Hot flushes

Stearns, Vered; Ullmer, Lynda; López, Juan F.; Smith, Yolanda R.; Isaacs, Claudine; Hayes, Daniel F.

doi:10.1016/s0140-6736(02)11774-0

Cited by 360 publications

(242 citation statements)

References 129 publications

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“…Although the pathophysiology of hot flashes remains unknown, a decline in sex hormone concentrations might lead to alterations in brain neurotransmitters and to instability in the hypothalamic thermoregulatory setpoint 1 . In the present study, although all patients were medically castrated, there were considerable differences in the clinical feature of hot flashes between the two treatment groups.…”

Section: Commentmentioning

confidence: 99%

“…Hot flashes are the most common symptom in menopausal women and are also a common and potentially chronic problem in men with prostate cancer who undergo androgen deprivation therapy (ADT). 1 Up to 80% of patients treated with a luteinizing hormone-releasing hormone (LHRH) agonist report hot flashes, and up to 27% report this as the most troublesome adverse effect. 2 Hot flashes can significantly affect quality of life (QOL) for men undergoing ADT.…”

Section: Introductionmentioning

confidence: 99%

“…However, the characteristics of hot flashes in men undergoing ADT have not been widely studied. 1 Methods to avoid or reduce these unpleasant side effects as much as possible have been investigated. In particular, the hot flash-preventive and -improving effects of steroidal antiandrogens have been reported.…”

Section: Introductionmentioning

confidence: 99%

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Hot Flashes During Androgen Deprivation Therapy With Luteinizing Hormone-Releasing Hormone Agonist Combined With Steroidal or Nonsteroidal Antiandrogen for Prostate Cancer

Sakai

Igawa

Tsurusaki

et al. 2009

Urology

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Objectives:We conducted a prospective, randomized study to investigate hot flashes and quality of life (QOL) during combined androgen blockade (CAB) therapy using steroidal or nonsteroidal antiandrogens. Methods:A total of 151 patients with prostate cancer, enrolled into this study between May 2001and June 2003, were randomized to receive CAB therapy using an LHRH agonist (leuprorelin) combined with a steroidal antiandrogen (chlormadinone) or a nonsteroidal antiandrogen (bicalutamide). The incidence of, frequency of, and distress due to hot flashes were evaluated with a self-entry questionnaire over 2 years. General and disease-specific QOL outcomes were also measured with the Functional Assessment of Cancer Therapy-Prostate (FACT-P) questionnaire.Results: Data were available for analysis on 124 patients. Although the incidence of hot flashes largely tended to be higher in the bicalutamide group than in the chlormadinone group, no significant difference was noted in the cumulative incidence of hot flashes at 2 years. The median frequency of hot flashes per day was 1.3 and 2.2 for warmth/flushing (P = 0.16) and 1.0 and 3.6 for sweating (P = 0.021) in the chlormadinone and bicalutamide groups, respectively. Patients in the chlormadinone group were significantly less likely to be distressed due to warmth/flushing 4 (OR 0.47, P < 0.001) and sweating (OR 0.61, P = 0.01) than those in the bicalutamide group.The time course of FACT-P scores showed no inter-group differences. Conclusions:Our results suggest that CAB using a steroidal antiandrogen such as chlormadinone may induce fewer and less distressing hot flashes than CAB with bicalutamide.

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Section: Commentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hot Flashes During Androgen Deprivation Therapy With Luteinizing Hormone-Releasing Hormone Agonist Combined With Steroidal or Nonsteroidal Antiandrogen for Prostate Cancer

Sakai

Igawa

Tsurusaki

et al. 2009

Urology

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“…Hot flushes are also experienced by men and women treated with tamoxifen for breast cancer, men undergoing androgen-ablation therapy for prostate cancer, young oophorectomized women, and hypogonadal men (2,3). A hot flush is characterized by episodic activation of heat dissipation effectors, including cutaneous vasodilatation, sweating, and behavioral thermoregulation.…”

mentioning

confidence: 99%

Role for kisspeptin/neurokinin B/dynorphin (KNDy) neurons in cutaneous vasodilatation and the estrogen modulation of body temperature

Mittelman-Smith

Williams

Krajewski-Hall

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

161

110

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Estrogen withdrawal in menopausal women leads to hot flushes, a syndrome characterized by the episodic activation of heat dissipation effectors. Despite the extraordinary number of individuals affected, the etiology of flushes remains an enigma. Because menopause is accompanied by marked alterations in hypothalamic kisspeptin/neurokinin B/dynorphin (KNDy) neurons, we hypothesized that these neurons could contribute to the generation of flushes. To determine if KNDy neurons participate in the regulation of body temperature, we evaluated the thermoregulatory effects of ablating KNDy neurons by injecting a selective toxin for neurokinin-3 expressing neurons [NK 3 -saporin (SAP)] into the rat arcuate nucleus. Remarkably, KNDy neuron ablation consistently reduced tail-skin temperature (T SKIN ), indicating that KNDy neurons facilitate cutaneous vasodilatation, an important heat dissipation effector. Moreover, KNDy ablation blocked the reduction of T SKIN by 17β-estradiol (E 2 ), which occurred in the environmental chamber during the light phase, but did not affect the E 2 suppression of T SKIN during the dark phase. At the high ambient temperature of 33°C, the average core temperature (T CORE ) of ovariectomized (OVX) control rats was significantly elevated, and this value was reduced by E 2 replacement. In contrast, the average T CORE of OVX, KNDy-ablated rats was lower than OVX control rats at 33°C, and not altered by E 2 replacement. These data provide unique evidence that KNDy neurons promote cutaneous vasodilatation and participate in the E 2 modulation of body temperature. Because cutaneous vasodilatation is a cardinal sign of a hot flush, these results support the hypothesis that KNDy neurons could play a role in the generation of flushes.reproduction | gonadotropin-releasing hormone | thermoregulation E strogen withdrawal leads to hot flushes in the majority of menopausal women (1). Hot flushes are also experienced by men and women treated with tamoxifen for breast cancer, men undergoing androgen-ablation therapy for prostate cancer, young oophorectomized women, and hypogonadal men (2, 3). A hot flush is characterized by episodic activation of heat dissipation effectors, including cutaneous vasodilatation, sweating, and behavioral thermoregulation. After a flush is initiated, the activation of heat dissipation mechanisms is so effective that core temperature frequently drops (4). Despite the vast numbers of individuals affected, the etiology of flushes remains an enigma.Hot flushes are closely timed with luteinizing hormone (LH) pulses, providing a clue that the generation of flushes is linked to the hypothalamic neural circuitry controlling pulsatile gonadotropin-releasing hormone (GnRH) secretion (5, 6). Current evidence suggests that pulsatile GnRH secretion is modulated by a subpopulation of neurons in the arcuate (infundibular) nucleus that express estrogen receptor α (ERα), neurokinin 3 receptor (NK 3 R), kisspeptin, neurokinin B (NKB), and dynorphin (7-11). In the hypothalamus of postmenopausal women, ...

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“…Fluctuations in circulating estrogens are thought to be responsible for these changes in part through an action on hypothalamic neurons [1][2][3][4]. The hypothalamic proopiomelanocortin (POMC) neurons are target of estrogen and are critical neurons in the hypothalamic circuits controlling energy homeostasis [5,6].…”

Section: Introductionmentioning

confidence: 99%

Modulation of hypothalamic neuronal activity through a novel G-protein-coupled estrogen membrane receptor

2008

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Estrogens are involved in the hypothalamic control of multiple homeostatic functions including reproduction, stress responses, energy metabolism, sleep cycles, temperature regulation, and motivated behaviors. The actions of 17β-estradiol (E 2 ) in the brain have been attributed to the activation of estrogen receptors α and β, as well as G-protein coupled or other membraneassociated estrogen receptors. Recently, we have identified a putative membrane-associated estrogen receptor that is coupled to desensitization of GABA B receptors in guinea pig and mouse hypothalamic neurons including proopiomelanocortin (POMC) neurons. We have synthesized a new nonsteroidal compound, STX, which selectively targets the Gαq-coupled phospholipase Cprotein kinase C-protein kinase A pathway, and have established that STX is more potent than E 2 in mediating this desensitization in an ICI 182, 780-sensitive manner in both guinea pig and mouse neurons. Both E 2 and STX are fully efficacious in estrogen receptor α, β knockout mice. Finally, we observed that the putative membrane-associated estrogen receptor is different from GPR30 in arcuate neurons using whole-cell patch recording in hypothalamic slices from GPR30 knockout mice. Collectively, these findings suggest that the mER is distinct from ERα, ERβ or GPR30.

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Hot flushes

Cited by 360 publications

References 129 publications

Hot Flashes During Androgen Deprivation Therapy With Luteinizing Hormone-Releasing Hormone Agonist Combined With Steroidal or Nonsteroidal Antiandrogen for Prostate Cancer

Hot Flashes During Androgen Deprivation Therapy With Luteinizing Hormone-Releasing Hormone Agonist Combined With Steroidal or Nonsteroidal Antiandrogen for Prostate Cancer

Role for kisspeptin/neurokinin B/dynorphin (KNDy) neurons in cutaneous vasodilatation and the estrogen modulation of body temperature

Modulation of hypothalamic neuronal activity through a novel G-protein-coupled estrogen membrane receptor

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