European journal of gastroenterology & hepatology · 2011
Helicobacter pylori infection and fundic gastric atrophy are not associated with esophageal squamous cell carcinoma: a case-control study.
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Venerito Marino, Kohrs Sabine, Wex Thomas, Adolf Daniela, Kuester Doerthe, Schubert Daniel, Peitz Ulrich, Mönkemüller Klaus, Malfertheiner Peter
Аннотация
OBJECTIVE: Recent studies from Asia and Northern Europe suggest that apart from alcohol intake and smoking, fundic gastric atrophy (FGA) may also increase the risk of esophageal squamous cell carcinoma (OSCC). However, because of the wide geographic variation of this cancer and the changing prevalence of the Helicobacter pylori infection, these findings need to be confirmed in other ethnic groups. The aim of this case-control study was to investigate whether H. pylori infection and FGA carry an increased risk for OSCC.
PATIENTS AND METHODS: FGA was evaluated, by histology and serology, in 75 patients with OSCC, and 75 sex-matched and age-matched controls. Pepsinogen (PG) I levels 70 μg/ml or less and PG I/II ratio of 3 or less were indicative for FGA. H. pylori infection was defined as positivity to at least one test among histology, rapid urease test, and serology for both general anti-IgG and anti-CagA.
RESULTS: Overall, the prevalence of H. pylori infection was identically high (70.7%) in both patients with OSCC and controls. FGA diagnosed by serology and histology was not associated with an increased risk for OSCC [odds ratio (OR)=1.17; 95% confidence interval (CI)=0.54-2.56 and OR=1.91; 95% CI=0.6-5.99, respectively]. ORs (95% CI) for hazardous alcohol consumption, smoking, and the presence of both risk factors were 5.75 (2.20-15.05), 22.18 (9.41-52.28), and 31.69 (8.39-119.67), respectively.
CONCLUSIONS: 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.
PATIENTS AND METHODS: FGA was evaluated, by histology and serology, in 75 patients with OSCC, and 75 sex-matched and age-matched controls. Pepsinogen (PG) I levels 70 μg/ml or less and PG I/II ratio of 3 or less were indicative for FGA. H. pylori infection was defined as positivity to at least one test among histology, rapid urease test, and serology for both general anti-IgG and anti-CagA.
RESULTS: Overall, the prevalence of H. pylori infection was identically high (70.7%) in both patients with OSCC and controls. FGA diagnosed by serology and histology was not associated with an increased risk for OSCC [odds ratio (OR)=1.17; 95% confidence interval (CI)=0.54-2.56 and OR=1.91; 95% CI=0.6-5.99, respectively]. ORs (95% CI) for hazardous alcohol consumption, smoking, and the presence of both risk factors were 5.75 (2.20-15.05), 22.18 (9.41-52.28), and 31.69 (8.39-119.67), respectively.
CONCLUSIONS: 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.