Helicobacter pylori infection and fundic gastric atrophy are not associated with esophageal squamous cell carcinoma

Venerito, Marino; Kohrs, S; Wex, Thomas; Adolf, Daniela; Kuester, Doerthe; Schubert, Daniel; Peitz, Ulrich; Mönkemüller, Klaus; Malfertheiner, Peter

doi:10.1097/meg.0b013e3283496469

Cited by 20 publications

(31 citation statements)

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“…In this study, we could not detect any association between infection with cagA -positive H. pylori strains and OSCC risk, which is in contrast to the results from the study among low-risk Swedish population (Ye et al , 2004), Japanese alcoholic males (Yokoyama et al , 2009), and in accordance to the reports from studies in Linxian of China (Kamangar et al , 2007), Magdeburg of Germany (Venerito et al , 2011), and among Finnish male smokers (Cook et al , 2010). Spontaneous disappearance of H. pylori over time or H. pylori eradication is possibly common in endemic areas.…”

Section: Discussionsupporting

confidence: 54%

“…Pepsinogen II (PGII) is synthesised in most parts of the gastric mucosa and part of the duodenum and some studies have shown its importance in detecting inflammation (He et al , 2011) or gastric cancer screening (Abnet et al , 2011). Magnitude of the reported associations between serological gastric atrophy and OSCC varied from null to eightfold (Iijima et al , 2007; de Vries et al , 2009; Ren et al , 2009; Cook et al , 2010; Venerito et al , 2011). …”

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confidence: 99%

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Gastric atrophy and oesophageal squamous cell carcinoma: possible interaction with dental health and oral hygiene habit

et al. 2012

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Background:Gastric fundal atrophy has been hypothesised to increase the risk of oesophageal squamous cell carcinoma (OSCC), but studies have shown inconsistent results.Methods:We measured serum pepsinogen I (PGI) and pepsinogen II (PGII) among 293 incident cases and 524 matched neighbourhood controls in a high-risk area of Northern Iran. Conditional logistic regression model was used to estimate odds ratios (ORs) and their 95% confidence intervals (CIs).Results:After controlling for age, sex, residence area and other potential confounders, gastric atrophy (defined by a validated criterion, PGI <55 μg dl−1) was associated with a two-fold increased risk (OR=2.01, 95% CI: 1.18, 3.45) of OSCC in the absence of nonatrophic pangastritis (defined as PGII <11.8 μg dl−1). Stratification by PGII decreased the misclassification errors due to cancer-induced gastritis. Presence of both poor dental health, indicated by higher than median sum of decayed, missing, and filled teeth (DMFT score), and gastric atrophy further increased the risk of OSCC (OR=4.15, 95% CI: 2.04, 8.42) with relative excess risk due to interaction (RERI) of 1.47 (95% CI: −1.15, 4.1). Coexistence of poor oral hygiene habit with gastric atrophy elevated OSCC risk eight times (OR=8.65, 95% CI: 3.65, 20.46) and the additive interaction index was marginally statistically significant (RERI=4.34, 95% CI: −1.07, 9.76).Conclusion:Gastric atrophy is a risk factor for OSCC, and poor dental health and oral hygiene habit may act synergistically in increasing the risk.

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Section: Discussionsupporting

confidence: 54%

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confidence: 99%

Gastric atrophy and oesophageal squamous cell carcinoma: possible interaction with dental health and oral hygiene habit

et al. 2012

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“…The literature search identified 948 potentially relevant articles. Based on our inclusion criteria, a total of 28 studies [13][14][15][17][18][19][20][21][22][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47] were included in qualitative synthesis (Fig. 1).…”

Section: Characteristics Of Studiesmentioning

confidence: 99%

“…Detailed characteristics of the aggregated data for the 28 studies are summarized in Table 1. In total, nine studies 14,17,18,33,36,38,40,41,46 concerned EAC, 15 concerned ESCC, 13,15,20,22,[29][30][31][32]34,35,39,[42][43][44][45] and four 19,21,37,47 concerned both. There were 13 studies in Asian populations and 15 studies in non-Asian subjects.…”

Section: Characteristics Of Studiesmentioning

confidence: 99%

Association ofHelicobacter pyloriinfection with esophageal adenocarcinoma and squamous cell carcinoma: a meta-analysis

et al. 2014

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To evaluate the relationship of Helicobacter pylori and cytotoxin-associated gene A (CagA) positive strains with esophageal neoplasm, including esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC), the authors conducted a meta-analysis using a predefined protocol. PubMed, Web of Science, China biology medical literature database, Wanfang, and China National Knowledge Infrastructure were searched for relevant articles from the first available year to April 8, 2013. The fixed or random effect pooled measure was selected based on heterogeneity among studies, which was evaluated using Q test and the I(2) of Higgins and Thompson. Metaregression was used to explore the sources of between-study heterogeneity. Publication bias was analyzed by Begg's funnel plot and Egger's regression test. The association was assessed by odds ratio (OR) with 95% confidence interval (CI). A total of 28 eligible studies were included in the meta-analysis. There was a significant inverse association between H. pylori infection (pooled OR, 0.57; 95% CI, 0.44-0.73) and EAC; CagA-positive H. pylori strains were less likely to be associated with EAC compared with CagA-negative strains (pooled OR, 0.64; 95% CI, 0.52-0.79). However, there was no statistically significant association between H. pylori/CagA-positive H. pylori strains infection and ESCC, and the pooled ORs were 1.16 (95% CI, 0.83-1.60) and 0.97 (95% CI, 0.79-1.19). But significant associations between CagA-positive H. pylori strains infection and ESCC risk were found in the stratified analysis of the study location (Asian and non-Asian), and the summary ORs were 0.74 (95% CI, 0.57-0.97) and 1.41 (95% CI, 1.02-1.94). H. pylori infection and CagA-positive strains are associated with decreased risk of EAC in the overall population. No significant association was found between H. pylori infection/CagA-positive strains and ESCC. But CagA-positive strains might have a positive association with ESCC in non-Asian population and an inverse association in Asian population.

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“…According to the current evidence, the causes of oxyntic gastric atrophy (OGA) are (1) H. pylori infection (environmental aetiology), (2) AIG (primary autoimmunity) and (3) combined H. pylori -autoimmune aetiology 4–6. OGA independent of its aetiology is a condition associated with hypo- or achlorhydria, and low serum pepsinogen (PG) I concentrations 7. In patients with autoimmune OGA, secondary hypergastrinaemia, antral G cell hyperplasia and corpus enterochromaffin-like (ECL) cell hyperplasia are commonly observed 8.…”

Section: Introductionmentioning

confidence: 99%

Oxyntic gastric atrophy inHelicobacter pylorigastritis is distinct from autoimmune gastritis

et al. 2016

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Helicobacter pylori infection and fundic gastric atrophy are not associated with esophageal squamous cell carcinoma

Abstract: Hazardous alcohol consumption and smoking increase synergistically the risk for developing OSCC. In our population neither H. pylori infection nor FGA was associated with an increased risk for OSCC.

Cited by 20 publications

References 33 publications

Gastric atrophy and oesophageal squamous cell carcinoma: possible interaction with dental health and oral hygiene habit

Gastric atrophy and oesophageal squamous cell carcinoma: possible interaction with dental health and oral hygiene habit

Association ofHelicobacter pyloriinfection with esophageal adenocarcinoma and squamous cell carcinoma: a meta-analysis

Oxyntic gastric atrophy inHelicobacter pylorigastritis is distinct from autoimmune gastritis

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