for gastric cancer prevention should be undertaken in populations at high risk. Statement 18: Factors to be considered for prevention strategies include: the incidence of gastric cancer in the community to be targeted; likely future trends in cancer incidence if intervention is not employed; the availability of primary care facilities and other logistics; the likely compliance of the chosen population; the availability of funding; the possibility of retesting and re-treatment in the event of eradication failure. Evidence level: not quotable Grade of recommendation: A Several factors should be considered when identifying popu- lations in whom a prevention strategy is planned. The incidence of gastric cancer in the community to be targeted is relevant. 199
The likely future trends in the incidence of gastric cancer if intervention is not provided must be considered and the general availability of primary care facilities and other logistics such as funding are also important. 315e317 The likely compliance of the target population is another factor to be taken into consideration. Reinfection with H pylori after eradication is rare in developed countries but more common in developing countries at around 13%. So the need for retesting and re-treatment in the event of eradication failure or reinfection must be kept in mind when considering a preventive strategy. 318
Statement 19: The antibiotic combination should be chosen according to local H pylori antibiotic resistance patterns. Evidence level: 2b Grade of recommendation: B Antibiotic resistance is the most important factor responsible for the falling success rate of H pylori eradication treatment. 319 320 Local surveillance of H pylori antibiotic resistance is mandatory and the antibiotic combination for H pylori eradication treat- ment should be chosen according to the local resistance patterns. A wider range of effective treatments is urgently required. Statement 20: Vaccination would be the best option for eliminating H pylori infection in the population. A major effort to develop a vaccine should be made. Evidence level: 4 Grade of recommendation: A In 2010, the worldwide prevalence of H pylori infection ranged between 7% and 87%. The average prevalence in Europe is around 30%, a high immigration background needs to be taken into account. 321
A vaccination strategy would be the best option for eliminating H pylori infection in the population. 322 A vaccine 658 Gut 2012;61:646e664. doi:10.1136/gutjnl-2012-302084 Guidelines
against H pylori is feasible in animals both for prevention and treatment. Its potential in humans requires further research. 323 324 A major effort should be made to develop a vaccine against H pylori in humans. Statement 21: (a) Preneoplastic high-risk conditions require endoscopic follow-up. (b) Prospective studies are needed to determine the correct timing of follow-up. Evidence level: 2c Grade of recommendation: A Patients
with high-risk conditions such
as atrophic
gastritis and IM are at an increased risk of developing gastric cancer.
17 223 325 Whether these lesions merit endoscopic follow-up and the optimal timing for this, require evaluation in prospective studies.
< Preneoplastic conditions to be considered for endoscopic follow-up – when there is a firm diagnosis of pernicious anaemia with histological con firmation of type A autoimmune atrophic gastritis; – if there are histological and/or serological signs of subtotal or total atrophic gastritis with hypo- or achlorhydria; – if there has been a diagnosis/removal of gastric adenoma(s). < Regular follow-up should be considered in moderate to severe atrophy at 2e3 years intervals and 3e6 month intervals where there is dysplasia. Key aspects related to gastric cancer prevention strategies involving H pylori are listed in table 4. Author footnote Disclosures The following participants disclosed no financial relationship relevant to this publication: LP Andersen, A Axon, F Bazzoli, A Burette, L Coelho, KM Fock, G Gasbarrini, G Gensini, J Gisbert, KL Goh, R Hunt, VA Isakov, L Kupcinskas, S Koletzko, EJ Kuipers, S Ladas, M Leja, JC Machado, Y Niv, A Ristima ¨ki, T Rokkas, R Rugge, R Stockbru ¨gger, M Vieth. The following participants disclosed a financial relationship: J Atherton: is a consultant for Axcan Pharma, Danone and Clinova Ltd X. Calvet:has participated in advisory boards of AstraZeneca, has served as speaker for AstraZeneca and Almirall-Prodesfarma and has received research support from AstraZeneca and Janssen-Cilag. F Chan: consultant: Pfizer, speaker’s honoraria: AstraZeneca, Pfizer, Takeda, Steering Committee/Adjudication: Pfizer. Commitee member for the CONDOR study. JC Delchier: is consultant for Aptalis Pharma in relation with the treatment of H pylori with Pylera. F Di Mario: none declared. E El-Omar: none declared. W Fischbach: research grant: Deutsche Krebshilfe, speaker’s honoraria: Abbott, Aptalis, Falk, Merck Serono, Norgine, Novartis, Nycomed, Pfizer, Roche, Sanofi-Aventis, Shire. Consultant: Fresenius Biotech, Norgine, Pfizer, Vifor Pharma. DY Graham: is an unpaid consultant for Novartis in relation to vaccine development for treatment or prevention of H pylori infection. He is also a paid consultant for Otsuka Pharmaceuticals regarding diagnostic testing and until recently has received royalties from Baylor College of Medicine on patients covering materials related to [ 13 C]urea breath test. P Hungin: has received research funding, travel and speakers fee from Reckitt Benckiser for upper gastrointestinal problems. M Kist: research support by Nycomed Deutschland GmbH, Honorary: Aptalis. Scientific Advisory Board: Aptalis. A Lanas: is advisor to AstraZeneca, Pfizer and Bayer. P Malfertheiner: speaker’s fee: Aptalis, Falk Foundation, Abbott, AstraZeneca. Research grant: Novartis. K McColl: received consultancy fees from Reckitt Benckiser. V Mahachai: is currently obtaining grant support from Daiichi Sankyu, Japan. F Megraud: received research grants and served as consultant for Aptalis Pharma, Danone Research, and speaker for Aptalis Pharma, AstraZeneca. C O’Morain: has received research grants from Abbott and MSD and served on advisory boards of Abbott, Aptalis, Falk Pharma, MSD and Shire. A Pilotto: none declared. K Sugano: research grants from Astellas, AstraZeneca, Eisai and Takeda, fees for advisory board from Takeda and AstraZenecaand a lecture fee from Takeda. D Vaira: none declared. N Vakil: is concultant for AstraZeneca, Takeda, Otsuka, Ironwood, Orexo. Stock options: Meridian Diagnostics, Orexo. Scientific secretaries P Lehours, A O’Connor, M Selgrad. We acknowledge the editorial assistance of Mrs. D. Deutschla ¨nder
Contributors LP Andersen (Denmark), J Atherton (UK), A Axon (UK), F Bazzoli (Italy), A Burette (Belgium), X Calvet (Spain), F Chan (Hongkong), L Coelho (Brazil), JC Delchier (France), F Di Mario (Italy), E El-Omar (UK), W Fischbach (Germany), KM Fock (Singapore), G Gasbarrini (Italy), G Gensini (Italy), J Gisbert (Spain), KL Goh (Malaysia), DY Graham (USA), P Hungin (UK), R Hunt (Canada), VA Isakov (Russia), M Kist (Germany), S Koletzko (Germany), EJ Kuipers (The Netherlands), L Kupcinskas (Kaunas), S Ladas (Greece), A Lanas (Spain), M Leja (Lattvia), JC Machado (Portugal), V Mahachai (Thailand) P Malfertheiner (Germany), K McColl (England), F Megraud (France), Y Niv (Israel), C O’Morain (Ireland), A Pilotto (Italy), A Ristimaki (Finland), T Rokkas (Greece), M Rugge (Italy), R Stockbru ¨gger (Italy), K Sugano (Japan), D Vaira (Italy), N Vakil (USA), M Vieth (Germany). Funding This study was supported by an unrestricted grant: Menarini Foundation (Firenze, Italy). Competing interests None. Provenance and peer review Not commissioned; externally peer reviewed. REFERENCES 1. Malfertheiner P, Megraud F, O’Morain C, et al. Current European concepts in the management of helicobacter pylori infectionethe Maastricht consensus report. The European helicobacter pylori study group (EHPSG). Eur J Gastroenterol Hepatol 1997;9:1e2. 2. Malfertheiner P, Megraud F, O’Morain C, et al. Current concepts in the management of Helicobacter pylori infectionethe Maastricht 2-2000 Consensus Report. Aliment Pharmacol Ther 2002;16:167e80. 3. Malfertheiner P, Megraud F, O’Morain C, et al. Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report. Gut 2007;56:772e81. 4. Howden CW, Hunt RH. Guidelines for the management of Helicobacter pylori infection. Ad Hoc Committee on practice Parameters of the American College of gastroenterology. Am J Gastroenterol 1998;93:2330e8. 5. Vaira D, Malfertheiner P, Megraud F, et al. Diagnosis of Helicobacter pylori infection with a new non-invasive antigen-based assay. HpSA European study group. Lancet 1999;354:30e3. 6. Chiba N, Van Zanten SJ, Sinclair P, et al. Treating Helicobacter pylori infection in primary care patients with uninvestigated dyspepsia: the Canadian adult dyspepsia empiric treatment-Helicobacter pylori positive (CADET-Hp) randomised controlled trial. BMJ 2002;324:1012e16. 7. Moayyedi P, Axon AT. The usefulness of the likelihood ratio in the diagnosis of dyspepsia and gastroesophageal reflux disease. Am J Gastroenterol 1999;94:3122e5. 8. Ikenberry SO, Harrison ME, Lichtenstein D, et al. The role of endoscopy in dyspepsia. Gastrointest Endosc 2007;66:1071e5. 9. Niv Y, Niv G, Koren R. 13C-urea breath test for diagnosis of Helicobacter pylori infection in the elderly. Dig Dis Sci 2004;49:1840e4. 10.
Moayyedi P, Deeks J, Talley NJ, et al. An update of the Cochrane systematic review of Helicobacter pylori eradication therapy in nonulcer dyspepsia: resolving the discrepancy between systematic reviews. Am J Gastroenterol 2003;98:2621e6. 11.
Harvey RF, Lane JA, Nair P, et al. Clinical trial: prolonged beneficial effect of Helicobacter pylori eradication on dyspepsia consultations - the Bristol Helicobacter Project. Aliment Pharmacol Ther 2010;32:394e400. 12.
Maconi G, Sainaghi M, Molteni M, et al. Predictors of long-term outcome of functional dyspepsia and duodenal ulcer after successful Helicobacter pylori eradicationea 7-year follow-up study. Eur J Gastroenterol Hepatol 2009;21:387e93. 13.
Moayyedi P. The health economics of Helicobacter pylori infection. Best Pract Res Clin Gastroenterol 2007;21:347e61. 14. Gwee KA, Teng L, Wong RK, et al. The response of Asian patients with functional dyspepsia to eradication of Helicobacter pylori infection. Eur J Gastroenterol Hepatol 2009;21:417e24. 15. Jin X, Li YM. Systematic review and meta-analysis from Chinese literature: the association between Helicobacter pylori eradication and improvement of functional dyspepsia. Helicobacter 2007;12:541e6. 16. El-Omar EM, Oien K, El-Nujumi A, et al. Helicobacter pylori infection and chronic gastric acid hyposecretion. Gastroenterology 1997;113:15e24. 17.
De Vries AC, van Grieken NC, Looman CW, et al. Gastric cancer risk in patients with premalignant gastric lesions: a nationwide cohort study in the Netherlands. Gastroenterology 2008;134:945e52. 18.
Cullen D, Hawkey G, Greenwood D, et al. H. pylori and gastroesophageal reflux disease: a community-based study. Helicobacter 2008;13:352e60. 19. O’Connor HJ. Review article: helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management. Aliment Pharmacol Ther 1999;13:117e27. 20. Rokkas T, Pistiolas D, Sechopoulos P, et al. Relationship between Helicobacter pylori infection and esophageal neoplasia: a meta-analysis. Clin Gastroenterol Hepatol 2007;5:1413e17, 1417. 21. Yaghoobi M, Farrokhyar F, Yuan Y, et al. Is there an increased risk of GERD after Helicobacter pylori eradication?: a meta-analysis. Am J Gastroenterol 2010;105:1007e13. 22. Moayyedi P, Bardhan C, Young L, et al. Helicobacter pylori eradication does not exacerbate reflux symptoms in gastroesophageal reflux disease. Gastroenterology 2001;121:1120e6. 23. Qian B, Shijie M, Shang L, et al. Effect of H. pylori eradication on gastroesophageal reflux disease. Helicobacter 2011;16:255e65. 24.
Klinkenberg-Knol EC, Nelis F, Dent J, et al. Long-term omeprazole treatment in resistant gastroesophageal reflux disease: efficacy, safetyand influence on gastric mucosa. Gastroenterology 2000;118:661e9. Gut 2012;61:646e664. doi:10.1136/gutjnl-2012-302084 659 Guidelines 25. Di Mario F, Ingegnoli A, Dal Bo ` N, et al. Early epigastric pain after PPI administration: exacerbation of Helicobacter pylori corpus gastritis? Helicobacter 2004;9:92e4. 26.
Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non- steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet 2002;359:14e22. 27.
Chan FK, Sung JJ, Chung SC, et al. Randomised trial of eradication of Helicobacter pylori before non-steroidal anti-inflammatory drug therapy to prevent peptic ulcers. Lancet 1997;350:975e9. 28.
Chan FK, To KF, Wu JC, et al. Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long-term treatment with non-steroidal anti-inflammatory drugs: a randomised trial. Lancet 2002;359:9e13. 29.
de Leest HT, Steen KS, Lems WF, et al. Eradication of Helicobacter pylori does not reduce the incidence of gastroduodenal ulcers in patients on long-term NSAID treatment: double-blind, randomized, placebo-controlled trial. Helicobacter 2007;12:477e85. 30. Lai KC, Lau CS, Ip WY, et al. Effect of treatment of Helicobacter pylori on the prevention of gastroduodenal ulcers in patients receiving long-term NSAIDs: a double-blind, placebo-controlled trial. Aliment Pharmacol Ther 2003;17:799e805. 31. Hawkey CJ, Tulassay Z, Szczepanski L, et al. Randomised controlled trial of Helicobacter pylori eradication in patients on non-steroidal anti-inflammatory drugs: HELP NSAIDs study. Helicobacter Eradication for Lesion Prevention. Lancet 1998;352:1016e21. 32.
Vergara M, Catalan M, Gisbert JP, et al. Meta-analysis: role of Helicobacter pylori eradication in the prevention of peptic ulcer in NSAID users. Aliment Pharmacol Ther 2005;21:1411e18. 33.
Chan FK, Chung SC, Suen BY, et al. Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen. N Engl J Med 2001;344:967e73. 34.
Lai KC, Lam SK, Chu KM, et al. Lansoprazole for the prevention of recurrences of ulcer complications from long-term low-dose aspirin use. N Engl J Med 2002;346:2033e8. 35.
Chan F, Ching J, Suen B, et al. H. pylori eradication on the long-term incidence of recurrent ulcer bleeding in high-tisk aspirin users: a 10-year prospective cohort study (abstr). Gastroenterology 2011;140:S173e4. 36.
Schenk BE, Kuipers EJ, Nelis GF, et al. Effect of Helicobacter pylori eradication on chronic gastritis during omeprazole therapy. Gut 2000;46:615e21. 37. Lundell L, Havu N, Miettinen P, et al. Changes of gastric mucosal architecture during long-term omeprazole therapy: results of a randomized clinical trial. Aliment Pharmacol Ther 2006;23:639e47. 38. Moayyedi P, Wason C, Peacock R, et al. Changing patterns of Helicobacter pylori gastritis in long-standing acid suppression. Helicobacter 2000;5:206e14. 39.
Kuipers EJ, Lundell L, Klinkenberg-Knol EC, et al. Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Engl J Med 1996;334:1018e22. 40.
Hagiwara T, Mukaisho K, Nakayama T, et al. Long-term proton pump inhibitor administration worsens atrophic corpus gastritis and promotes adenocarcinoma development in Mongolian gerbils infected with Helicobacter pylori. Gut 2011;60:624e30. 41. Fox JG, Kuipers EJ. Long-term proton pump inhibitor administration, H pylori and gastric cancer: lessons from the gerbil. Gut 2011;60:567e8. Yüklə 0,54 Mb. Dostları ilə paylaş:
|