Lipid Changes During Endocrine Therapy in Breast Cancer Patients: The Results of a 5-Year Real-World Retrospective Analysis.

Tao He,Qing Lv,Jie Chen,Yunhao Wu,Zhoukai Fu,Jiayuan Li,Zhu Wang,Xu Li,Ting Luo,Xiusong Li,Yuan Fan,Xiaorong Zhong

doi:10.3389/fonc.2021.670897

Abstract

BackgroundThe aim of this study was to investigate the status of serum lipids during endocrine therapy.MethodsWe retrospectively analysed lipid profiles during the 5-year treatment of 1487 consecutive postoperative BC patients. Lipid parameters included triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL-C) and high-density lipoprotein (HDL-C). Those biomarkers were measured at baseline and 1, 2, 3, 4 and 5 years following the initiation of endocrine therapy.ResultsFor premenopausal BC patients, LDL levels rapidly decreased at 1 year in the tamoxifen (TAM) group compared with baseline levels (p<0.05), and this decline remained for the following 4 years. Additionally, LDL levels were significantly lower in the TAM group than in the nonendocrine group at all assessment time points (p<0.05). Similarly, TC levels also decreased in the TAM group compared with baseline levels at all assessment time points (p<0.05), and compared with the levels in the nonendocrine group, TC levels were also lower for the first 4 years. For postmenopausal BC patients, there was no significant difference in the lipid profiles (TG, TC, LDL and HDL) in the letrozole (LET), anastrozole (ANA) or exemestane (EXE) groups compared with the nonendocrine group. For patients who received TAM, compared with the nonendocrine group, TC levels decreased at 1 year, and LDL levels decreased at 1 and 2 years.ConclusionsTAM may improve LDL and TC levels in premenopausal BC patients. In postmenopausal BC patients, aromatase inhibitors (AIs) may have no adverse effects on lipid profiles, and TAM may have limited beneficial effects on serum lipids.

Highlights

The aim of this study was to investigate the status of serum lipids during endocrine therapy
The inclusion criteria were as follows: [1] female patients aged ≥18 years; [2] patients pathologically diagnosed with Breast cancer (BC); [3] postoperative BC patients and the method of operation were according to the NCCN guidelines [4] stage I-III BC patients; [5] postoperative systemic therapies including endocrine therapy, chemotherapy, targeted therapy, and radiotherapy were recommended according to the NCCN guidelines, [6]patients who did not receive endocrine therapy or patients who received one of the following endocrine drugs: tamoxifen (TAM), letrozole (LET), anastrozole (ANA), or exemestane (EXE); and [7] patients who had adequate organ function before surgery and Eastern Cooperative Oncology Group (ECOG) ≤2
The variables of interest included height, weight, body mass index (BMI), age at diagnosis, menopausal status, tumour location, surgical procedures, TNM (Tumour, Node, Metastasis) stage [22], ER, progesterone receptor (PR), human epidermal growth factor receptor-2 (HER-2), Ki-67 status and lipid parameters at baseline and at 1, 2, 3, 4 and 5 years following the initiation of endocrine therapy

Summary

Introduction

The aim of this study was to investigate the status of serum lipids during endocrine therapy. Hormone receptor (HR)positive BC, accounting for 65%-75% of BC cases, is the most common type deserving urgent exploration [3,4,5]. Extensive studies have shown that the better prognosis of HR-positive BC patients may be due to adjuvant endocrine therapy, which substantially reduces recurrence rates and improves overall survival [6]. Prior studies have demonstrated that oestrogen plays a vital role in the development and progression of HR-positive BC [7, 8], and deregulation of oestrogen signalling may be the basic therapeutic strategy for endocrine therapy. Endocrine drugs include selective oestrogen receptor modulators (SERMs) and aromatase inhibitors (AIs) [9, 10]. AIs (including letrozole, anastrozole and exemestane) inhibit the aromatase enzyme, which is the rate-limiting enzyme in the conversion of androgens to oestrogens, leading to the reduction of plasma and intratumoural oestrogen levels [12, 13]

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