PS3-12: Obesity and Risk of Proliferative Hyperplastic Lesions

Abstract

Background and Aims: Obesity is a risk factor for breast cancer for postmenopausal women. Aromatization of androstenedione to estradiol in the peripheral adipose tissue and low levels of sex-hormone binding globulin as well as increased serum levels of insulin-like growth factors have been proposed as the underlying biological mechanisms. Women diagnosed with hyperplastic lesions with/without atypia have increased risk for a subsequent breast cancer. We conducted a retrospective study with the primary objective of assessing the association between body weight and the diagnosis of hyperplastic lesions. Our specific aims were: to compare the prevalence of biopsies prior to the diagnosis of breast cancer and to estimate the risk of hyperplastic lesions after adjusting for Body Mass Index (BMI), and other potential confounders. Methods: This case-series study benefits from an existing cohort of women (N= 882), ages 40 years and older, diagnosed with and treated for their first primary invasive breast cancer at the Geisinger Health System between 2001 and 2007. Data were obtained from Geisinger’s electronic health record; the diagnosis atypical ductal hyperplasia (ADH) was the outcome of interest. Women were categorized according to their BMIs as normal, overweight or obese. All statistical tests were two-sided and analyses were performed using SAS version 9.3 (SAS Institute, Inc. Cary, NC). Results: The prevalence of biopsy prior to the diagnosis of breast cancer was not statistically different among the three groups of women. The risk of hyperplastic lesions was elevated for overweight (OR= 13.58; 95% CI= 1.03–178.84; P= 0.047) and obese (OR= 14.76; 95% CI= 1.09–200.09; P= 0.043) women relative to women in their ideal body weight. The association between BMI and other risk factors for breast cancer did not reach the level of statistical significance. Conclusions: Preliminary results suggest that excess body weight increases the risk of hyperplastic lesions in postmenopausal women. Biologically, this observed risk may be the result of higher serum levels of unbound estradiol in overweight and obese women. Future larger studies should validate our findings.