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林奇综合征患者饮食的炎症潜能与结直肠癌风险

Inflammatory potential of the diet and colorectal tumor risk in persons with Lynch syndrome.

作者信息

Brouwer Jesca Gm, Makama Maureen, van Woudenbergh Geertruida J, Vasen Hans Fa, Nagengast Fokko M, Kleibeuker Jan H, Kampman Ellen, van Duijnhoven Fränzel Jb

机构信息

Division of Human Nutrition, Wageningen University & Research, Wageningen, Netherlands.

Christelijke Hogeschool, Ede, Netherlands.

出版信息

Am J Clin Nutr. 2017 Nov;106(5):1287-1294. doi: 10.3945/ajcn.117.152900. Epub 2017 Sep 20.

Abstract

Persons with Lynch syndrome (LS) have high lifetime risk of developing colorectal tumors (CRTs) because of a germline mutation in one of their mismatch repair (MMR) genes. An important process in the development of CRTs is inflammation, which has been shown to be modulated by diet. We aimed to investigate the association between the inflammatory potential of the diet and the risk of CRTs in persons with LS. We used the dietary intake of 457 persons with LS from a prospective cohort study to calculate the adapted dietary inflammatory index (ADII). The ADII was split into tertiles in which the highest tertile reflects the most proinflammatory potential of the diet. Cox proportional hazard models, with robust sandwich variance estimates to adjust for dependency within families, were used to calculate HRs and 95% CIs of CRTs by ADII tertile. HRs were adjusted for age, smoking status, and education level, and number of colonoscopies as a time-dependent variable. A potential effect measure modification was explored by stratifying the results by mutated MMR gene, sex, and a history of CRTs. We performed sensitivity analyses by repeating the analyses in non-nonsteroidal anti-inflammatory drug (NSAID) users ( = 315). During a median follow-up time of 59 mo, 200 participants (43.8%) developed CRTs. No significant association was shown between highest compared with lowest ADII tertiles (HR for highest compared with lowest tertiles: 1.37; 95% CI: 0.80, 2.34). Stratification by mutated MMR gene, sex, and CRT history did not show significantly differential associations (-interactions ≥ 0.64). In non-NSAID users, an HR of 1.60 (95% CI: 0.88, 2.93) for highest compared with lowest tertiles was shown. No significant effect modification was shown in this group either (-interactions ≥ 0.24). A proinflammatory potential of the diet does not seem to be significantly associated with CRT risk in persons with LS.

摘要

林奇综合征(LS)患者由于其错配修复(MMR)基因之一发生种系突变,一生中患结直肠肿瘤(CRT)的风险很高。CRT发生过程中的一个重要过程是炎症,研究表明炎症会受到饮食的调节。我们旨在研究饮食的炎症潜能与LS患者发生CRT的风险之间的关联。我们利用一项前瞻性队列研究中457名LS患者的饮食摄入量来计算适应性饮食炎症指数(ADII)。ADII被分为三个三分位数,其中最高三分位数反映了饮食中最强的促炎潜能。使用Cox比例风险模型,并采用稳健的三明治方差估计来调整家庭内部的相关性,以计算按ADII三分位数划分的CRT的风险比(HR)和95%置信区间(CI)。HR根据年龄、吸烟状况、教育水平以及作为时间依赖性变量的结肠镜检查次数进行了调整。通过按突变的MMR基因、性别和CRT病史对结果进行分层,探索了潜在的效应测量修正。我们通过在非非甾体抗炎药(NSAID)使用者(n = 315)中重复分析进行了敏感性分析。在中位随访时间59个月期间,200名参与者(43.8%)发生了CRT。与最低ADII三分位数相比,最高三分位数之间未显示出显著关联(最高三分位数与最低三分位数相比的HR:1.37;95%CI:0.80,2.34)。按突变的MMR基因、性别和CRT病史分层未显示出显著的差异关联(P交互作用≥0.64)。在非NSAID使用者中,最高三分位数与最低三分位数相比的HR为1.60(95%CI:0.88,2.93)。该组也未显示出显著的效应修正(P交互作用≥0.24)。饮食的促炎潜能似乎与LS患者的CRT风险无显著关联。

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