Chemoprevention of Gastric Dysplasia: Randomized Trial of Antioxidant Supplements and Anti-Helicobacter pylori Therapy

Gail, Mitchell H.; Brown, Linda Morris; You, Wei‐Cheng

doi:10.1093/jnci/92.23.1881

Cited by 627 publications

(491 citation statements)

References 23 publications

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“…Several studies have reported annual incidences of MGC after H. pylori eradication, ranging from 0.1 to 0.5 % in healthy individuals or peptic ulcer patients [26][27][28][29][30][31][32][33], and from 0.8 to 4.1 % in patients after endoscopic resection for early gastric cancer [9,[11][12][13][14][15]. Individuals after endoscopic resection had a higher risk of MGC compared with those who were healthy or had peptic ulcers.…”

Section: Discussionmentioning

confidence: 99%

Incidence of and risk factors for metachronous gastric cancer after endoscopic resection and successful Helicobacter pylori eradication: results of a large-scale, multicenter cohort study in Japan

Mori

Nakajima

Asada³

et al. 2015

Gastric Cancer

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Background A previous multicenter prospective randomized study from Japan showed that Helicobacter pylori eradication reduced the development of metachronous gastric cancer (MGC) after endoscopic resection for early gastric cancer. MGC risk, however, is not eliminated; yet few studies have evaluated its long-term incidence and risk factors. In this study, we investigated the incidence of and risk factors for MGC in patients who underwent endoscopic resection for early gastric cancer with successful H. pylori eradication. Methods A total of 594 patients who underwent endoscopic resection for early gastric cancer and successful H. pylori eradication at three institutions (National Cancer Center Hospital, University of Tokyo Hospital, and Wakayama Medical University Hospital) were analyzed retrospectively. Annual endoscopic surveillance was performed after initial endoscopic resection. MGC was defined as a gastric cancer newly detected at least 1 year after successful H. pylori eradication. Results Ninety-four MGCs were detected in 79 patients during the 4.5-year median follow-up period. KaplanMeier analysis showed the cumulative incidence of MGC 5 years after successful H. pylori eradication was 15.0 %; the incidence of MGC calculated by use of the person-year method was 29.9 cases per 1000 person-years. Multivariate analysis using the Cox proportional hazards model revealed that male sex, severe gastric mucosal atrophy, and multiple gastric cancers before successful H. pylori eradication were independent risk factors for MGC. Eleven percent of MGCs (10 of 94) were detected more than 5 years after successful H. pylori eradication. Conclusion Surveillance endoscopy for MGC in patients who have undergone endoscopic resection for early gastric cancer should be performed even after successful H. pylori eradication.

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Section: Discussionmentioning

confidence: 99%

Incidence of and risk factors for metachronous gastric cancer after endoscopic resection and successful Helicobacter pylori eradication: results of a large-scale, multicenter cohort study in Japan

Mori

Nakajima

Asada³

et al. 2015

Gastric Cancer

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“…This study did not observe any association with plasma levels of a-or b-carotene and GC risk, whereas previous prospective studies have shown lower plasma levels of b-carotene in GC cancer cases vs controls in a Western population (Eichholzer et al, 1996) and either an inverse association (Yuan et al, 2004), no association or a positive association (You et al, 2000) with GC risk in high-risk Chinese populations. Intervention studies with b-carotene, however, have shown no effect on GC risk in low-risk populations (Hennekens et al, 1996), and either no effect (Varis et al, 1998) or mild protective effects in high-risk populations (Blot et al, 1995;Correa et al, 2000). In the present study, no GC risk associations were observed for dietary b-carotene and in a concurrent study of fruit and vegetable intake based on the entire EPIC cohort, no GC risk association was observed with the intake of fruiting and root vegetables , which are good sources of carotenes (Al Delaimy et al, 2005a).…”

Section: Discussionmentioning

confidence: 99%

Plasma and dietary carotenoid, retinol and tocopherol levels and the risk of gastric adenocarcinomas in the European prospective investigation into cancer and nutrition

Jenab¹,

Riboli²,

Ferrari³

et al. 2006

Br J Cancer

111

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Despite declining incidence rates, gastric cancer (GC) is a major cause of death worldwide. Its aetiology may involve dietary antioxidant micronutrients such as carotenoids and tocopherols. The objective of this study was to determine the association of plasma levels of seven common carotenoids, their total plasma concentration, retinol and a-and g-tocopherol, with the risk of gastric adenocarcinoma in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), a large cohort involving 10 countries. A secondary objective was to determine the association of total sum of carotenoids, retinol and a-tocopherol on GCs by anatomical subsite (cardia/noncardia) and histological subtype (diffuse/intestinal). Analytes were measured by high-performance liquid chromatography in prediagnostic plasma from 244 GC cases and 645 controls matched by age, gender, study centre and date of blood donation. Conditional logistic regression models adjusted by body mass index, total energy intake, smoking and Helicobacter pylori infection status were used to estimate relative cancer risks. After an average 3.2 years of follow-up, a negative association with GC risk was observed in the highest vs the lowest quartiles of plasma b-cryptoxanthin (odds ratio (OR) ¼ 0.53, 95% confidence intervals (CI) ¼ 0.30-0.94, P trend ¼ 0.006), zeaxanthin (OR ¼ 0.39, 95% CI ¼ 0.22-0.69, P trend ¼ 0.005), retinol (OR ¼ 0.55, 95% CI ¼ 0.33-0.93, P trend ¼ 0.005) and lipid-unadjusted a-tocopherol (OR ¼ 0.59, 95% CI ¼ 0.37-0.94, P trend ¼ 0.022). For all analytes, no heterogeneity of risk estimates or significant associations were observed by anatomical subsite. In the diffuse histological subtype, an inverse association was observed with the highest vs lowest quartile of lipid-unadjusted a-tocopherol (OR ¼ 0.26, 95% CI ¼ 0.11-0.65, P trend ¼ 0.003). These results show that higher plasma concentrations of some carotenoids, retinol and a-tocopherol are associated with reduced risk of GC.

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“…Ingesta de compostos nitrogenados, dieta rica em sal e pobre em frutas, verduras e vitamina C, bem como tabagismo e ocorrência de refluxo biliar parecem estar relacionados a maior ocorrência de lesões pré-neoplásicas e câncer gástrico (9,18,19,25,42,43) .…”

Section: Discussionunclassified

Prevalência da infecção por Helicobacter pylori e das lesões precusoras do câncer gástrico em pacientes dispéticos

Müller

Fagundes

Moraes

et al. 2007

Arq. Gastroenterol.

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RESUMO -Racional -A infecção pelo Helicobacter pylori é fator importante no desenvolvimento da carcinogênese gástrica, mas somente uma fração dos pacientes infectados irá desenvolver câncer gástrico. A infecção pelo H. pylori determina gastrite crônica não-atrófica, que pode evoluir para gastrite atrófica e metaplasia intestinal e, finalmente, para displasia e adenocarcinoma. , 3% e 15% das biopsias, respectivamente. A infecção por H. pylori determinou uma razão de chances 10 vezes (IC95% 6.50 -17%) maior de se encontrar algum grau de alteração histológica na mucosa gástrica. A razão de chances dos pacientes infectados apresentarem gastrite crônica não-atrófica, foi igual a 3 (IC95% 2,2 -3,4). A razão de chances dos pacientes infectados apresentarem gastrite atrófica e metaplasia intestinal foi menor que 1. Conclusão -A prevalência da infecção por H. pylori foi alta (76%) e os indivíduos infectados apresentaram probabilidade 10 vezes maior para a ocorrência de lesão da mucosa gástrica. Gastrite crônica não-atrófica apresentou prevalência de 77%, gastrite atrófica 3% e metaplasia intestinal 15%. A infecção pelo H. pylori determinou uma probabilidade 3 vezes maior para o desenvolvimento de gastrite crônica não-atrófica e não determinou risco para a ocorrência de gastrite atrófica e metaplasia intestinal, sugerindo que possivelmente outros fatores de risco, além do H. pylori, estejam envolvidos no processo da carcinogênese gástrica. DESCRITORES -Infecções por Helicobacter. Neoplasias gástricas. Condições pré-cancerosas. Dispepsia. INTRODUÇÃOO câncer gástrico é a segunda causa mais comum de morte por câncer no mundo e quase dois terços dos casos ocorrem em países em desenvolvimento (28) . Progresso significante na etiologia do câncer gástrico foi a identificação do Helicobacter pylori (H. pylori) e as evidências acumuladas que levaram a sua classificação como fator importante ligado ao processo da carcinogênese gástrica. No entanto, tem-se observado grande heterogeneidade entre as populações, no que diz respeito ao risco do desenvolvimento de câncer gástrico associado à infecção pelo H. pylori, notando-se que nas populações com alta prevalência da infecção somente uma fração da mesma irá desenvolver câncer gástrico (15) .Estudos da mucosa gástrica em populações de alto risco têm revelado uma série de lesões que, seqüencialmente, evoluiriam da condição normal para gastrite crônica não-atrófica (GCNA), que evoluiria para gastrite atrófica (GA) e metaplasia intestinal (MI) e, finalmente, para displasia e adenocarcinoma (7,8,10,35) . Portanto, a infecção pelo

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Chemoprevention of Gastric Dysplasia: Randomized Trial of Antioxidant Supplements and Anti-Helicobacter pylori Therapy

Cited by 627 publications

References 23 publications

Incidence of and risk factors for metachronous gastric cancer after endoscopic resection and successful Helicobacter pylori eradication: results of a large-scale, multicenter cohort study in Japan

Incidence of and risk factors for metachronous gastric cancer after endoscopic resection and successful Helicobacter pylori eradication: results of a large-scale, multicenter cohort study in Japan

Plasma and dietary carotenoid, retinol and tocopherol levels and the risk of gastric adenocarcinomas in the European prospective investigation into cancer and nutrition

Prevalência da infecção por Helicobacter pylori e das lesões precusoras do câncer gástrico em pacientes dispéticos

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