Chlebowski Rowan T, Schottinger Joanne E, Shi Jiaxiao, Chung Joanie, Haque Reina
Los Angeles Biomedical Research Institute at Harbor-University of California Los Angeles, Torrance, California.
Department of Research and Evaluation, Kaiser Permanente Southern California, Pasadena, California.
Cancer. 2015 Jul 1;121(13):2147-55. doi: 10.1002/cncr.29332. Epub 2015 Mar 10.
The risks of both endometrial cancer and postmenopausal breast cancer are increased by obesity and higher endogenous estrogen levels. Although aromatase inhibitors reduce breast cancer incidence, their influence on endometrial cancer is uncertain.
The authors investigated this issue in a cohort of 17,064 women who were diagnosed with hormone receptor-positive breast cancer in an integrated group practice health plan. Information on demographics, comorbidities, and the receipt of adjuvant endocrine therapy was available from electronic medical records and pharmacy records, respectively. Endometrial cancer information was obtained from the health plan's Surveillance, Epidemiology, and End Results-affiliated tumor registry, and rates were compared across endocrine therapy groups (aromatase inhibitor, n = 5303; tamoxifen, n = 5155; switchers: both [n = 3787] or none [n = 2819]) using multivariable adjusted Cox proportional-hazards models.
Endometrial cancer incidence was a statistically significant 48% lower in the aromatase inhibitor group versus the tamoxifen group (hazard ratio, 0.52; 95% confidence interval, 0.31-0.87; P = .01). Endometrial cancer incidence was 29% lower in the aromatase inhibitor group versus the no endocrine therapy group (hazard ratio, 0.71; 95% confidence interval, 0.37-1.35; P = .30) and 33% lower in the aromatase inhibitor group versus the tamoxifen group (hazard ratio, 0.67; 95% confidence interval, 0.42-1.06; P = .08), but neither difference was statistically significant. Associations were stronger among those with good drug adherence.
In a community-based, integrated health plan setting, endometrial cancer incidence was lower in women who were receiving an aromatase inhibitor compared with those who were receiving tamoxifen. In addition, aromatase inhibitors may mitigate the incidence of tamoxifen-associated endometrial cancer. Although there were somewhat fewer endometrial cancers in the aromatase inhibitor group versus the no endocrine therapy group, further studies are needed for the definitive assessment of this potential association.
肥胖和较高的内源性雌激素水平会增加子宫内膜癌和绝经后乳腺癌的风险。虽然芳香化酶抑制剂可降低乳腺癌发病率,但其对子宫内膜癌的影响尚不确定。
作者在一个综合团体医疗健康计划中,对17064名被诊断为激素受体阳性乳腺癌的女性队列进行了此项研究。人口统计学、合并症以及辅助内分泌治疗的信息分别来自电子病历和药房记录。子宫内膜癌信息从该健康计划的监测、流行病学和最终结果相关肿瘤登记处获取,并使用多变量调整的Cox比例风险模型比较各内分泌治疗组(芳香化酶抑制剂组,n = 5303;他莫昔芬组,n = 5155;转换组:两者都用[n = 3787]或都不用[n = 2819])的发病率。
与他莫昔芬组相比,芳香化酶抑制剂组的子宫内膜癌发病率在统计学上显著降低48%(风险比,0.52;95%置信区间,0.31 - 0.87;P = 0.01)。与未接受内分泌治疗组相比,芳香化酶抑制剂组的子宫内膜癌发病率降低29%(风险比,0.71;95%置信区间,0.37 - 1.35;P = 0.30),与他莫昔芬组相比降低33%(风险比,0.67;95%置信区间,0.42 - 1.06;P = 0.08),但这两个差异均无统计学意义。在药物依从性良好的人群中关联更强。
在基于社区的综合健康计划环境中,接受芳香化酶抑制剂治疗的女性子宫内膜癌发病率低于接受他莫昔芬治疗的女性。此外,芳香化酶抑制剂可能会降低他莫昔芬相关子宫内膜癌的发病率。虽然与未接受内分泌治疗组相比,芳香化酶抑制剂组的子宫内膜癌病例数略少,但需要进一步研究以明确评估这种潜在关联。