scholarly journals Hypothalamic amenorrhea with normal body weight: ACTH, allopregnanolone and cortisol responses to corticotropin-releasing hormone test

2000 ◽  
Vol 142 (3) ◽  
pp. 280-285 ◽  
Author(s):  
B Meczekalski ◽  
A Tonetti ◽  
P Monteleone ◽  
F Bernardi ◽  
S Luisi ◽  
...  
Keyword(s):  
Body Weight ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Amenorrhea ◽  
Releasing Hormone ◽  
Normal Body ◽  
Adrenal Axis ◽  
Normal Body Weight ◽  
Cortisol Responses ◽  
Pituitary Adrenal Axis

OBJECTIVE: Hypothalamic amenorrhea (HA) is a functional disorder caused by disturbances in gonadotropin-releasing hormone (GnRH) pulsatility. The mechanism by which stress alters GnRH release is not well known. Recently, the role of corticotropin-releasing hormone (CRH) and neurosteroids in the pathophysiology of HA has been considered. The aim of the present study was to explore further the role of the hypothalamic-pituitary-adrenal axis in HA. DESIGN: We included 8 patients (aged 23.16+/-1.72 years) suffering from hypothalamic stress-related amenorrhea with normal body weight and 8 age-matched healthy controls in the follicular phase of the menstrual cycle. METHODS: We measured basal serum levels of FSH, LH, and estradiol and evaluated ACTH, allopregnanolone and cortisol responses to CRH test in both HA patients and healthy women. RESULTS: Serum basal levels of FSH, LH, and estradiol as well as basal levels of allopregnanolone were significantly lower in HA patients than in controls (P<0.001) while basal ACTH and cortisol levels were significantly higher in amenorrheic patients with respect to controls (P<0.001). The response (area under the curve) of ACTH, allopregnanolone and cortisol to CRH was significantly lower in amenorrheic women compared with controls (P<0.001, P<0.05, P<0.05 respectively). CONCLUSIONS: In conclusion, women with HA, despite the high ACTH and cortisol levels and, therefore, hypothalamus-pituitary-adrenal axis hyperactivity, are characterized by low allopregnanolone basal levels, deriving from an impairment of both adrenal and ovarian synthesis. The blunted ACTH, allopregnanolone and cortisol responses to CRH indicate that, in hypothalamic amenorrhea, there is a reduced sensitivity and expression of CRH receptor. These results open new perspectives on the role of neurosteroids in the pathogenesis of hypothalamic amenorrhea.

scholarly journals The Role of Corticotropin-Releasing Hormone at Peripheral Nociceptors: Implications for Pain Modulation

Biomedicines ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 623
Author(s):  
Haiyan Zheng ◽  
Ji Yeon Lim ◽  
Jae Young Seong ◽  
Sun Wook Hwang
Keyword(s):  
Signal Transmission ◽  
Brain Regions ◽  
Pain Modulation ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Inhibitory Function ◽  
Peripheral Pain ◽  
Functional Profiles ◽  
Pituitary Adrenal Axis

Peripheral nociceptors and their synaptic partners utilize neuropeptides for signal transmission. Such communication tunes the excitatory and inhibitory function of nociceptor-based circuits, eventually contributing to pain modulation. Corticotropin-releasing hormone (CRH) is the initiator hormone for the conventional hypothalamic-pituitary-adrenal axis, preparing our body for stress insults. Although knowledge of the expression and functional profiles of CRH and its receptors and the outcomes of their interactions has been actively accumulating for many brain regions, those for nociceptors are still under gradual investigation. Currently, based on the evidence of their expressions in nociceptors and their neighboring components, several hypotheses for possible pain modulations are emerging. Here we overview the historical attention to CRH and its receptors on the peripheral nociception and the recent increases in information regarding their roles in tuning pain signals. We also briefly contemplate the possibility that the stress-response paradigm can be locally intrapolated into intercellular communication that is driven by nociceptor neurons. Such endeavors may contribute to a more precise view of local peptidergic mechanisms of peripheral pain modulation.

Opioid Control of the Hypothalamus-Pituitary-Adrenal Axis Cyclically Fails in Menstrual Migraine

Cephalalgia ◽  
1990 ◽  
Vol 10 (1) ◽  
pp. 51-56 ◽  
Author(s):  
Fabio Facchinetti ◽  
Emilia Martignoni ◽  
Loridine Fioroni ◽  
Grazia Sances ◽  
Andrea R Genazzani
Keyword(s):  
Menstrual Cycle ◽  
Follicular Phase ◽  
Menstrual Migraine ◽  
Cycle Phase ◽  
Corticotropin Releasing Hormone ◽  
Menstrual Cycle Phase ◽  
Releasing Hormone ◽  
Adrenal Axis ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

To assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma b-endorphin (b-EP) and cortisol responses to naloxone (8 mg iv) and corticotropin releasing hormone (100 μg iv) were evaluated in both the follicular phase and the premenstrual period in 7 patients suffering from menstrual migraine and in 7 healthy, asymptomatic control volunteers. In the controls, naloxone evoked a significant release of both b-EP (F = 5.86, p < 0.002) and cortisol (F = 4.43, p < 0.008), independently of the menstrual cycle phase (F = 0.31 and 1.04, for b-EP and cortisol, respectively). Menstrual migraine patients, on the other hand, showed a significant hormone response only in the follicular phase, not in the premenstrual period. Corticotropin releasing hormone significantly increased b-EP and cortisol in both the controls and the menstrual migraine patients, independently of the menstrual cycle phase. In both the naloxone and corticotropin releasing hormone testings, the basal b-EP levels measured in the premenstrual period were lower than those observed in the follicular phase ( p < 0.02). These data demonstrate a cyclical, premenstrual dysfunction of the hypothalamic control exerted by opioids on the hypothalamus-pituitary-adrenal axis. Impairment of this fundamental adaptive mechanism (involved in stress responses and in pain control) could establish a causal relationship between menstrual-related migraine attacks and premenstrual opioid hyposensitivity.

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