BACKGROUND & AIMS: Atrophic corpus gastritis (ACG) is believed to be an early precursor of gastric adenocarcinoma. We aimed to investigate trends of ACG in Northern Sweden, from 1990 through 2009, and to identify possible risk factors.
METHODS: We randomly selected serum samples collected from 5284 participants in 1990, 1994, 1999, 2004, and 2009, as part of the population-based, cross-sectional Northern Sweden Multinational Monitoring of Trends and Determinants in Cardiovascular Disease study (ages 35-64 y). Information was collected on sociodemographic, anthropometric, lifestyle, and medical factors using questionnaires. Serum samples were analyzed for levels of pepsinogen I, to identify participants with functional ACG; data from participants with ACG were compared with those from frequency-matched individuals without ACG (controls). Blood samples were analyzed for antibodies against H pylori and CagA. Associations were estimated with unconditional logistic regression models.
RESULTS: Overall, 305 subjects tested positive for functional ACG, based on level of pepsinogen I. The prevalence of ACG in participants 55-64 y old decreased, from 124/1000 to 49/1000 individuals, between 1990 and 2009. However, the prevalence of ACG increased, from 22/1000 to 64/1000 individuals among participants 35-44 y old during this time period. CagA seropositivity was associated with risk for ACG (odds ratio, 2.29; 95% confidence interval, 1.69-3.12). Other risk factors included diabetes, low level of education, and high body mass index. The association between body mass index and ACG was confined to individuals 35-44 y old; in this group, overweight and obesity were associated with a 2.8-fold and 4.7-fold increased risk of ACG, respectively.
CONCLUSIONS: Among residents of Northern Sweden, the prevalence of ACG increased from 1990 through 2009 specifically among adults 35-44 y old. The stabilizing seroprevalence of H pylori and increasing prevalence of overweight and obesity might contribute to this unexpected trend; studies are needed to determine whether these changes have affected the incidence of gastric cancer.
2015. Vol. 13, no 9, 1592-1600 p.