{'fraction_non_alphanumeric': 0.043094496365524405, 'fraction_numerical': 0.029075804776739357, 'mean_word_length': 5.2973856209150325, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Helicobacter pylori infection, chronic atrophic gastritis and risk of stomach and esophagus cancer: Results from the prospective population‐based ESTHER cohort study

Helicobacter pylori (H. pylori) infection is considered as principal cause of gastric cancer. It is further associated with a reduced risk of esophageal adenocarcinomas. In a large prospective population‐based cohort study including 9,949 subjects with average observation time of 13.8 years, we assessed the risk of invasive gastric and esophageal cancer according to H. pylori infection and presence of chronic atrophic gastritis (CAG). Incidence rates and hazard ratios (HR) derived by Cox proportional hazards models and adjusted for relevant confounders were derived by seroprevalence of H. pylori and cytotoxin‐associated gene A (CagA) antibodies and presence of CAG based on serological markers at baseline, respectively. During follow‐up, 30 cases of noncardia gastric cancer and 33 cases of esophageal cancer were observed. Infection by H. pylori without and with expression of CagA was associated with a 5.2‐fold (95% confidence interval 1.00–27.1) and an 18.2‐fold (4.3–77.4) increase of noncardia gastric cancer incidence. A 0.65‐fold decreased risk of esophageal adenocarcinomas (HR 0.35, 0.12–0.97) was observed among H. pylori‐infected individuals. In participants infected with CagA expressed H. pylori, the presence of mild/moderate and severe CAG was associated with a 6.4‐fold (1.3–31.0) and an 11.8‐fold (3.1–45.4) increase of gastric cancer incidence, respectively. The results of this prospective population‐based cohort study may contribute relevant evidence to the ongoing research of H. pylori‐related cancers. The results may furthermore enhance the empirical basis for risk stratification among H. pylori‐infected people and for recommendations regarding H. pylori screening and treatment among older adults in a Western population.