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Gonadotropin-releasing hormone agonist in premenopausal women does not alter hypothalamic-pituitary-adrenal axis response to corticotropin-releasing hormone.
Am J Physiol Endocrinol Metab 2018; 315(2):E316-E325AJ

Abstract

Sex hormones appear to play a role in the regulation of hypothalamic-pituitary-adrenal (HPA) axis activity. The objective was to isolate the effects of estradiol (E2) on central activation of the HPA axis. We hypothesized that the HPA axis response to corticotropin-releasing hormone (CRH) under dexamethasone (Dex) suppression would be exaggerated in response to chronic ovarian hormone suppression and that physiologic E2 add-back would mitigate this response. Thirty premenopausal women underwent 20 wk of gonadotropin-releasing hormone agonist therapy (GnRHAG) and transdermal E2 (0.075 mg per day, GnRHAG + E2, n = 15) or placebo (PL) patch (GnRHAG + PL, n = 15). Women in the GnRHAG + PL and GnRHAG + E2 groups were of similar age (38 (SD 5) yr vs. 36 (SD 7) yr) and body mass index (27 (SD 6) kg/m2 vs. 27 (SD 6) kg/m2). Serum E2 changed differently between the groups (P = 0.01); it decreased in response to GnRHAG + PL (77.9 ± 17.4 to 23.2 ± 2.6 pg/ml; P = 0.008) and did not change in response to GnRHAG + E2 (70.6 ± 12.4 to 105 ± 30.4 pg/ml; P = 0.36). The incremental area under the curve (AUCINC) responses to CRH were different between the groups for total cortisol (P = 0.03) and cortisone (P = 0.04) but not serum adrenocorticotropic hormone (ACTH) (P = 0.28). When examining within-group changes, GnRHAG + PL did not alter the HPA axis response to Dex/CRH, but GnRHAG + E2 decreased the AUCINC for ACTH (AUCINC, 1,623 ± 257 to 1,211 ± 236 pg/ml·min, P = 0.004), cortisone (1,795 ± 367 to 1,090 ± 281 ng/ml·min, P = 0.009), and total cortisol (7,008 ± 1,387 to 3,893 ± 1,090 ng/ml·min, P = 0.02). Suppression of ovarian hormones by GnRHAG therapy for 20 wk did not exaggerate the HPA axis response to CRH, but physiologic E2 add-back reduced HPA axis activity compared with preintervention levels.

Authors+Show Affiliations

Division of Geriatric Medicine, School of Medicine, University of Colorado Anschutz Medical Campus , Aurora, Colorado. Geriatric Research, Education and Clinical Center, Veterans Affairs Eastern Colorado Heath Care System, Denver, Colorado.Division of Geriatric Medicine, School of Medicine, University of Colorado Anschutz Medical Campus , Aurora, Colorado. Geriatric Research, Education and Clinical Center, Veterans Affairs Eastern Colorado Heath Care System, Denver, Colorado.Division of Geriatric Medicine, School of Medicine, University of Colorado Anschutz Medical Campus , Aurora, Colorado.Department of Preventative Medicine and Biostatistics, University of Colorado Anschutz Medical Campus , Aurora, Colorado.Division of Geriatric Medicine, School of Medicine, University of Colorado Anschutz Medical Campus , Aurora, Colorado. Geriatric Research, Education and Clinical Center, Veterans Affairs Eastern Colorado Heath Care System, Denver, Colorado.Division of Endocrinology, Metabolism and Diabetes, University of Colorado Anschutz Medical Campus , Aurora, Colorado.Division of Geriatric Medicine, School of Medicine, University of Colorado Anschutz Medical Campus , Aurora, Colorado. Geriatric Research, Education and Clinical Center, Veterans Affairs Eastern Colorado Heath Care System, Denver, Colorado.

Pub Type(s)

Journal Article
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

29631362

Citation

Gavin, Kathleen M., et al. "Gonadotropin-releasing Hormone Agonist in Premenopausal Women Does Not Alter Hypothalamic-pituitary-adrenal Axis Response to Corticotropin-releasing Hormone." American Journal of Physiology. Endocrinology and Metabolism, vol. 315, no. 2, 2018, pp. E316-E325.
Gavin KM, Shea KL, Gibbons E, et al. Gonadotropin-releasing hormone agonist in premenopausal women does not alter hypothalamic-pituitary-adrenal axis response to corticotropin-releasing hormone. Am J Physiol Endocrinol Metab. 2018;315(2):E316-E325.
Gavin, K. M., Shea, K. L., Gibbons, E., Wolfe, P., Schwartz, R. S., Wierman, M. E., & Kohrt, W. M. (2018). Gonadotropin-releasing hormone agonist in premenopausal women does not alter hypothalamic-pituitary-adrenal axis response to corticotropin-releasing hormone. American Journal of Physiology. Endocrinology and Metabolism, 315(2), pp. E316-E325. doi:10.1152/ajpendo.00221.2017.
Gavin KM, et al. Gonadotropin-releasing Hormone Agonist in Premenopausal Women Does Not Alter Hypothalamic-pituitary-adrenal Axis Response to Corticotropin-releasing Hormone. Am J Physiol Endocrinol Metab. 2018 08 1;315(2):E316-E325. PubMed PMID: 29631362.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gonadotropin-releasing hormone agonist in premenopausal women does not alter hypothalamic-pituitary-adrenal axis response to corticotropin-releasing hormone. AU - Gavin,Kathleen M, AU - Shea,Karen L, AU - Gibbons,Ellie, AU - Wolfe,Pamela, AU - Schwartz,Robert S, AU - Wierman,Margaret E, AU - Kohrt,Wendy M, Y1 - 2018/04/06/ PY - 2018/4/11/pubmed PY - 2019/7/10/medline PY - 2018/4/11/entrez KW - central adiposity KW - cortisol KW - estradiol KW - gonadotropin-releasing hormone agonist KW - menopause SP - E316 EP - E325 JF - American journal of physiology. Endocrinology and metabolism JO - Am. J. Physiol. Endocrinol. Metab. VL - 315 IS - 2 N2 - Sex hormones appear to play a role in the regulation of hypothalamic-pituitary-adrenal (HPA) axis activity. The objective was to isolate the effects of estradiol (E2) on central activation of the HPA axis. We hypothesized that the HPA axis response to corticotropin-releasing hormone (CRH) under dexamethasone (Dex) suppression would be exaggerated in response to chronic ovarian hormone suppression and that physiologic E2 add-back would mitigate this response. Thirty premenopausal women underwent 20 wk of gonadotropin-releasing hormone agonist therapy (GnRHAG) and transdermal E2 (0.075 mg per day, GnRHAG + E2, n = 15) or placebo (PL) patch (GnRHAG + PL, n = 15). Women in the GnRHAG + PL and GnRHAG + E2 groups were of similar age (38 (SD 5) yr vs. 36 (SD 7) yr) and body mass index (27 (SD 6) kg/m2 vs. 27 (SD 6) kg/m2). Serum E2 changed differently between the groups (P = 0.01); it decreased in response to GnRHAG + PL (77.9 ± 17.4 to 23.2 ± 2.6 pg/ml; P = 0.008) and did not change in response to GnRHAG + E2 (70.6 ± 12.4 to 105 ± 30.4 pg/ml; P = 0.36). The incremental area under the curve (AUCINC) responses to CRH were different between the groups for total cortisol (P = 0.03) and cortisone (P = 0.04) but not serum adrenocorticotropic hormone (ACTH) (P = 0.28). When examining within-group changes, GnRHAG + PL did not alter the HPA axis response to Dex/CRH, but GnRHAG + E2 decreased the AUCINC for ACTH (AUCINC, 1,623 ± 257 to 1,211 ± 236 pg/ml·min, P = 0.004), cortisone (1,795 ± 367 to 1,090 ± 281 ng/ml·min, P = 0.009), and total cortisol (7,008 ± 1,387 to 3,893 ± 1,090 ng/ml·min, P = 0.02). Suppression of ovarian hormones by GnRHAG therapy for 20 wk did not exaggerate the HPA axis response to CRH, but physiologic E2 add-back reduced HPA axis activity compared with preintervention levels. SN - 1522-1555 UR - https://www.unboundmedicine.com/medline/citation/29631362/Gonadotropin_releasing_hormone_agonist_in_premenopausal_women_does_not_alter_hypothalamic_pituitary_adrenal_axis_response_to_corticotropin_releasing_hormone_ L2 - http://www.physiology.org/doi/full/10.1152/ajpendo.00221.2017?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -