Is letrozole during ovarian stimulation useful in breast cancer patients undergoing fertility preservation to reduce early luteal progesterone levels following GnRH-agonist trigger?
Cryopreservation
Estrogen
Luteal phase
Luteinizing hormone
Ovarian stimulation
Progesterone
Journal
Reproductive biology and endocrinology : RB&E
ISSN: 1477-7827
Titre abrégé: Reprod Biol Endocrinol
Pays: England
ID NLM: 101153627
Informations de publication
Date de publication:
11 Jun 2022
11 Jun 2022
Historique:
received:
12
03
2022
accepted:
26
05
2022
entrez:
11
6
2022
pubmed:
12
6
2022
medline:
15
6
2022
Statut:
epublish
Résumé
In absence of contraindication, breast cancer patients of reproductive age can undergo fertility preservation with controlled ovarian stimulation for oocyte/embryo cryopreservation before the administration of potentially gonadotoxic treatments. High hormonal levels induced by ovarian stimulation might have an adverse impact on hormone-positive breast cancer. Whether letrozole supplementation during ovarian stimulation (COSTLES) reduces serum progesterone levels after GnRHa trigger remains unknown. We aimed to determine whether COSTLES might be useful for breast cancer patients undergoing fertility preservation to reduce early luteal progesterone levels following GnRH-agonist (GnRHa)trigger. All women who underwent COS with GnRH antagonist protocol with GnRHa trigger were included. Serum progesterone level measured 12 h after GnRHa trigger was compared between patients undergoing COS with letrozole supplementation (COSTLES group) and patients undergoing COS without letrozole (Control group) for fertility preservation purposes. A total of 246 patients were included, of which 84 patients (34.1%) in the COSTLES group and 162 patients (65.6%) in the Control group. All patients in the COSTLES group were BC patients (n = 84, 100%), while the Control group included 77 BC patients (47.5%). Patients in the two groups were comparable. The mean number of oocytes recovered and vitrified at metaphase 2 stage did not significantly differ between the two groups. Serum progesterone levels on the day after GnRHa trigger were significantly lower in the COSTLES group (8.6 ± 0.7 vs. 10.5 ± 0.5 ng/mL, respectively, p < 0.03), as well as serum E2 levels (650.3 ± 57.7 vs. 2451.4.0 ± 144.0 pg/mL, respectively, p < 0.01). However, the GnRHa-induced LH surge was significantly higher in in the COSTLES group (71.9 ± 4.6 vs. 51.2 ± 2.6 UI/L, respectively, p < 0.01). Our results show that COSTLES for fertility preservation in breast cancer patients using GnRHa trigger reduces serum progesterone levels compared to ovarian stimulation without letrozole. These findings encourage the use of COSTLES in this context to decrease the potential deleterious effect of elevated hormonal levels on hormone-positive breast cancer.
Sections du résumé
BACKGROUND
BACKGROUND
In absence of contraindication, breast cancer patients of reproductive age can undergo fertility preservation with controlled ovarian stimulation for oocyte/embryo cryopreservation before the administration of potentially gonadotoxic treatments. High hormonal levels induced by ovarian stimulation might have an adverse impact on hormone-positive breast cancer. Whether letrozole supplementation during ovarian stimulation (COSTLES) reduces serum progesterone levels after GnRHa trigger remains unknown. We aimed to determine whether COSTLES might be useful for breast cancer patients undergoing fertility preservation to reduce early luteal progesterone levels following GnRH-agonist (GnRHa)trigger.
METHODS
METHODS
All women who underwent COS with GnRH antagonist protocol with GnRHa trigger were included. Serum progesterone level measured 12 h after GnRHa trigger was compared between patients undergoing COS with letrozole supplementation (COSTLES group) and patients undergoing COS without letrozole (Control group) for fertility preservation purposes.
RESULTS
RESULTS
A total of 246 patients were included, of which 84 patients (34.1%) in the COSTLES group and 162 patients (65.6%) in the Control group. All patients in the COSTLES group were BC patients (n = 84, 100%), while the Control group included 77 BC patients (47.5%). Patients in the two groups were comparable. The mean number of oocytes recovered and vitrified at metaphase 2 stage did not significantly differ between the two groups. Serum progesterone levels on the day after GnRHa trigger were significantly lower in the COSTLES group (8.6 ± 0.7 vs. 10.5 ± 0.5 ng/mL, respectively, p < 0.03), as well as serum E2 levels (650.3 ± 57.7 vs. 2451.4.0 ± 144.0 pg/mL, respectively, p < 0.01). However, the GnRHa-induced LH surge was significantly higher in in the COSTLES group (71.9 ± 4.6 vs. 51.2 ± 2.6 UI/L, respectively, p < 0.01).
CONCLUSIONS
CONCLUSIONS
Our results show that COSTLES for fertility preservation in breast cancer patients using GnRHa trigger reduces serum progesterone levels compared to ovarian stimulation without letrozole. These findings encourage the use of COSTLES in this context to decrease the potential deleterious effect of elevated hormonal levels on hormone-positive breast cancer.
Identifiants
pubmed: 35690817
doi: 10.1186/s12958-022-00958-7
pii: 10.1186/s12958-022-00958-7
pmc: PMC9188055
doi:
Substances chimiques
Gonadotropin-Releasing Hormone
33515-09-2
Progesterone
4G7DS2Q64Y
Letrozole
7LKK855W8I
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
87Informations de copyright
© 2022. The Author(s).
Références
JAMA. 2013 Oct 2;310(13):1353-68
pubmed: 24084921
N Engl J Med. 2018 Jan 25;378(4):400
pubmed: 29372989
Reprod Biomed Online. 2017 Oct;35(4):400-406
pubmed: 28647355
Fertil Steril. 2019 Dec;112(6):1022-1033
pubmed: 31843073
FASEB J. 2007 Feb;21(2):586-95
pubmed: 17158782
Eur J Obstet Gynecol Reprod Biol X. 2019 May 11;4:100049
pubmed: 31673686
Ann Oncol. 2020 Dec;31(12):1664-1678
pubmed: 32976936
J Assist Reprod Genet. 2014 Jul;31(7):927-32
pubmed: 24854484
Front Endocrinol (Lausanne). 2020 Dec 08;11:572388
pubmed: 33363515
J Biol Chem. 1990 Nov 25;265(33):20533-8
pubmed: 1700790
Fertil Steril. 2017 Sep;108(3):407-415.e11
pubmed: 28739117
Nature. 2010 Jun 10;465(7299):803-7
pubmed: 20445538
Hum Reprod. 2007 Mar;22(3):676-87
pubmed: 17110397
Hum Reprod. 2000 Sep;15(9):1909-12
pubmed: 10966984
Hum Reprod Update. 2012 Sep-Oct;18(5):525-35
pubmed: 22647504
Endocrinology. 1996 Jan;137(1):166-74
pubmed: 8536609
J Natl Cancer Inst. 2006 Jul 19;98(14):1011-4
pubmed: 16849684
Hum Reprod. 2020 Jan 1;35(1):157-166
pubmed: 31967304
Reprod Biomed Online. 2010 Jun;20(6):783-8
pubmed: 20382080
J Clin Oncol. 2018 Jul 1;36(19):1994-2001
pubmed: 29620997
Fertil Steril. 2008 Jan;89(1):84-91
pubmed: 17462639
J Clin Endocrinol Metab. 2006 Oct;91(10):3885-90
pubmed: 16882752
CA Cancer J Clin. 2011 Nov-Dec;61(6):409-18
pubmed: 21969133
Endocr Rev. 2013 Feb;34(1):130-62
pubmed: 23303565
Hum Reprod. 2015 Sep;30(9):2184-9
pubmed: 26109617
J Clin Endocrinol Metab. 2016 Apr;101(4):1364-71
pubmed: 26751194
Fertil Steril. 2013 Dec;100(6):1673-80
pubmed: 23987516
Mol Cell Endocrinol. 2012 Jun 24;357(1-2):71-9
pubmed: 21945473
Clin Breast Cancer. 2008 Feb;8(1):65-9
pubmed: 18501060
J Clin Oncol. 2008 Jun 1;26(16):2630-5
pubmed: 18509175
J Clin Endocrinol Metab. 2003 Sep;88(9):4186-92
pubmed: 12970285
Eur J Pediatr Surg. 2013 Oct;23(5):418-22
pubmed: 23093430
Eur Rev Med Pharmacol Sci. 2017 Jul;21(13):3134-3138
pubmed: 28742191