Fulvestrant treatment is associated with cholesterol plasma level reduction in hormone-receptor-positive metastatic breast cancer patients.
BACKGROUND
Fulvestrant is a pure anti-estrogen hormoal agent formally lacking any estrogen-agonist activity. We analyze the effect(s) of fulvestrant treatment on estrogen target systems in hormoe-sensitive advanced breast cancer patients.


RESULTS
Patients received a median of five fulvestrant injections (range 3-19). We observed a partial response in one patient, disease stability in 21 and disease progression in 29 patients with a clinical benefit of 43.2% and a median time to progression of 5 [range 3-20] mo. Total cholesterol levels significantly decreased during treatment (219.8 +/- 45.3 vs. 201.4 +/- 42.1 mg/dl; p = 0.0054) together with LDL-cholesterol (129.7 +/- 41.39 vs. 112.3 +/- 37.1 mg/dl; p = 0.018). HDL-cholesterol and triglycerides did not show significant changes. Reduction of total and LDL-cholesterol was independent from last hormoal treatment or treatment duration. All coagulation indices and mean endometrial mucosa thickness value did not vary.


METHODS
Fifty-one patients [median age 65 (range 48-82) y] were enrolled. All patients received previous hormoal treatments, with 90.2% receiving > or =2 courses. Last hormoal treatment was exemestane, letrozole, anastrozole and other in 30-10-7-4/51 patients respectively. Median withdrawal time was 18 d (range 3-1456). Complete fasting lipid blood profile and coagulation indices were assessed before fulvestrant administration, every 3 mo and at discontinuation time. Endometrial mucosa thickness was evaluated before fulvestrant administration and at end-study time.


CONCLUSIONS
We observed a lipid lowering effect of fulvestrant possibly related to an influence on lipid metabolism by a mechanism in which a role could be played by progesterone receptor.
Camerini
Andrea
A
Medical Oncology, Versilia Hospital and Istituto Toscano Tumori, Lido di Camaiore, Italy. andreacamerini@katamail.com
Rondini
Marianna
M
Garrone
Ornella
O
Valsuani
Chiara
C
Donati
Sara
S
Siclari
Olimpia
O
Sgambato
Alessandro
A
Tartarelli
Gianna
G
Vincenti
Maura
M
Mattiot
Valentina Polla
VP
Porta
Romana Prosperi
RP
Puccetti
Cheti
C
Puccinelli
Paolo
P
Amoroso
Domenico
D
D000230:Adenocarcinoma / Q000097:blood / Q000188:drug therapy / Q000556:secondary*; D000368:Aged; D000369:Aged, 80 and over; D018931:Antineoplastic Agents, Hormonal / Q000494:pharmacology* / Q000627:therapeutic use; D047072:Aromatase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D002784:Cholesterol / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood; D004717:Endometrium / Q000187:drug effects / Q000648:ultrastructure; D004958:Estradiol / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D020847:Estrogen Receptor Modulators / Q000494:pharmacology* / Q000627:therapeutic use; D004967:Estrogens; D005260:Female; D000077267:Fulvestrant; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000032:analysis*; D009376:Neoplasms, Hormone-Dependent / Q000097:blood / Q000188:drug therapy / Q000473:pathology / Q000556:secondary*; D017698:Postmenopause; D011374:Progesterone; D011446:Prospective Studies; D011960:Receptors, Estrogen / Q000032:analysis* / Q000187:drug effects; D011980:Receptors, Progesterone / Q000032:analysis* / Q000187:drug effects / Q000502:physiology; D014280:Triglycerides / Q000097:blood
D018931:Antineoplastic Agents, Hormonal; D047072:Aromatase Inhibitors; D008078:Cholesterol, LDL; D020847:Estrogen Receptor Modulators; D004967:Estrogens; D009363:Neoplasm Proteins; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D014280:Triglycerides; D000077267:Fulvestrant; D011374:Progesterone; D004958:Estradiol; D002784:Cholesterol