Hormone therapy increases risk of ulcerative colitis but not Crohn's disease.
Hormone therapy increases risk of ulcerative colitis but not Crohn's disease.
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DOI：
10.1053/j.gastro.2012.07.096
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发表时间：
2012-11
期刊：
影响因子：
29.4
通讯作者：
Chan AT
中科院分区：
文献类型：
--
作者：
Khalili H;Higuchi LM;Ananthakrishnan AN;Manson JE;Feskanich D;Richter JM;Fuchs CS;Chan AT
雌激素被认为是通过影响胃肠道上皮细胞和免疫细胞上的雌激素受体来调节肠道炎症的。绝经后激素治疗对克罗恩病(CD)和溃疡性结肠炎(UC)风险的作用尚不清楚。我们对108,844名绝经后美国妇女(平均年龄54岁)进行了前瞻性队列研究，这些妇女在1976年参加了护士健康研究，但没有CD或UC的既往病史。每两年，我们都会更新有关绝经状态、绝经后激素使用和其他风险因素的信息。自我报告的CD和UC诊断是由两名对暴露信息视而不见的胃肠病医生通过病历审查确认的。我们使用COX比例风险模型来计算调整后的危险比(HR)和95%可信区间(CI)。通过2008年超过180万人的跟踪，我们记录了138起CD事件和138起UC事件。与从不使用激素的女性相比，目前使用激素的女性UC的多因素调整后HR为1.71(95%CI，1.07-2.74)，既往使用激素的女性UC的多变量调整后HR为1.65(95%CI，1.03-2.66)。UC的风险似乎随着激素使用时间的延长而增加(P趋势=0.04)，并且随着停药时间的延长而降低。根据使用的激素治疗类型(雌激素与雌激素+孕激素)，风险没有差异。相反，我们没有观察到当前激素使用与CD风险之间的关联(多变量调整后的HR，1.19 95%CI 0.78-1.82)。激素对UC和CD风险的影响不受年龄、体重指数或吸烟的影响。在一大批女性前瞻性队列中，绝经后激素治疗与UC风险增加有关，但与CD风险无关。提示雌激素相关通路可能参与了UC的发病机制。
Estrogen has been proposed to modulate gut inflammation through an effect on estrogen receptors found on gastrointestinal epithelial and immune cells. The role of postmenopausal hormone therapy on risk of Crohn’s disease (CD) and ulcerative colitis (UC) is unclear. We conducted a prospective cohort study of 108,844 postmenopausal US women (median age 54 years) enrolled in 1976 in the Nurses’ Health Study without a prior history of CD or UC. Every 2 years, we have updated information on menopause status, postmenopausal hormone use, and other risk factors. Self-reported CD and UC diagnoses were confirmed through medical record review by two gastroenterologists who were blinded to exposure information. We used Cox proportional hazards models to calculate adjusted hazard ratios (HR) and 95% confidence intervals (CIs). Through 2008 with over 1.8 million person years of follow up, we documented 138 incident cases of CD and 138 of UC. Compared to women who never used hormones, the multivariate-adjusted HR for UC was 1.71 (95% CI, 1.07-2.74) among women who currently used hormones and 1.65 (95% CI, 1.03-2.66) among past users. The risk of UC appeared to increase with longer duration of hormone use (Ptrend=.04) and decreased with time since discontinuation. There was no difference in risk according to the type of hormone therapy used (estrogen vs estrogen + progestin). In contrast, we did not observe an association between current use of hormones and risk of CD (multivariate-adjusted HR, 1.19 95% CI 0.78-1.82). The effect of hormones on risk of UC and CD was not modified by age, body mass index, or smoking. In a large prospective cohort of women, postmenopausal hormone therapy was associated with an increased risk of UC but not CD. These findings indicate that pathways related to estrogens might mediate the pathogenesis of UC.
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