Baseline estrogen levels in postmenopausal women participating in the MAP.3 breast cancer chemoprevention trial. Issue 6 (June 2020)

• Record Type: Journal Article
• Authors: Richardson, Harriet; Ho, Vikki; Pasquet, Romain; Singh, Ravinder J.; Goetz, Matthew P.; Tu, Dongsheng; Goss, Paul E.; Ingle, James N.
• Is Part Of: Menopause. Volume 27:Issue 6(2020)
• Publication Date: 2020-06
• Subjects: Estradiol -- Estrone -- Postmenopausal women; Menopause -- Periodicals; 618.175005
• DOI: 10.1097/GME.0000000000001568
• Languages: English
• ISSNs: 1072-3714

Abstract

Abstract: Objective: The aim of the study was to quantify baseline estradiol (E2) and estrone (E1) concentrations according to selected patient characteristics in a substudy nested within the MAP.3 chemoprevention trial. Methods: E2 and E1 levels were measured in 4, 068 postmenopausal women using liquid chromatography-tandem mass spectrometry. Distributions were described by age, years since menopause, race, body mass index (BMI), smoking status, and use and duration of hormone therapy using the Kruskal-Wallis test. Multivariable linear regression was also used to identify characteristics associated with estrogen levels. Results: After truncation at the 97.5th percentile, the mean (SD)/median (IQR) values for E2 and E1 were 5.41 (4.67)/4.0 (2.4-6.7) pg/mL and 24.7 (14.1)/21 (15-31) pg/mL, respectively. E2 and E1 were strongly correlated (Pearson correlation [ r ] = 0.8, P < 0.01). The largest variation in E2 and E1 levels was by BMI; mean E2 and E1 levels were 3.5 and 19.1 pg/mL, respectively for women with BMI less than 25 and 7.5 and 30.6 pg/mL, respectively, for women with BMI greater than 30. E2 and E1 varied by age, BMI, smoking status, and prior hormone therapy in multivariable models ( P < 0.01). Conclusions: There was large interindividual variability observed for E2 and E1 that varied significantly by participant characteristics, but with small absolute differences except in the case of BMI. Although the majority of participant characteristics were independently associated with E1 and E2, together, these factors only explained about 20% of the variation in E1 and E2 levels.