HELICOBACTER-PYLORI, DIETARY FACTORS, AND ATROPHIC GASTRITIS IN 5 JAPANESE POPULATIONS WITH DIFFERENT GASTRIC-CANCER MORTALITY
HELICOBACTER-PYLORI, DIETARY FACTORS, AND ATROPHIC GASTRITIS IN 5 JAPANESE POPULATIONS WITH DIFFERENT GASTRIC-CANCER MORTALITY
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DOI：
10.1007/bf00051331
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发表时间：
1993-07-01
影响因子：
2.3
通讯作者：
WATANABE, S
中科院分区：
文献类型：
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作者：
TSUGANE, S;KABUTO, M;WATANABE, S
在一项横断面研究中，从日本胃癌死亡率不同的五个地区随机挑选了634名年龄在40岁至49岁之间的男性，其中121名男性被评估为萎缩性胃炎，诊断标准为血清胃蛋白酶原1和70 ng/ml，胃蛋白酶原1(PGI)/胃蛋白酶原II(PGII)比率为3.0。我们研究了幽门螺杆菌抗体和饮食因素，包括血浆抗氧化剂微量营养素水平与萎缩性胃炎的关系。幽门螺杆菌抗体阳性与萎缩性胃炎发病风险增加相关(优势比[OR]=1.9，95%可信区间[CI]=1.1~3.3)。随着血浆β-胡萝卜素水平的升高，我们发现萎缩性胃炎的风险稳步下降(第二四分位数OR=0.7，第三四分位数=0.6，第四四分位数=0.4，CI=0.2-0.8)。经常摄入黄色蔬菜也与较低的风险相关，而频繁摄入大豆产品与风险增加相关。虽然幽门螺杆菌抗体、β-胡萝卜素水平和豆制品摄入量在多因素分析中都有显著意义，但这些因素并不能解释五个地区之间萎缩性胃炎患病率的差异。各胃蛋白酶原标志物的危险因素分析表明，虽然幽门螺杆菌感染和血浆β-胡萝卜素水平降低均与血清PGI/II比值降低有关，但前者源于萎缩性胃炎早期常见的PGII升高，后者源于重度萎缩性胃炎所特有的PGI降低。这一发现表明，幽门螺杆菌感染与萎缩性胃炎的形成有关，而β-胡萝卜素保护其进展和形成。
In a cross-sectional study of 634 men aged 40 to 49 years, randomly selected from five areas of Japan with different rates of gastric cancer mortality, 121 men of 624 evaluated were diagnosed as having atrophic gastritis through serum pepsinogen 1 < 70 ng/ml and the pepsinogen 1 (PGI)/pepsinogen II (PGII) ratio < 3.0. We examined the relation of Helicobacter pylori (H. pylori) antibodies and dietary factors, including plasma level of antioxidant micronutrients, to the presence of atrophic gastritis. Presence of H. pylori IgG antibodies was associated with increased risk of atrophic gastritis (odds ratio [OR] = 1.9, 95 percent confidence interval [CI] = 1.1-3.3). As the level of plasma beta-carotene increased, we found a steady decrease in the risk of atrophic gastritis (OR for second quartile = 0.7, third quartile = 0.6, fourth quartile = 0.4, with CI = 0.2-0.8). Frequent intake of yellow vegetables also was associated with lower risk, while frequent intake of soybean products was related to increased risk. Although H. pylori antibodies, beta-carotene level, and intake of soybean products were all significant in the multivariate analysis, these factors did not explain the differences in atrophic gastritis prevalence among the five regions. The analysis of these risk factors in relation to each pepsinogen marker showed that although both H. pylori infection and low plasma beta-carotene were associated with the decreased level of serum PGI/II ratio, the former was derived from the increase of PGII, which is common in early stage of atrophic gastritis, and the latter from the decrease of PGI, which is specific to severe atrophic gastritis. This finding suggests that H. pylori infection is associated with the formation of atrophic gastritis, while beta-carotene protects its advancement as well as formation.