Tobacco smoking and intestinal metaplasia: Systematic review and meta-analysis

Morais, Samantha; Rodrigues, Sandra; Amorim, Liliana; Peleteiro, Bárbara; Lunet, Nuno

doi:10.1016/j.dld.2014.08.034

Cited by 20 publications

(16 citation statements)

References 63 publications

(121 reference statements)

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“…Taken together, these may have contributed to conservative PAF estimates, though not compromising the comparison across regions. To further improve the accuracy of our estimates of PAF, we used sex-specific summary RRs, to account for differences in the patterns of smoking between men and women, and we assumed a time lag of approximately 10 years between exposure to smoking and occurrence of cancer, which is supported by the available evidence on the relation between smoking and gastric cancer precursor lesions [16]. This may have contributed to more accurate estimates of the burden of gastric cancer attributable to smoking than in previous studies, which took into account a smaller [21] or no lag time [26].…”

Section: Discussionmentioning

confidence: 99%

“…For this, we used country-specific data on smoking prevalence and gastric cancer incidence and published estimates of the magnitude of the association between smoking and gastric cancer. A time lag of approximately 10 years was assumed, based on the stronger associations observed between smoking and cancer or intestinal metaplasia [15,16] than with the preceding gastric lesions, indicative of an effect later in carcinogenesis.…”

Section: Methodsmentioning

confidence: 99%

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Worldwide Burden of Gastric Cancer Attributable to Tobacco Smoking in 2012 and Predictions for 2020

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Worldwide Burden of Gastric Cancer Attributable to Tobacco Smoking in 2012 and Predictions for 2020

et al. 2015

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“…Gastric and intestinal metaplasia upon nicotine administration was recently reported by Morais et al . (). The significant increase in gastrin concentrations in nicotine‐treated animals might explain the gastric erosions that have been seen upon macroscopic examination of the stomach of nicotine‐treated rats, because gastrin is an important stimulator to gastric acid secretion.…”

Section: Discussionmentioning

confidence: 97%

Effects of different routes of nicotine administration on gastric morphology and hormonal secretion in rats

Ali

Hamed

Ayuob

et al. 2015

Experimental Physiology

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New Findings r What is the central question of this study? Does chronic administration of nicotine by different routes affect gastric hormonal secretions and morphology in rats?r What is the main finding and its importance?Chronic nicotine administration increased levels of gastrin, ghrelin and histamine but decreased prostaglandin E 2 . Nicotine administered orally and by inhalation had a marked negative impact on the histological structure of the gastric mucosa compared with intraperitoneal administration. The negative impact of nicotine administration on gastric structure was associated with an increased concentration of gastrin and decreased prostaglandin E 2 , which might be the cause of gastric/peptic ulcers in heavy smokers. The increase in ghrelin concentration and its effect following chronic nicotine administration needs further investigation.The aim was to assess the effects of different routes of chronic nicotine administration on gastric morphology and hormonal secretion; mainly gastrin, ghrelin, histamine and prostaglandin E 2 (PGE 2 ). Forty adult male albino rats were randomly assigned into four groups (10 rats per group), treated for 21 days as follows: control group (given standard rat pellets and water only); oral nicotine-treated group [50 µg (ml drinking water)−1 ]; intraperitoneal nicotine-treated group [0.5 mg (kg body weight)−1 ]; and inhaled nicotine-treated group [0.5 mg (kg body weight)−1 ]. Concentrations of gastrin, ghrelin, PGE 2 and histamine in serum and gastric tissue homogenates were assessed using ELISA kits. Stomach fundus was processed for histopathology and immunohistochemistry using light and electron microscopy. Different routes of chronic nicotine administration resulted in a significant increase in serum and gastric homogenate gastrin and ghrelin concentrations and a significant decrease in serum and homogenate PGE 2 concentrations compared with the control group. Moreover, nicotine administration via oral and inhalation routes caused gastric erosion, transformation of peptic cells into the mucous variety, a significant increase in parietal cell numbers and an increase in expression of gastrin. In conclusion, the negative impact of nicotine administration on gastric structure that is associated with an increased concentration of gastrin and decreased concentration PGE 2 might be the leading cause of gastric/peptic ulcers in heavy smokers. The increased ghrelin concentration and

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“…Previous studies have also examined the relationship between smoking and the gastric IM (10)(11)(12). A recent meta-analysis with 19 articles reported a weak and statistically nonsignificant association of smoking with IM using available data but could not confirm smoking as an independent risk factor for IM (12).…”

Section: Discussionmentioning

confidence: 99%

“…Previously, the association between smoking and IM has been examined in observational studies, but the results are controversial (10,11). A recent study involving a meta-analysis reported a statistically nonsignificant association between smoking and IM, suggesting that further research is needed (12). Indeed, many studies were limited by their cross-sectional design, unclear temporality between exposure and outcome, insufficient sample size, and the use of self-report smoking status.…”

Section: Introductionmentioning

confidence: 99%

Smoking and Urinary Cotinine Levels Are Predictors of Increased Risk for Gastric Intestinal Metaplasia

et al. 2019

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Studies on a longitudinal relationship between smoking status and intestinal metaplasia (IM), a premalignant lesion of stomach cancer, are limited. Here we examined the association of smoking status and urinary cotinine levels, an objective measure of smoking, with the development of endoscopic IM. This cohort study included 199,235 Korean adults free of endoscopic IM who underwent upper endoscopy at baseline and subsequent visits and who were followed for up to 6.8 years (median, 3.7 years). Former and current smoking status and pack-years based on self-reports were associated with an increased risk of new-onset IM in men but not in women. However, urinary cotinine levels were positively associated with incident IM in a dose-response manner in both men and women. For men, the multivariable-adjusted HR [95% confidence interval (CI)] for incident IM comparing the urinary cotinine levels of 50 to 99 ng/mL, 100 to 499 ng/mL, and !500 ng/mL with <50 ng/mL were 1.20 (0.94-1.55), 1.26 (1.14-1.40), and 1.54 (1.44-1.64), respectively, whereas for women, corresponding HR (95% CI) were 0.75 (0.19-2.99), 1.86 (1.20-2.88), and 1.57 (1.07-2.30), respectively. These associations were observed when changes in smoking status and other confounders were updated during follow-up as timevarying covariates. In this large cohort of young and middleaged men and women, urinary cotinine levels were independently associated with an increased incidence of endoscopic IM in a dose-response manner. Collectively, these data confirm smoking as an independent risk factor for the development of gastric IM, a precursor lesion of stomach cancer. Significance: A large-scale cohort study of nearly 200,000 adults associates smoking with increased risk for gastric intestinal metaplasia, a precursor lesion of stomach cancer.

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Tobacco smoking and intestinal metaplasia: Systematic review and meta-analysis

Abstract: The weak and non-statistically significant association found through meta-analysis of the available evidence does not confirm smoking as an independent risk factor for intestinal metaplasia.

Cited by 20 publications

References 63 publications

Worldwide Burden of Gastric Cancer Attributable to Tobacco Smoking in 2012 and Predictions for 2020

Worldwide Burden of Gastric Cancer Attributable to Tobacco Smoking in 2012 and Predictions for 2020

Effects of different routes of nicotine administration on gastric morphology and hormonal secretion in rats

Smoking and Urinary Cotinine Levels Are Predictors of Increased Risk for Gastric Intestinal Metaplasia

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