Urinary prostaglandin E2 metabolite and gastric cancer risk in the Shanghai women's health study.
Urinary prostaglandin E2 metabolite and gastric cancer risk in the Shanghai women's health study.
复制标题
DOI：
10.1158/1055-9965.epi-09-0680
复制
发表时间：
2009-11
期刊：
影响因子：
--
通讯作者：
Abnet CC
中科院分区：
文献类型：
--
作者：
Dong LM;Shu XO;Gao YT;Milne G;Ji BT;Yang G;Li HL;Rothman N;Zheng W;Chow WH;Abnet CC
慢性炎症与胃癌的病因学有关。前列腺素E2（PGE 2）是考克斯-2途径的主要终产物之一，COX-2途径是一种重要的炎症介质。在上海妇女健康研究中，我们使用一种新的定量尿中PGE 2（PGE-M，11 α-羟基-9，15-二氧代-2，3，4，5-四去甲前列烷-1，20-二酸）的主要代谢产物的方法，评估了尿中PGE-M浓度与随后发生胃癌的风险的关系。上海妇女健康研究是一项基于大人群的前瞻性队列研究，采用巢式病例对照研究设计。对照组与153例胃癌病例按绝经状态、年龄、样本采集时间和日期、距最后一餐的时间间隔和尿液样本的可用性进行匹配（1：1）。采用条件Logistic回归分析计算比值比（OR）和95%置信区间（95%CI），并对潜在混杂因素进行校正。胃癌病例的基线尿PGE-M水平略高，中位肌酐为6.4 ng/mg（四分位距：3.4-11.2），而对照组为5.4 ng/mg（四分位距：2.8-9.0），但该差异无统计学显著性（Wilcoxon p值=0.34）。随着尿PGE-M水平四分位数的增加，胃癌风险的OR在四分位数2、3和4中增加：1.00（95%CI：0.48-2.08）、1.40（95%CI：0.67-2.91）和1.98（95%CI：0.95-4.13），趋势检验具有统计学意义（p=0.04）。在对H进行额外调整后，这种关联仍然存在。pylori状态，并在非NSAID使用者，H.幽门螺杆菌状态，以及研究入组后46个月内诊断的病例。我们的研究结果表明，较高水平的尿PGE-M，炎症标志物，可能与胃癌的风险。
Chronic inflammation has been implicated in the etiology of gastric cancer. Prostaglandin-E2(PGE2) is one of the major end products of the COX-2 pathway, an enzyme that is an important mediator of inflammation. Using a novel method of quantifying the primary urinary metabolite of PGE2(PGE-M, 11 alpha-hydroxy-9,15-dioxo-2,3,4,5-tetranorprostane-1,20-dioic acid), we evaluated urinary PGE-M concentrations in association with subsequent risk of development of gastric cancer in the Shanghai Women’s Health Study, a large population-based prospective cohort, using a nested case-control study design. Controls were matched(1:1) to 153 gastric cancer cases by menopausal status; age, time and date of sample collection; time interval since last meal and availability of urine sample. Odds ratios(OR) and 95% confidence intervals(95%CI) were calculated using conditional logistic regression adjusted for potential confounders. Baseline urinary PGE-M levels were slightly higher among gastric cancer cases with a median of 6.4 ng/mg creatinine (interquartile range: 3.4–11.2) compared to 5.4 among controls (interquartile range: 2.8–9.0) but this difference was not statistically significant (Wilcoxon p-value=0.34). With increasing quartiles of urinary PGE-M levels, the ORs for risk of gastric cancer increased in quartiles 2, 3, and 4: 1.00 (95%CI:0.48–2.08), 1.40 (95%CI:0.67–2.91) and 1.98 (95%CI:0.95–4.13), with a statistically significant test for trend (p=0.04). The association persisted after additional adjustment for H. pylori status, and was slightly strengthened among non-NSAID users, subjects with positive H. pylori status, and for cases diagnosed within 46 months after study enrollment. Our findings suggest that higher levels of urinary PGE-M, a marker of inflammation, may be associated with gastric cancer risk.