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doi:10.1111/j.1440-1746.2008.05314.

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S P E C I A L A RT I C L E

Asia–Pacific consensus guidelines on gastric cancer prevention
Kwong Ming Fock,* Nick Talley,† Paul Moayyedi,‡ Richard Hunt,‡ Takeshi Azuma,§ Kentaro Sugano,¶ Shu Dong Xiao,** Shiu Kum Lam,†† Khean Lee Goh,‡‡ Tsutomu Chiba,§§ Naomi Uemura,¶¶ Jae G Kim,*** Nayoung Kim,††† Tiing Leong Ang,* Varocha Mahachai,‡‡‡ Hazel Mitchell,§§§ Abdul Aziz Rani,¶¶¶ Jyh Ming Liou,**** Ratha-korn Vilaichone†††† and Jose Sollano‡‡‡‡
*Changi General Hospital, Singapore; †Mayo Clinic College of Medicine, Rochester, USA; ‡McMaster University Medical Center, Ontario, Canada; § University of Fukui, Fukui, ¶Jichi Medical University, Tochigi, §§Kyoto University, Kyoto, ¶¶Kure Kyousai General Hospital, Kure, Japan; **Shanghai Institute of Digestive Disease, Shanghai, ††University of Hong Kong, Hong Kong, China; ‡‡University of Malaya, Kuala Lumpur, Malaysia; ***Chung Ang University College of Medicine, †††Seoul National University College of Medicine, Seoul, Korea; ‡‡‡Chulalongkorn University Hospital, Bangkok, ††††Thammasat University Hospital, Pathumthani, Thailand; §§§University of New South Wales, Sydney, New South Wales, Australia; ¶¶¶University of Indonesia, Jakarta, Indonesia; ****National Taiwan University Hospital, Taipei, Taiwan; and ‡‡‡‡University of Santo Tomas, Manila, Philippines

Key words gastric cancer, guidelines, Helicobacter pylori, prevention. Accepted for publication 22 November 2007. Correspondence Professor Kwong Ming Fock, Division of Gastroenterology, Department of Medicine, Changi General Hospital, 2 Simei Street 3, Singapore 529889. Email: kwong_ming_fock@cgh.com.sg

Abstract
Background and Aim: Gastric cancer is a major health burden in the Asia–Pacific region but consensus on prevention strategies has been lacking. We aimed to critically evaluate strategies for preventing gastric cancer. Methods: A multidisciplinary group developed consensus statements using a Delphi approach. Relevant data were presented, and the quality of evidence, strength of recommendation, and level of consensus were graded. Results: Helicobacter pylori infection is a necessary but not sufficient causal factor for non-cardia gastric adenocarcinoma. A high intake of salt is strongly associated with gastric cancer. Fresh fruits and vegetables are protective but the use of vitamins and other dietary supplements does not prevent gastric cancer. Host–bacterial interaction in H. pylori infection results in different patterns of gastritis and differences in gastric acid secretion which determine disease outcome. A positive family history of gastric cancer is an important risk factor. Low serum pepsinogens reflect gastric atrophy and may be useful as a marker to identify populations at high risk for gastric cancer. H. pylori screening and treatment is a recommended gastric cancer risk reduction strategy in high-risk populations. H. pylori screening and treatment is most effective before atrophic gastritis has developed. It does not exclude the existing practice of gastric cancer surveillance in high-risk populations. In populations at low risk for gastric cancer, H. pylori screening is not recommended. Firstline treatment of H. pylori infection should be in accordance with national treatment guidelines. Conclusion: A strategy of H. pylori screening and eradication in high-risk populations will probably reduce gastric cancer incidence, and based on current evidence is recommended by consensus.

Introduction
Gastric cancer is a major public health burden. Globally, it is the fourth most common cancer and the second leading cause of cancer-related death, with 700 000 deaths annually.1 The risk of gastric cancer varies among the countries and populations in the Asia–Pacific region. High-risk areas include East Asian countries such as China, Japan and Korea, where the age-standardized incidence rate (ASR) is greater than 20 per 100 000. Intermediate risk

countries (ASR 11–19/100 000) include Malaysia, Singapore and Taiwan, while low-risk areas (ASR < 10/100 000) include countries such as Australia, New Zealand, India and Thailand.1 Gastric cancer carcinogenesis is a multifactorial process, related to an interaction of host factors, H. pylori infection and environmental factors such as diet. There is a precancerous cascade, in which the gastric mucosa undergoes a series of changes resulting in gastritis, atrophy, intestinal metaplasia, and dysplasia, before developing eventually into gastric cancer.2 At an early stage,
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Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd

Once an acceptable recommendation based on available evidence was established. a strategy of population screening for gastric cancer is being adopted in Japan. C. For data related to therapeutic interventions. This was followed by a period of discussion. Voting on the recommendations† a. specifically. Evidence obtained from at least one randomized controlled trial. when compared to surgery. Consensus statements Each statement below is followed by a brief summary in which the quality of supporting evidence. Preparation process and format of the report The manuscript was drafted by a working group. formal voting for each statement of recommendation was undertaken (Table 1). Evidence obtained from expert committee reports or opinions and/or clinical experience of respected authorities. III.4 In addition.8 To reduce the morbidity and mortality from gastric cancer. B. it would be necessary to diagnose gastric cancer at an early stage. host and bacterial factors. In order to address this major health problem. Methods Nature and extent of background preparation The Asia–Pacific Gastric Cancer Consensus Conference was convened specifically to address three main areas relevant to the prevention of gastric cancer and. Requires evidence obtained from expert committee reports or opinions and/or clinical experience of respected authorities.B. IV. The consensus conference was sponsored by the Asian Pacific Association of Gastroenterology. Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd . a classification of the recommendation and the results of voting are summarized. without randomization. (ii) gastric cancer surveillance and H. Thailand. a recommendation with specific wording was formulated. who approved the final draft. as many of the statements could not be evaluated by randomized controlled trials. and explore means of gastric cancer prevention by addressing modifiable environmental risk factors such as diet and H. depending on the depth of mucosal infiltration and degree of differentiation. and (iii) H. Disagree d.5. with lower morbidity. Requires the availability of well-conducted clinical studies. in general. patients have advanced cancer at diagnosis. pylori eradication to prevent gastric cancer. (N. d. pylori screening. and this was then circulated to and reviewed by conference participants. At the end of this discussion. correlation studies and case studies. pylori infection varies among countries in the Asia–Pacific region. Sixteen Asian gastroenterologists and four external experts were invited to participate in the consensus conference on the basis of their expertise (Appendix I). Evidence obtained from well-designed non-experimental descriptive studies.Asia–Pacific gastric cancer consensus KM Fock et al.11 No formal programs exist in other countries. Acceptance of a statement required that at least 352 two-thirds of the votes were in categories ‘a (strongly agree)’ or ‘b (agree)’. host and bacterial factors Statement 1: The prevalence of H. the quality of the evidence and the classification of evidence relative to the recommendation were assessed.3. either in terms of gastric cancer screening or screening for modifiable factors such as H.) Consensus statements I: Epidemiology. Agree c. Classification of recommendations A. Ib. The Journal of Gastroenterology and Hepatology Foundation provided financial support for the conference through an unrestricted educational grant. may also be suitable for endoscopic mucosal resection or submucosal dissection. Evidence obtained from at least one other type of well-designed quasi-experimental study. gastric adenocarcinoma. the level of evidence and the grade of recommendation are not included with every statement for the epidemiology section. in most countries. assess the evidence for current and potential intervention strategies and to decide whether it is timely to adopt a bold proactive approach towards gastric cancer prevention by recommending H. The consensus conference was held from 11 to 12 November 2006 in Bangkok. 0%. Requires at least one randomized controlled trial as part of a body of literature of overall good quality and consistency addressing the specific recommendation. related to age. when diagnosed at an advanced stage. gastric cancer may be clinically silent and. but also to ethnicity Level of agreement: a. early gastric cancer. IIa. in which the existing data were evaluated and critiqued. Indicates an absence of directly applicable clinical studies of good quality. This difference is. Currently. None of the participants were remunerated for their participation in the meeting. c. classification of recommendations and voting scheme Quality of evidence Ia.6 However. 5-year survival rates may be only in the range of 10–20%. When diagnosed at an early stage. Evidence obtained from at least one well-designed controlled study. Reject † Accept statement when more than two-thirds of participants voted a or b. pylori infection. but no randomized clinical trials on the topic of the recommendation. Selected papers relevant to the topics to be discussed were circulated and an overview of each topic based on comprehensive literature searches was presented by selected participants based on their specific expertise. 0%.7. 0%. 5-year survival rates for gastric cancer exceed 90%. b.9 Korea10 and Matsu Island in Taiwan. IIb. pylori screening and eradication. Table 1 Level of evidence. These areas were: (i) epidemiology. Each of the three topics chosen for evaluation and formulation of clinical recommendations was addressed independently. Strongly agree b. the The Asia–Pacific Gastric Cancer Consensus Conference was convened in order to review and synthesize the most current information. pylori infection. Evidence obtained from meta-analysis of randomized trials. 100%. but similar efficacy. socioeconomic circumstances.

In these studies.42 In a prospective cohort study from Japan.43 In a recent Swedish cohort study. pylori. pylori serology were collected more than 10 years before cancer diagnosis (OR: 5. 0. a negative association was possible for total vegetable intake and onion and garlic intake.45–0. c.5%. However. 0%.9 was the best estimate of the relative risk of non-cardia cancer associated with H.24 A metaanalysis of cohort studies showed an inverse association between fruit intake and gastric cancer incidence (RR: 0. Asia–Pacific gastric cancer consensus The prevalence of H. 100%. the respective importance of high salt and nitrate intake for gastric cancer mortality was assessed at the population level in 24 countries. Grade of recommendation: A. whereas no significant association was observed for fruit consumption. It is clear that those countries with high gastric cancer ASR have a high seroprevalence of H. As illustrated by a recent study. In animal model studies.73– 0. respectively.13 Thailand14 and Vietnam15 have been reported to be especially high at 92%. 95% CI: 0. This statement addressed the importance of H. the prevalence rates in Chinese.3). b.00) for fruits. but host factors have also been implicated.70 (95% CI: 0.KM Fock et al. the RR was 0. H. 95% CI: 0. 54% and 31%. 46 For vegetables.64 (95% CI: 0. pylori infection but a purportedly low gastric cancer ASR.24 The relationship of H. 95% CI: 0. whereas in more industrialized and developed countries such as Japan. the prevalence rate was 54%. pylori was found to be restricted to non-cardia cancers (odds ratio [OR]: 3.19 Within a country. Statement 3: For non-cardia gastric adenocarcinoma.3–3. The relationship of gastric cancer mortality with sodium was stronger than with nitrate. 95% CI: 3.24 Statement 5: Fresh fruits and vegetables are associated with a reduced risk of gastric cancer Level of agreement: a. b.8) and was stronger when blood samples for H.44 In a multicenter European study. the prevalence rates in Chinese. Statement 4: A high intake of salt is strongly associated with gastric cancer in both epidemiological and animal model studies Level of agreement: a.79. salt ingestion has been shown to cause gastritis and enhance the effects of gastric carcinogens. 0%.45 A case–control study from Malaysia also showed that a high intake of fresh fruits and vegetables was protective against gastric cancer.83). In Japan. there are also populations with a high seroprevalence of H.92) for yellow vegetables. pylori infection varies markedly in different Asian countries. d.2%. pylori with gastric cancer has been examined in a combined analysis of 12 case–control studies.52–0.48 (95% CI: 0. respectively. In the AngloCeltic population in Australia. pylori is a necessary but not sufficient causal factor Level of agreement: a. the seroprevalence of H. the seroprevalence rate may vary between geographic regions.9. bacterial virulence factors38 and other environmental factors. pylori infection. pylori infection increased with age from 3% in children below 5 years of age to 71% in adults above 65 years. 0%. 0%.16 Korea17 and Singapore. a high intake of salted fish and vegetables was found to be significantly associated with gastric cancer. These factors are individually addressed in the statements that follow. pylori infection. the relative risk associated with intake of Ն 1 days per week compared to < 1 day per week was 0. c. apart from H.25–0.20 whereas in nearby Taiwan. Gastric cancer is a multifactorial disease.9 would imply that between approximately 65% and 80% of non-cardia gastric cancers were attributable to H.16 the seroprevalence rates decreased from 73% in 1974 to 55% in 1984 and finally to 39% in 1994. In Table 2. 100%. c.13) using all incidence studies and 0. 0%. b. b. pylori infection and diet are believed to be major contributors to gastric carcinogenesis.39. such as India and Thailand. Level of evidence: I. Several prospective studies have reported significant reductions in gastric cancer risk arising from consumption of fresh fruits and vegetables. pylori infection.0. 0%. pylori infection as a causal factor for the development of non-cardia gastric adenocarcinoma. pylori of 35% in developed countries and 85% in developing countries. 0%. pylori infection. 100%.93) and this was stronger for follow-up periods of Ն 10 years (RR: 0.22 In Malaysia.71 (95% CI: 353 Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd . pylori infection and potentially preventable.93) but not in women (RR: 1. blood samples for H.4–10. the prevalence rate in urban areas was 52% compared to 39% in rural areas. an OR of 5. a high overall plant food intake was associated with reduced risk of gastric cancer in men (relative risk [RR]: 0.18.18 the seroprevalence of H. Malays and Indians were 27–57. The prevalence rates in developing Asian countries such as Bangladesh.21 There is also a temporal and age-related change in the prevalence rate of H. pylori infection and the age-standardized incidence rates (ASR) of gastric cancer in selected countries in the Asia–Pacific region are listed. 95% CI: 0.18 the rates are somewhat lower at 39%.67–0. d. 0%.89) for white vegetables and 0. In mainland China. it was observed that for intestinal type non-cardia cancer. 12–29% and 49–52%.93–1. It was concluded that 5.25 The prospective design of the studies26–37 helped to circumvent the problem of classification bias in retrospective studies. In Singapore.8%.88 (95% CI: 0. Within a country. In a recent study from Malaysia. 28% and 48%. c. It was further concluded that based on an average prevalence of H. d. pylori infection and the circulating antibody response could be lost with development of cancer.40 In an ecological study.49–1. vegetable consumption was inversely associated with risk of gastric cancer. 81%. 74% and 75%. Environmental factors such as H. It also recognized the fact that not all patients with non-cardia gastric adenocarcinoma are positive for H. respectively.50).66. in which H. In the Cancer Prevention Study II.69–1. 95% CI: 2.41 There was a significant correlation of gastric cancer mortality with sodium as well as nitrate in both men and women. respectively. 0%. d. other risk factors such as ethnicity and diet were also independently associated with noncardia gastric adenocarcinoma. These differences are postulated to be related to host genetic factors. 0%. pylori serology were collected before diagnosis of gastric cancer. 36.82. differences in prevalence rates between ethnic groups exist. it is approximately 38%.12 India. In Singapore. Malays and Indians were 46%. 63. 0%.23 Statement 2: Gastric cancer is a multifactorial disease Level of agreement: a. The association with H. Salt-preserved food and dietary nitrite are potentially carcinogenic. and that other factors are involved as well.

9–29. 95% CI: 1. Statement 6: There is a protective role of ascorbic acid Level of agreement: a. Table 2 Country Prevalence of H.5% 20–29 years: 55% 30–49 years: 75% 74. Level of evidence: Ib.5% 26.3% 46. vitamin E. but may be mediated through anti-oxidant vitamins such as ascorbic acid.48 Individuals were assigned to receive H. 100%.8 3.1% 54. 47. pylori infection. Corresponding relative risk of regression in subjects with intestinal metaplasia was 3.47 However.7 1.4 6. Although epidemiological evidence suggested that a diet rich in fresh fruit and vegetables could be a protective factor against gastric cancer.1 Australia19 China20 Changle Hong Kong India13 Japan16 38% 86% 58.94) when considering only those with a longer follow up.8 18. b. 0%.1–9.53–0.7–57.8 6. with about half agreeing and half disagreeing. Correa et al.Asia–Pacific gastric cancer consensus KM Fock et al. the precise factors involved are probably more than individual vitamins and anti-oxidants.0.6 6 26. 0%.3 19. examined the effect of dietary supplementation with vitamin C. Decreased gastric juice dehydroascorbic acid concentrations were observed in patients with gastric atrophy and intestinal metaplasia.5% 11.3% 27. Only the study by Correa et al. or their corresponding placebos.2% 49. pylori-associated carcinogenesis. 0%.9 2. c. showed that dietary supplementation with ascorbic acid and beta-carotene resulted in statistically significant increases in the rates of regression of precancerous gastric lesions.3 8.5). The specific nutrients that may be protective remain unclear. results of specific interventional trials have largely been unconvincing. Level of evidence: Ib. Epidemiological evidence suggested that a diet rich in fresh fruit and vegetables could be a protective factor against gastric cancer. beta-carotene. pylori (%) Age-standardized incidence rate (per 100 000) Male Female 6. 52.8 81.7% 5–9 years: 17.48 In three other chemoprevention studies.4%.6%. conducted a randomized. There was no consensus on this statement.6 5.4% < 5 years: 22–57% > 20 years: 80–90% 1974: 72.9% 48. three other randomized controlled trials showed that ascorbic acid supplementation was not helpful in preventing progression of gastric precancerous lesions.4–52.7 10.1 Korea17 Malaysia23 Chinese Malay Indian Singapore22 Chinese Malay Indian Taiwan21 Thailand14 58 25 11.8 8. This statement was rejected. and beta-carotene on the progression and regression of Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd .6 12. b.9 21.9 62.3 (95% CI: 1.49–51 dietary interventions had no effect on prevention of precancerous gastric lesions. Mucosal ascorbic acid concentrations were also significantly lower in patients with H. Grade of recommendation: A. c. Ascorbic acid is an important anti-oxidant and may inhibit tumor cell mitotic activity without affecting normal cell growth.5 31. controlled chemoprevention trial in subjects with histological diagnoses of multifocal atrophy and/or intestinal metaplasia.4) in subjects with atrophy.6% 13. Grade of recommendation: A.6% 1994: 39. Ascorbic acid interventions resulted in statistically significant increases in the rates of regression (RR: 5.9 10. pylori eradication triple therapy and/or 354 dietary supplementation with ascorbic acid.9 Vietnam15 23. these epidemiological associations do not establish beyond doubt that dietary interventions will reduce gastric cancer incidence.1 10.7% 1984: 54.3% Overall: 46.6 7.7 9. These findings may have implications in H. d.49–51 Statement 7: The current evidence does not support the use of vitamins and other dietary supplements to prevent gastric cancer Level of agreement: a. Plummer et al. However. 0%.8 0.7–14.5 2.6% Age > 40 years: 78. d.3 7. pylori and gastric cancer in the Asia–Pacific region Seroprevalence of H. 0%. However.

61 Statement 9: Currently identified IL-1b polymorphisms in the Asia–Pacific region may not be associated with gastric cancer Level of agreement: a. pylori infection is the initiation of an inflammatory response in which the main mediators are cytokines. in the presence of H.and 2. 15. Patients with antralpredominant gastritis.59 Genetic polymorphisms of the IL-8 promoter were significantly associated with an increased risk of gastric cancer. c.54 The observation that relatives of patients with gastric cancer had a higher prevalence of atrophy and hypochlorhydria suggested genetic predisposition to the development of atrophy. The key pathophysiological event in H. and 10% of cases of gastric cancer show familial clustering. 0%.64 whereas others did not show any association. when combined with pro-inflammatory IL-1b gene polymorphisms.3) for non-cardia gastric cancer.8%.50 No statistically significant favorable effects were seen for garlic or vitamin supplements. H. b. H.53 Compared to H. IL-1b is a potent proinflammatory cytokine and is involved in the host’s response to many antigenic challenges. the prevalence of cagA in Asia is high.9 Korea10 and Matsu island in Taiwan. pylori infection results in different patterns of gastritis and consequent differences in gastric acid secretion which determine disease outcome Level of agreement: a. studied the correlation of these IL-1b genotypes with hypochlorhydria and gastric atrophy in a Caucasian population of gastric cancer relatives. whereas patients with corpus-predominant gastritis and multifocal atrophy are more likely to have gastric ulcers. You et al.53 A body of evidence supports the role of host factors in determining progression to gastric cancer in H. and increased prevalence of body atrophy and intestinal metaplasia. b. pylori-infected patients have histological gastritis and approximately 80% are asymptomatic. The key determinants of these outcomes are the severity and distribution of the H. 0%. Gastric cancer of the cardia was not associated with H. 5. Some studies are in agreement63.0-fold (95% CI: 1.2–2.9-fold. When compared with controls.52 Statement 8: Host genetic factors are important in the response to H. infection with cagApositive strains further increased the risk for gastric cancer 1. d.2) overall and 2. pylori-infected populations.2–3. 10.6-fold (95% CI: 1.68 Statement 10: Currently identified cagA genotypes in the Asia–Pacific region may not be associated with gastric cancer Level of agreement: a. pylori colonization.51 There was no association between gastric cancer mortality and regular use of vitamin E or multivitamins regardless of the duration of use. pylori infection or cagA-positive strains of H. pylori-induced gastritis. body-predominant colonization and gastritis.8%.77 In contrast.61 and TNF-a65 polymorphisms has been proposed. 63. pylori and cagA seropositivity significantly increased the risk for gastric cancer by 2. progressive gastric atrophy. 100%. the results of Asian studies are conflicting. 0%.5%. pylori gastritis.7%.2%. pylori infection.4%. population-based screening is being undertaken in Japan. Among H. and an increased risk of gastric cancer. the precursor of gastric cancer.KM Fock et al. pylori infection and disease outcome Level of agreement: a. patients with H. conducted a meta-analysis to estimate the magnitude of the risk for gastric cancer associated with cagA seropositivity. conducted a randomized trial to test the effect of one-time H. Asia–Pacific gastric cancer consensus precancerous gastric lesions. gastric carcinoma. gastritis that involved the acid-secreting corpus region resulted in hypochlorhydria.11 These are 355 Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd . The risk of developing gastric cancer is increased up to three-fold in individuals with an immediate relative suffering from gastric cancer.2%.4%. Huang et al. pylori eradication therapy and long-term vitamin or garlic supplements in reducing the prevalence of advanced precancerous gastric lesions. d.55 However. an association with other genetic markers such as IL-860.65–67 However. 0%. 10–15% develop peptic ulcer.69 H. 1–2% develop gastric cancer and a very small proportion develop gastric mucosa-associated lymphoid tissue lymphoma. Genetic polymorphisms in the IL-1 gene cluster significantly increased the risk of precancerous gastric lesions. 47. Jacobs et al. b. examined the association between gastric cancer mortality and regular use (Ն 15 times per month) of vitamin C supplements.3.78 Statement 12: Population-based screening for gastric cancer is currently undertaken at the national level in two countries and at the local level in one country Currently. the most common form of H. vitamin E supplements. pylori infection is associated with divergent clinical outcomes that range from simple asymptomatic gastritis to serious conditions such as peptic ulcer disease and gastric neoplasia. c. pylori. and currently identified cagA genotypes in the Asia–Pacific region are not associated with gastric cancer. 36. A meta-analysis of the role of IL-1b and IL-1 receptor antagonist gene polymorphisms in gastric cancer risk showed an association in Caucasians.69–76 Statement 11: The host bacterial interaction in H.58 Genetic polymorphisms in tumor necrosis factor (TNF)-a and IL-10. El Omar et al. d. but not in Asians. 0%. 47. were shown to result in a high-risk genotype with a 27-fold or greater risk of developing gastric cancer. c. d. ultimately. 73. A Finnish study of over 29 000 people also failed to show that any upper aerodigestive cancers were prevented by daily supplementation with alpha-tocopheryl acetate and/or betacarotene in older male smokers. gastric atrophy.62 A positive association between these genotypes and gastric cancer was confirmed in a follow-up study.54 A strong association between pro-inflammatory polymorphisms in the interleukin (IL)-1b gene cluster and an increased risk of developing gastric cancer has been demonstrated in Western populations55–57 as well as in Japan. c. respectively. and multivitamins. are predisposed to duodenal ulcers. 0%.60. However. pylorinegative healthy volunteers. 0%. intestinal metaplasia and. pylori infection. the hypochlorhydric subjects had less dense H. pylori-related duodenal ulcers had significantly higher basal and maximal acid output. b.49 There was no statistically significant difference in the progression rate or regression rate between vitamin and placebo groups.

3%. but significantly lower among Malay subjects.62 They found that among the relatives of cancer patients.9–66.92 There are. Appropriate approaches may include screening of high-risk populations.2%. d.90%. 31.4) for gastric cancer overall and an OR of 16 (95% CI: 3. pylori strains had an OR of 8. b. H. 0%. Both are produced by the chief and mucus neck cells in the gastric fundus and corpus. 21. mild inflammation leads to elevated levels of both PG I and PG II in the circulation initially. 95% CI: 1. 57.83 Statement 16: Low serum pepsinogen I levels and low PG I/II ratio may be useful as a marker to identify populations at high risk for gastric cancer Level of agreement: a. 0%. subjects with both a positive family history and infection with cagA-positive H. the PG I/II ratio was significantly lower in the gastric cancer group than in the normal and chronic gastritis groups (OR: 2.7%. pylori infection within families. Since the 1990s. but not PG I.84–90 The results have shown that PG testing is useful in detecting early-stage gastric cancer. while in Taiwan. but not for the Indian subjects. Level of evidence: IIa. Statement 15: Low serum pepsinogen I levels and low PG I/II ratio reflect gastric atrophy Level of agreement: a. both were independently and strongly associated with a risk for gastric cancer. late diagnosis. pylori. Grade of recommendation: B. but the negative predictive value varied between 99. Brenner et al. The prevalence of cagA in Asia is high. PG II. due to frequent late presentation and. the EUROGAST Study Group correlated gastric cancer rates with low serum PG levels in men from the same population. c. 52. c.4) for noncardia gastric cancer. 0%. Statement 14: A positive family history of gastric cancer is an important risk factor Level of agreement: a. Germany. exceptions with respect to the utility of serum pepsinogen levels.25%. pylori infection in first-degree relatives of patients with gastric cancer. Low serum pepsinogen (PG) has been used as a surrogate marker for atrophic gastritis. 78. pylori infection and a positive family history of gastric cancer are both risk factors for the disease. c. as disease severity increases further. populations with high gastric cancer risks.80). In Japan.8%. 36. A familial association may be partly related to clustering of H.1%. 0%.10–4.3%. In Korea. 0%. The gastric cancer incidence rates correlated with H. while the level of PG I and.9%. examined the prevalence of atrophy and hypochlorhydria and their association with H. and resolution of hypochlorhydria and atrophy in 50% of the subjects. Miki91 performed a meta-analysis of the sensitivity and specificity results from 42 individual studies. c. There is a need to further reduce the incidence of gastric cancer in high-risk populations and this should be based on development of national policies. 73. A study from Singapore examined whether racial differences in the prevalence of H. There is considerable morbidity and mortality associated with gastric cancer. Compared with uninfected subjects without a family history. b.79 They found that although H.9%. Eradication of H. on a trial basis.6%.80–84 PG. c. pylori infection. endoscopy is used.08% and 99. the precursor of pepsin.70–76 As such. Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd . d. there is no role for it as a marker for gastric cancer risk in an individual. The positive predictive value was low and varied between 0. pylori infection. pylori seroprevalence was similar between Chinese and Indian subjects. 0% Level of evidence: IIa. Statement 13: There is a pressing need for the development of national policies to reduce the incidence of gastric cancer which is now feasible Level of agreement: a. b. consequently.6%. The prevalence of low PG was highest in Indian subjects even when adjusted for gender and the presence of H. 21%.8%. 5. individuals are first screened using serum pepsinogen and. statewide case–control study in Saarland. The differential changes in PG levels are indicative of the histological state of the gastric mucosa. H. d. For instance. is also produced by the pyloric glands in the 356 Statement 17: Neither cagA serology nor the presence of the cagA gene has been shown to be a useful marker for gastric cancer risk in an individual Level of agreement: a. the prevalence of both gastric cancer and H. chief cells are replaced by pyloric glands and the level of PG II remains elevated. PG I level Յ 70 ng/mL and PG I/II ratio Յ 3 had a sensitivity of 77% and false-positive rate of 27%. endoscopy is performed. the prevalence of atrophy and hypochlorhydria was increased only in those with evidence of H. 0%. antrum and Brunner’s glands in the proximal duodenum. hence.2–30. exists as two main types: types I and II. are reduced. as well as by addressing known risk factors. pylori infection and family history were positively related. 5. b. in particular. In a case–control study from Thailand. pylori and serum PG could account for a racial difference in gastric cancer incidence. carried out a population-based. 15. 84. As gastritis progresses. and currently identified cagA genotypes in the Asia–Pacific region have not been associated with gastric cancer. to identify people who would benefit most from gastric cancer screening in Japan. pylori infection produced resolution of the gastric inflammation in each subject. serum PG as a marker for chronic atrophic gastritis has been incorporated into gastric cancer screening programs.Asia–Pacific gastric cancer consensus KM Fock et al. 15. In contrast.2 (95% CI: 2.8%.3. In Asia. This highlighted the limited usefulness of serum PG in the Indian population for gastric cancer screening. pylori infection to the risk of gastric carcinoma. however. screening is performed in individuals aged over 40 years using double-contrast barium or endoscopy. if the level is low. to assess the individual and joint contributions of family history and H. d. pylori infection remain high. El Omar et al. d. b. Utilizing PG as surrogate markers for gastric atrophy. pylori seropositivity for the Chinese and Malay subjects. the PG I/II ratio.22 The H.77% and 1. However.

pylori eradication therapy against antisecretory therapy without long-term maintenance therapy. d. enrolled in a community screening program in the UK were randomized to eradication therapy or placebo and followed up after 10 years. and public health measures to monitor the patterns of drug resistance would be needed. Statement 20: Population H. Grade of recommendation: A.6% versus 5. 0%. b. 0%. 70%. Eradication of H.42–1. A recent paper on public awareness of breast cancer and screening showed that increased awareness led to increased referrals and screening for breast cancer. 0%. pylori screening and treatment. The number needed to treat to cure one case of dyspepsia was 14 (95% CI: 10–25). The savings were greater than the initial cost of H. pylori eradication in the management of dyspepsia symptoms in patients with functional dyspepsia was assessed in a meta-analysis.25. eradication therapy was compared to placebo or pharmacological therapies in H. 0%. reduce recurrence of peptic ulcers and reduce incidence of bleeding peptic ulcers in clinical trials. 75%. there was a strong concern by the participants of the meeting that H.96 There was a 10% relative risk reduction in the H. Comparing H. d. 95% CI: 0. NNT: 20.73. pylori infection was more effective than antisecretory therapy (with or without long-term maintenance therapy) in preventing recurrent bleeding from peptic ulcer. 10%. Level of evidence: III. pylori screening and treatment will reduce peptic ulcer disease and its complications. 95% CI: 0. pylori status. 95% CI: 0.25). c. pylori-positive peptic ulcers.53).97 In that study. 20%. 95% CI: 0. However.10). Level of evidence: I. b.93 In a Cochrane review.98 This will be especially so in the context of non-compliance to treatment.08–0. 25%. Screening program for H.6% (OR: 0.76). There was a significant 10-year mean saving in total dyspepsiarelated costs of US$117 per person (95% CI: 11–220).KM Fock et al. pylori screening. 90%. A recent study investigated the effect of screening for H.103.105 357 Statement 19: Population H. c. pylori screening and treatment will result in a modest reduction of dyspepsia symptoms and costs Level of agreement: a. Asia–Pacific gastric cancer consensus II. A recent systemic review of 21 studies involving 10 146 patients showed that ulcers were more common in H.25.17. b. pylori screening could possibly increase cancer anxiety.99–102 In Europe.94 In duodenal ulcer healing. pylori screening and treatment will increase antibiotic resistance in the community Level of agreement: a.37.83-fold. The risk of ulcer was 17. There was concern about the problem of increased antibiotic resistance in the community with population H. anxiety and cancer phobia. pylori on dyspepsia and dyspepsia-related resource use over 10 years. 0%. pylori-negative non-users and the presence of both H. especially to a level disproportionate to the actual risk of disease.58– 0.104 Ensuring compliance to treatment would be important in preventing the selection of resistant strains. 0%. no significant differences were detected between eradication therapy and maintenance therapy with acid suppressants (RR of ulcer recurring: 0.20. An association has been found between the consumption level of antibiotics and the rate of bacterial resistance to antimicrobials. In gastric ulcer healing.76. the rebleeding rate was 1. irrespective of H. pylori to macrolides was noted in countries with the highest consumption of these drugs. 95% CI: 0.29. c. 95%. Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd . the efficacy was similar between eradication therapy and acid suppressants (RR: 1.10–0. pylori and NSAIDs increased the risk of bleeding 20. pylori screening will increase cancer anxiety in the population Level of agreement: a. Level of evidence: I. 95% CI: 0. In preventing gastric ulcer recurrence. without an actual increase in detection rates. aged 40–49 years. The widespread use of antimicrobials constitutes a risk for antimicrobial resistance. 10%. b. d. 2324 H pylori-positive individuals. irrespective of NSAID use. pylori infection as well as non-steroidal anti-inflammatory drug(s) (NSAIDs) use. pyloripositive than in H. 95% CI: 0. pylori eradication against antisecretory therapy with long-term maintenance therapy.88–1. Grade of recommendation: C. Comparing H. number needed to treat [NNT]: 7.54-fold higher in H. pylori eradication therapy versus antisecretory therapy for the prevention of recurrent bleeding from peptic ulcer was assessed in another Cochrane review.66. pylori infection and gastric cancer Statement 18: Population H. An economic model suggested that this modest benefit may be cost-effective.26).20– 0. pylori-negative patients (OR: 4. The role of H. pylori eradication regimens as well as the efficacy of antibiotics against other infections.9% versus 20% (OR: 0. There are no published data on the association of cancer anxiety in the population with H. eradication therapy was superior to acid suppressants (RR of ulcer persisting: 0. 95% CI: 12–100). leading the authors to conclude that while it was encouraging that media campaigns raised awareness. a trend toward a higher resistance of H. 95% CI: 5–11). Grade of recommendation: C. and more common in NSAID users than in nonusers (OR: 3. pylori infection has been shown to facilitate peptic ulcer healing. d. pylori screening and eradication. Level of evidence: IV. there may be a detrimental effect with increased radiation exposure. This provides evidence that population H. Statement 21: Population H. Peptic ulcers are independently related to both H. pylori eradication group (95% CI: 6–14%) compared to placebo. 5%. 0%. c. Grade of recommendation: A.26–0.76) and no treatment (RR: 0. the rebleeding rate was 2. The efficacy of H. pylori screening and treatment will reduce peptic ulcer disease and its complications Level of agreement: a. eradication therapy was superior to no treatment (RR: 0.95 It was shown that treatment of H.32. In preventing duodenal ulcer recurrence.15–0. This may potentially impact on the efficacy of H. pylori-positive NSAID users than in H. 95% CI: 0.03). but eradication therapy was superior to no treatment (RR: 0.42).

pylori eradication prevented the progression of precancerous gastric lesions.Asia–Pacific gastric cancer consensus KM Fock et al.109 showed that H.119 although this has not been a universal observation. The results were similar for studies conducted in patients with pre-existing GERD110–112 and in the general population. In a prospective observational study. the issue of the optimal population age cut-off for treatment of infection to prevent cancer remains unknown.106 However. c. pylori eradication in reducing the risk of gastric cancer can be considered indirectly from studies that assessed its effect on precancerous lesions and directly from its effect on cancer development.40. pylori eradication would almost certainly outweigh any theoretical impact on Barrett’s cancer.56 (95% CI: 0. pylori eradication had a direct impact on gastric cancer occurrence. 0%. Level of evidence: I. c. pylori negative had. 15% more regression and 358 Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd . pylori infection and GERD or Barrett’s esophagus. pylori positive. randomized.127 At the end of the follow-up period. b. 0%. 0%. b. d. 0%. pylori eradication seemed to reduce the incidence of gastric cancer in patients without baseline precancerous gastric lesions. Two other prospective. significantly more patients (4% vs 1. Even though this metaanalysis relies on the results of two studies128. pylori eradication in the prevention of subsequent gastric neoplasia.121 Results of the 6-year follow-up evaluation showed that H.5%) in the H. Level of evidence: I. Correa et al. with an OR of 2. One Japanese study in patients having endoscopic mucosal resection for gastric adenocarcinoma did show a significant effect of H.124 Uemura et al. pylori-positive subjects and in those in whom H. Statement 22: H.50. Another prospective.122 Those who were H.131 that have yet to be published in peer-reviewed journals. Grade of recommendation: C. 0.128–130 evaluating H. pylori eradication produced a significant increase in the rates of regression for intestinal metaplasia and gastric atrophy. randomized study was performed by Leung et al. subjects with persistent H.41–3. The sole rejection in the voting was made on the basis that the actual age of cut-off remained unknown. data. on average. metachronous gastric cancer developed in 9% of those not treated.118.113. assessed the effect of H.50. pylori CagA seropositivity was inversely and strongly associated with a risk of esophageal adenocarcinoma. placebocontrolled. H.123 At 5 years follow up. 5%. five randomized placebo-controlled H. the association with Barrett’s esophagus may be spurious and the benefits of H. Statement 25: Eradication of H.114 These data support the statement that H pylori eradication does not increase reflux symptoms in the community. Level of evidence: III. pylori has been shown to reduce the incidence of gastric cancer development even at a late age Level of agreement: a. d. but not in uninfected persons. 0%. double-blind. d. pylori was eradicated. pylori infection would depend on local resources and ethical considerations. unpubl. 0%. 0%. pylori-positive group developed gastric cancer.131 A meta-analysis was performed (Moayyedi P. 45%. 90%. first provided evidence that H. H.24). GU MACH and DU MACH108. With H. Grade of recommendation: A. Grade of recommendation: A.129 Hence. 55%. pylori eradicated. After a 3-year follow-up period. placebo-controlled studies conducted in China reached similar conclusions. the same group also showed that gastric cancer developed in persons infected with H. These findings were subsequently confirmed at the end of the 12-year follow-up period. c. a post hoc metaanalysis of eight double-blind studies of H.121–130 the results of both randomized and non-randomized studies suggested that in a subpopulation of treated subjects.125 They conducted a non-randomized H. b. pylori screening and treatment in the general population and all showed a non-significant trend towards risk reduction for gastric cancer with H. pylori eradication for ulcer disease did not lead to development of erosive esophagitis or new symptomatic GERD or worsening of symptoms in patients with pre-existing GERD. pylori eradication. the consensus meeting concluded that the evidence is very suggestive. pylori eradication.13 (95% CI: 1.8). 10%. The choice of an arbitrary age cut-off for population screening and eradication for H. Grade of recommendation: A. 0%. pylori screening and treatment does not increase the risk for esophageal adenocarcinoma Level of agreement: a. pylori eradication. Level of evidence: I. Some data suggested an inverse association between H. pylori infection had a significantly higher risk of progression to intestinal metaplasia than those with successful eradication. pylori eradication and gastric cancer Statement 24: H. 85%. pylori. The potential benefit of H.126 A recent non-randomized. pylori eradication107 and a large post hoc analysis of the peptic ulcer trials.120 There was consensus that since there was no association between GERD and H. Labenz et al. 100%. 10%. initially suggested that an increase in the prevalence of gastroesophageal reflux disease (GERD) occurred after H. 2007) using the raw data from these five studies. pylori eradication trial in patients with early gastric cancer treated by endoscopic resection. pylori eradication trials have been conducted in Asia to address this issue. compared with 0% in patients with H. d.115–117 There are epidemiological studies that showed H. As elaborated in the discussion following statement 24. subsequently. pylori eradication does not increase reflux symptoms in the community Level of agreement: a. 14% less progression of precancerous gastric lesions than subjects who were H. c. III. pylori. However. pylori eradication reduces the risk of developing gastric cancer Level of agreement: a. multifocal atrophy and dysplasia in a high gastric cancer risk region of Colombia. the pooled relative risk of developing gastric cancer was 0. To date. b. Statement 23: Current data suggest that population-based H.128–131 There were four studies50. H. interventional trial evaluated gastric cancer development after 3 years in H. pylori eradication therapy on intestinal metaplasia.

pylori positive. All these studies were conducted in high-risk populations. affordability would be a major concern and. Level of evidence: I. it is not recommended at this time to adopt a strategy of H. This is clear from studies that used occurrence of precancerous gastric lesions as a surrogate outcome measure for gastric cancer development. Grade of recommendation: A. approximately one-third of the patients successfully treated still experienced progression of precancerous gastric lesions. there are data that suggest that screening for H pylori and eradicating it would reduce total dyspepsia-related health-care costs. c. Level of evidence: IV. 25%. The occurrence of gastric cancer after successful H. pylori infection were to be eradicated. Grade of recommendation: A. Ogura et al. pylori eradication in those patients who have already developed advanced precancerous gastric lesions does not prevent gastric cancer development and.5 years. c. at the end of the 12-year follow-up period. By targeting high-risk populations. b. 20%. noted that progression of precancerous lesions occurred in 45% in the active treatment group versus 49% in the placebo group. Grade of recommendation: A. quite apart from gastric cancer prevention. 0%. in high-risk populations such as Japan and Korea. Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd .50 Similar findings were noted by Zhou et al. Level of evidence: I. 4% in the H. pylori screen and treat is a gastric cancer risk reduction strategy in high-risk populations Level of agreement: a. 0%. pylori eradication to prevent precancerous gastric lesions and gastric cancer have been conducted in high-risk populations. 0%. screening for H. In light of the data concerning the relationship between 359 Statement 27: H. 0%. Asia–Pacific gastric cancer consensus Statement 26: Gastric cancer can still occur despite eradication of the infection Level of agreement: a. Grade of recommendation: C. endoscopic surveillance may continue to be performed. c. pylori eradication and its impact on the progression of precancerous gastric lesions and occurrence of gastric cancer discussed earlier. pylori eradication was able to induce regression of precancerous gastric lesions. pylori was successfully eradicated. 90%. You et al. 0%. pylori eradication may represent a primary chemopreventive strategy. d. c. these data suggest that although H. To date. 55%. reported that at the 3-year follow up. 0. Grade of recommendation: C. all randomized controlled trials on H. pylori-positive group and 1. population screening and treatment of H. 80%. pylori-negative group developed gastric cancer. if this eradication occurred before the development of advanced precancerous gastric lesions. the benefit is not universal because advanced precancerous changes may continue to progress. economic modeling using efficacy data from the meta-analysis presented in statement 24 and randomized controlled trial data97 with Asian costs applied suggested this strategy would be cost-effective in developed countries where gastric cancer rates were high. pylori screening and eradication with the aim of decreasing the already low incidence of gastric cancer in low-risk populations. pylori infection is the strategy of choice Level of agreement: a. 0%. although those who were H. d. b. after a follow-up period of 7 years. up to 45% of treated subjects would still show disease progression. pylori eradication has also been assessed. pylori is not recommended Level of agreement: a. 0%. Current evidence suggests that H. pylori negative had more regression and less progression of precancerous gastric lesions than subjects who remained H. However.121–130 it was felt that screening for H. pylori infection and eradicating it in high-risk populations would have an impact on reduction of gastric cancer incidence. as well as those that directly assessed the incidence of gastric cancer. Level of evidence: I.123 In another prospective randomized trial. particularly in those with early and non-severe lesions. the limited published data on H.. Level of evidence: I. 10%.129 Statement 28: In high gastric cancer-risk populations in the Asia–Pacific region. Even within these high-risk populations. 20%. pylori infection offers the possibility to reduce the risk of peptic ulcer disease and gastric cancer Level of agreement: a. In a study from Colombia.122 In a study by Leung et al. To date.124 Collectively. d. However. c.5% in the H. 0%. during the period of follow-up of 7.3% of placebo developed gastric cancer.KM Fock et al. pylori screening and treatment does not exclude the existing practice of gastric cancer surveillance in high-risk populations such as in Japan and Korea Level of agreement: a. b. 80%. d. H. d. pylori eradication might represent a primary chemopreventive strategy in a subset of subjects without advanced precancerous gastric lesions. 75%. 0%. b. 0%.9% of treated subjects and 1. b. if H. 100%. Hence. progression of intestinal metaplasia was found in approximately one-third of patients in whom H. Level of evidence: IV. Statement 29: H. pylori eradication and gastric cancer prevention have been from high-risk populations. Even though H. on a national level. Grade of recommendation: A. The effect of H. pylori eradication therapy on precancerous gastric lesions such as intestinal metaplasia. there would be a better return for the economic resources that need to be committed for such a strategy. 0%. Statement 30: In populations at low risk for gastric cancer. c. gastric cancer may still develop despite successful eradication therapy. Based on the results of the published data on H. 0%. as such.97 Statement 31: Opportunistic testing and treating of H. 0%. Indeed. individual strategies need to be developed. d. In the long term.127 In the study by Wong et al. multifocal atrophy and dysplasia was assessed by several studies. it may even mean that endoscopic surveillance for gastric cancer may no longer be necessary. For developing countries in the Asia–Pacific region. b. 45%.

pylori eradication before the onset of irreversible precancerous changes. Grade of recommendation: C. and that it takes time for precancerous lesions to occur.134 Statement 34: A serological test for H. pylori infection to prevent gastric cancer is not recommended. Grade of recommendation: B. d. 100%. Level of evidence: IV. Level of evidence: I. pylori infection as part of the screening strategy is not necessary Level of agreement: a. 0%. However. 10%.132. It was unanimously agreed that first-line treatment of H. clarithromycin and amoxicillin or metronidazole for at least 7 days. as H. Grade of recommendation: C. 0%. 20%. The program would therefore also be less financially attractive from a third-party payer perspective. pylori infection is recommended 10–20 years before the take-off age for gastric cancer Level of agreement: a. in the subgroup of patients with no precancerous lesions (gastric atrophy. pylori and gastric cancer. pylori infection is most effective before atrophic gastritis has developed Level of agreement: a. the risk of false-negative results are minimal and do not justify the costs of repeated testing for H.25 and peptic ulcer disease. However. d. 0%. However. Statement 32: In a high-risk population. the diagnostic accuracy is low at approximately 80–84%. 0%. The occurrence of precancerous lesions may represent a stage of irreversibility in the pathogenesis of gastric cancer. 95%. 20%. However. pylori eradication and. b. and were used in population screening for H.129 During the period of follow up. 100%. Grade of recommendation: B.136 There is also an increased risk of reinfection after successful eradication therapy in childhood when compared to adulthood. Statement 33: In high-risk populations. pylori infection is usually acquired in childhood. pylori infection. pylori infection should be in accordance with national treatment guidelines.94 and the data that showed reduced occurrence of gastric cancer125. pylori screening are the adults in high-risk populations. pylori that has been locally validated is recommended for population screening Level of agreement: a. 0%. screening for H.133 Statement 36: Repeated testing for H. Standard first-line H. Local validation is 360 Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd .Asia–Pacific gastric cancer consensus KM Fock et al. pylori strains differ across geographic locations. b. However some kits have a high accuracy rate (> 90%) and may be used when locally validated. 65%. 0%. The participants based their decision on the indirect evidence from the randomized controlled study by Wong et al. Childhood screening of H. 75%.139 As such. for which reason they are useful for epidemiological studies. pylori antigens. pylori infection 10–20 years before the take-off age for gastric cancer in the population would allow H. They are widely available and inexpensive. 25%. 5%. screening for H. c. d. could help prevent gastric cancer later in life. Infections are generally acquired during childhood. These first-choice H.135. pylori eradication. 0%. c. Serological tests for diagnosis of H. it was felt that opportunistic testing and treating of H.53 Serological tests. pylori infection should be in accordance with national treatment guidelines Level of agreement: a. pylori infection in epidemiological studies. d. 0%.02). Level of evidence: IIa. b. H. It was felt that screening for H. the incidence of gastric cancer development at the population level was similar between those who received H. or gastric dysplasia) at presentation. Grade of recommendation: B. Level of evidence: IV.137 The interval between screening and preventing gastric cancer would be lengthened and therefore payers for the program would have to wait a longer time before seeing any return on their investment. pylori infection to prevent gastric cancer is not recommended Level of agreement: a. 80%. pylori eradication and controls. pylori eradication compared to 6% in controls (P = 0. and as children would not have not harbored the organism for long enough to have developed precancerous lesions. the issue of costs and affordability of this strategy of screening and subsequent treatment for H. The unanimous consensus was based on knowledge that the occurrence of gastric cancer goes through a cascade. thus. c. pylori infection offered a possibility to reduce the risk of peptic ulcer disease and gastric cancer. b. pylori eradication have not been addressed in the region. 0%. pylori treatments are recommended worldwide. are immunogenic and long-lasting.134 Statement 35: Childhood screening of H. c. Grade of recommendation: A. 5%. d. no patient developed gastric cancer after H. pylori prevalence and the incidence of gastric cancer are low in childhood. widespread population screening programs would be enormously expensive and not justifiable at a national level. intestinal metaplasia. pylori infection rely on the detection of immunoglobulin (Ig)G antibodies to H. 0%. d. Statement 37: First-line treatment of H. H.138. childhood is theoretically an attractive time for H. b. Level of evidence: IIb. c. and that the decision to treat for 1 or 2 weeks would also depend on the results of locally validated data. 0%.83 Overall. optimal because H.126 and peptic ulcer disease94 after H. in particular antibodies against the specific antigen CagA. pylori eradication regimens are based on triple therapy comprising twice daily proton pump inhibitors. 0%. This strategy assumes reinfection would be low in adults successfully treated. it is recognized that the exact choice of antimicrobials may differ based on local patterns of antibiotic resistance. c. b. Level of evidence: III. The targeted group for H.

For the individual patient. Survival after surgical treatment of early gastric cancer: surgical techniques and long-term survival. pylori One-off treatment according to local guideline. Ferlay J. Current evidence suggests that H. 5%. pylori eradication is not practical or cost-effective to consider on a population basis Level of agreement: a.134 In clinical practice.140 However. Global cancer statistics 2005. Statement 38: Confirmation of H. screening in low-risk populations is not currently recommended. although it is acknowledged that supporting data are lacking and such a strategy is not recommended at this time. b. d. Katada N. Major causes of treatment failure are poor patient compliance and antibiotic resistance. pylori eradication is not practical or cost-effective to consider. 35%. The future of gastric cancer prevention. and it has come time to try and intervene to prevent this cancer at the population level. 2005. Gastric Cancer. Bray F. At the same time. 2004.g. pylori negative positive Continue program of gastric cancer surveillance based on national guidelines Qualified reassurance. 0%. pylori screening and eradication in high-risk populations (Fig. at the population level. Langenbecks Arch. One may however. pylori screening and eradication in populations at high or intermediate risk for gastric cancer. 3 Kikuchi S. consider retesting and follow-up therapy on a case by case basis. CA Cancer J. 389: 69–74. e. 2 Correa P.KM Fock et al. pylori eradication by using non-serological tests. 55: 74–108. one may assess the success of H. Grade of recommendation: C. Clin. Eradicate H. pylori eradication by using non-serological tests at least 4 weeks posttherapy and institute a second-line therapy in the event of treatment failure. pylori eradication probably reduces the incidence of gastric cancer. there should be confirmation of the success of H. c. the current gastric surveillance programs in populations at high risk for gastric cancer such as in Japan and Korea should be continued. gastric cancer. Pisani P. Sakuramoto S et al. H. pylori eradication. which should be performed at least 4 weeks after treatment has been completed. Level of evidence: IV. 2004. 60%. pylori eradication can prevent the progression of precancerous gastric lesions and. confirmation of H. Finally. On a case-by-case basis. Camargo MC. perform 2nd test on individualized basis. 7: 9–16. Figure 1 Strategy of H. Surg. References 1 Parkin DM. approximately 20% of patients will fail to eradicate H. in those without advanced precancerous lesions. Piazuelo MB. Asia–Pacific gastric cancer consensus Populations with a high or intermediate risk of gastric cancer Patients with dyspepsia Asymptomatic individuals (18–60 years) Investigate dyspepsia One-off screening with locally validated serology test for H. pylori infection with the recommended treatment regimens. Conclusion After carefully reviewing the literature and weighing the evidence and uncertainties. 1-week triple therapy. pylori infection and Journal of Gastroenterology and Hepatology 23 (2008) 351–365 © 2008 The Authors Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd 361 . because of the costs involved and the resources required. 1) should reduce gastric cancer incidence and is recommended by this consensus conference. This approach may be considered in intermediate-risk populations. such as in patients with dyspepsia symptoms and those who request confirmation of successful H. this consensus conference has concluded that there is a definite causal link between H. A strategy of H.

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Appendix I List of participants and contributors Australia: Professor Nick Talley. Aliment. Vaughan D. Gastroenterol. Natl Cancer Inst. Best Pract. Indonesia: Professor Abdul Aziz Rani. Cancer Epidemiol. Gastroenterology 2001. Uemura N. Gastroenterology 2006. Gut 2007. 96: 396–402. Effect of Helicobacter pylori eradication on subsequent development of cancer after endoscopic resection of early gastric cancer. Am. Sonnenberg A. Res. 117: 336–41. Sung JJ. Dig. 2004. J. Held M. 116: 11–14. 2007. 2005. Ogura K. Rohan T et al. An inverse relation between CagA+ strains of Helicobacter pylori infection and risk of esophageal gastric cardia adenocarcinoma. Zhou LY. Fontham ET. O’morain C et al. Kraaz W. Correa P. 2): A4. 291: 187–94. J. Saito D. Blot WJ et al. (Engl. Asia–Pacific gastric cancer consensus 118 119 120 121 122 123 124 125 126 127 128 129 130 131 with GERD. Inadomi JM. Gut 2004. J. Chin J. 2000. Natl Cancer Inst. Review article: medical decision models of Helicobacter pylori therapy to prevent gastric cancer. Korea: Professor Jae G Kim. Kumar D. 58: 588–90. Gastroenterol. Boku N.KM Fock et al. 103: 815–21. Rowland M. pylori eradication. Bernstein L et al. 12 (Suppl. Professor Nayoung Kim. Am. J. Role of Helicobacter pylori Cag A+ strains and risk of adenocarcinoma of the stomach and esophagus. 345: 784–9. Dr Ratha-korn Vilaichone. Professor Richard Hunt. Held M. Dr Tiing Leong Ang. J. Barrett’s esophagus.