Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Department of Clinical Chemistry, Hallands Sjukhus Halmstad, Halmstad, Sweden.
Clin Gastroenterol Hepatol. 2015 Sep;13(9):1592-600.e1. doi: 10.1016/j.cgh.2015.04.001. Epub 2015 Apr 6.
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.
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 Helicobacter pylori and Cag pathogenicity island protein A. Associations were estimated with unconditional logistic regression models.
Overall, 305 subjects tested positive for functional ACG, based on their level of pepsinogen I. The prevalence of ACG in participants age 55 to 64 years old decreased from 124 per 1000 to 49 per 1000 individuals between 1990 and 2009. However, the prevalence of ACG increased from 22 per 1000 to 64 per 1000 individuals among participants age 35 to 44 years old during this time period. Cag pathogenicity island protein A 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 age 35 to 44 years old; in this group, overweight and obesity were associated with a 2.8-fold and a 4.7-fold increased risk of ACG, respectively.
Among residents of Northern Sweden, the prevalence of ACG increased from 1990 through 2009, specifically among adults age 35 to 44 years old. The stabilizing seroprevalence of H pylori and the 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.
萎缩性 corpus 胃炎（ACG）被认为是胃腺癌的早期前体。我们旨在调查从 1990 年到 2009 年，瑞典北部 ACG 的趋势，并确定可能的危险因素。
我们随机选择了 1990 年、1994 年、1999 年、2004 年和 2009 年作为基于人群的、横断性北瑞典多国监测趋势和心血管疾病决定因素研究（年龄 35-64 岁）的一部分收集的 5284 名参与者的血清样本。使用问卷收集了社会人口统计学、人体测量学、生活方式和医疗因素信息。血清样本用于检测胃蛋白酶原 I 的水平，以确定功能性 ACG 参与者；将有 ACG 的参与者的数据与没有 ACG（对照组）的频率匹配个体的数据进行比较。血液样本用于分析幽门螺杆菌和 Cag 致病岛蛋白 A 的抗体。使用非条件逻辑回归模型估计关联。
总体而言，根据胃蛋白酶原 I 的水平，有 305 名参与者检测出功能性 ACG 阳性。在 55 至 64 岁的参与者中，ACG 的患病率从 1990 年至 2009 年期间从每 1000 人 124 例降至每 1000 人 49 例。然而，在此期间，35 至 44 岁的参与者中 ACG 的患病率从每 1000 人 22 例增加到每 1000 人 64 例。Cag 致病岛蛋白 A 血清阳性与 ACG 风险相关（比值比，2.29；95%置信区间，1.69-3.12）。其他危险因素包括糖尿病、低教育水平和高体重指数。体重指数与 ACG 之间的关联仅限于 35 至 44 岁的个体；在该组中，超重和肥胖分别与 ACG 风险增加 2.8 倍和 4.7 倍相关。
在瑞典北部的居民中，ACG 的患病率从 1990 年到 2009 年增加，特别是在 35 至 44 岁的成年人中。幽门螺杆菌稳定的血清流行率和超重和肥胖的流行率增加可能导致这种意外趋势。需要研究这些变化是否影响胃癌的发病率。
