scholarly journals Gonadotropin-releasing hormone agonist in premenopausal women does not alter hypothalamic-pituitary-adrenal axis response to corticotropin-releasing hormone

2018 ◽  
Vol 315 (2) ◽  
pp. E316-E325 ◽  
Author(s):  
Kathleen M. Gavin ◽  
Karen L. Shea ◽  
Ellie Gibbons ◽  
Pamela Wolfe ◽  
Robert S. Schwartz ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Area Under The Curve ◽  
Premenopausal Women ◽  
Gonadotropin Releasing Hormone ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Pituitary Adrenal ◽  
Releasing Hormone ◽  
Gonadotropin Releasing Hormone Agonist ◽  
Total Cortisol ◽  
Hpa Axis Activity

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.

Consistent Reduction of ACTH responses to stimulation with CRH, Vasopressin and Hypoglycaemia in Patients with Major Depression

1989 ◽  
Vol 155 (4) ◽  
pp. 468-478 ◽  
Author(s):  
Roger G. Kathol ◽  
Richard S. Jaeckle ◽  
Juan F. Lopez ◽  
William H. Meller
Keyword(s):  
Major Depression ◽  
Hpa Axis ◽  
Negative Correlation ◽  
Arginine Vasopressin ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Pituitary Adrenal ◽  
Releasing Hormone ◽  
Control Subjects ◽  
Basal Cortisol ◽  
Cortisol Responses

Eleven patients with major depression and 12 control subjects were administered corticotropin-releasing hormone (CRH), aqueous arginine vasopressin (AVP), and insulin hypoglycaemia (IH) to test for differences in hypothalamic–pituitary–adrenal (HPA) axis function. Patients with major depression demonstrated lower ACTH responses to CRH when compared with controls, and a trend toward such after administration of AVP. Despite lower ACTH responses in patients with depression, there were no differences in Cortisol responses to these stimuli. In the CRH and AVP tests, there was no correlation between the basal Cortisol and ACTH responses in either controls or patients, but in the IH test there was a negative correlation between these responses for both groups. The ACTH responses to CRH and AVP were positively correlated in controls and patients. Cortisol responses to all three provocative stimuli were positively correlated in both subject groups. These findings are consistent with the hypothesis that hypothalamic or supra-hypothalamic overactivity may be involved in the development of HPA-axis abnormalities in patients with depression.

THE HYPOTHALAMIC-PITUITARY-ADRENAL (HPA) AXIS OF PATIENTS WITH SEVERE SEPSIS: ALTERED RESPONSE TO CORTICOTROPIN-RELEASING HORMONE (CRH)

1999 ◽  
Vol 27 (Supplement) ◽  
pp. A144
Author(s):  
Stefan Schroeder ◽  
Maria Wichers ◽  
Lutz E Lehmann ◽  
Christian Putensen ◽  
Andreas Hoeft ◽  
...  
Keyword(s):  
Severe Sepsis ◽  
Hpa Axis ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Pituitary Adrenal ◽  
Releasing Hormone ◽  
Altered Response

scholarly journals Hypothalamic–pituitary–adrenal axis activity in adults who were prenatally exposed to the Dutch famine

2006 ◽  
Vol 155 (1) ◽  
pp. 153-160 ◽  
Author(s):  
Susanne R de Rooij ◽  
Rebecca C Painter ◽  
David I W Phillips ◽  
Clive Osmond ◽  
Robert P J Michels ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Area Under The Curve ◽  
Later Life ◽  
Hypothalamic Pituitary Adrenal ◽  
Adult Age ◽  
Suppression Test ◽  
Design And Methods ◽  
Prenatal Famine ◽  
Hpa Axis Activity ◽  
Dexamethasone Suppression

Objective: The hypothalamic–pituitary–adrenal (HPA) axis has been proposed to be susceptible to fetal programming, the process by which an adverse fetal environment elicits permanent physiological and metabolic alterations predisposing to disease in later life. It is hypothesized that fetal exposure to poor circumstances alters the set point of the HPA axis, leading to increased HPA axis activity and subsequent increased cortisol concentrations. In this study, we tested the hypothesis that prenatal exposure to famine during different periods of gestation is associated with increased activity of the HPA axis. Design and methods: We assessed plasma cortisol concentrations after a dexamethasone suppression and an ACTH1–24-stimulation test in a group of 98 men and women randomly sampled from the Dutch famine birth cohort. Cohort members were born as term singletons around the 1944–1945 Dutch famine. Results: Cortisol profiles after dexamethasone suppression and ACTH1–24 stimulation were similar for participants exposed to famine during late, mid- or early gestation (P=0.78). Cortisol concentrations after dexamethasone suppression test did not differ between those exposed and those unexposed to famine in utero (mean difference −2% (95% confidence interval (CI) −27 to 23)). Neither peak cortisol concentration (20 nmol/l (95% CI −27 to 66)), cortisol increment (−5 nmol/l (95% CI −56 to 47)) or cortisol area under the curve post-ACTH1–24 injection (4% (95% CI −4 to 12)) differed between exposed and unexposed participants. Conclusions: Prenatal famine exposure does not seem to affect HPA axis activity at adult age, at least not at the adrenal level. This does not exclude altered HPA axis activity at the levels of the hippocampus and hypothalamus.

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