Hot flashes, core body temperature, and metabolic parameters in breast cancer survivors

Carpenter, Janet S.; Gilchrist, Janet M.; Chen, Kong; Gautam, Shiva; Freedman, Robert R.

doi:10.1097/01.gme.0000113848.74835.1a

Cited by 51 publications

(42 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Physiological hot flash frequency was evaluated using weekly 24-hour ambulatory sternal skin conductance monitoring as previously described and validated [15,[23][24][25]. Sternal skin conductance monitoring is more specific in detecting hot flashes than other measures of core or peripheral temperature (for review, see [3]) and is highly correlated with self-reported hot flashes under controlled conditions [16].…”

Section: Methodsmentioning

confidence: 99%

Randomized, Double-Blind, Placebo-Controlled Crossover Trials of Venlafaxine for Hot Flashes After Breast Cancer

et al. 2007

Self Cite

View full text Add to dashboard Cite

LEARNING OBJECTIVESAfter completing this course, the reader will be able to:1. Discuss the efficacy of venlafaxine in alleviating hot flashes and improving secondary outcomes.2. Identify the week of treatment that venlafaxine was most effective.3. List three side effects associated with venlafaxine.Access and take the CME test online and receive 1 AMA PRA Category 1 Credit ™ at CME.TheOncologist.com CME CME ABSTRACT Background. Although venlafaxine reduces self-reported hot flashes, no data have established the drug's impact on physiologically documented hot flashes. Two randomized, double-blind, placebo-controlled crossover trials examined the efficacy of two doses of venlafaxine in relation to physiological and self-reported hot flashes and other outcomes, including negative affect, fatigue, sleep, and quality of life.Methods. Sample: 57 breast cancer survivors in the low-dose study; 20 in the high-dose study. Setting: university cancer clinics in the Southeast and Midwest. Intervention: 37.5 mg of venlafaxine (low-dose study) or 75 mg of venlafaxine (high-dose study). Measures: hot flash frequency (physiological monitor, diary, and event marker), hot flash severity (diary), hot flash bother (diary), and questionnaires for hot flash impact on daily life, negative affect, fatigue, sleep, and quality of life.

show abstract

Section: Methodsmentioning

confidence: 99%

Randomized, Double-Blind, Placebo-Controlled Crossover Trials of Venlafaxine for Hot Flashes After Breast Cancer

et al. 2007

Self Cite

View full text Add to dashboard Cite

show abstract

“…We did not observe an increase in time spent in stage N1, but there may not have been enough objective hot flashes per night to detect a change in N1. Alternatively, the transient increase in core body temperature of up to 0.1°C that usually precedes each flash may also induce an awakening, [19][20][21] as has been observed in other clinical settings. 22 However, it is also plausible that N1 sleep and brief awakenings are more closely linked with hot flashes because neural factors that drive wakefulness also increase susceptibility to hot flashes, which are similarly triggered by cortical activation.…”

Section: Discussionmentioning

confidence: 99%

Nocturnal Hot Flashes: Relationship to Objective Awakenings and Sleep Stage Transitions

Bianchi

Kim

Galvan

et al. 2016

Journal of Clinical Sleep Medicine

View full text Add to dashboard Cite

Study Objectives: While women report sleep interruption secondary to nighttime hot flashes, the sleep disrupting impact of nocturnal hot flashes (HF) is not well characterized. We utilized a model of induced HF to investigate the relationship of nighttime HF to sleep architecture and sleep-stage transitions. Methods: Twenty-eight healthy, premenopausal volunteers received the depot gonadotropin-releasing hormone agonist (GnRHa) leuprolide to rapidly induce menopause, manifesting with HF. Sleep disruption was measured on 2 polysomnograms conducted before and after 4-5 weeks on leuprolide, when HF had developed. Results: 165 HF episodes were recorded objectively during 48 sleep studies (mean 3.4 HF/night). After standardizing to sleep-stage time distribution, the majority of HF were recorded during wake (51.0%) and stage N1 (18.8%). Sixty-six percent of HF occurred within 5 minutes of an awakening, with 80% occurring just before or during the awakening. Objective HF were not associated with sleep disruption as measured by increased transitions to wake or N1, but self-reported nocturnal HF correlated with an increase from pre-to post-leuprolide in the rate of transitions to wake (p = 0.01), and to N1 (p = 0.008). Conclusions: By isolating the effect of HF on sleep in women without the confound of age-related sleep changes associated with natural menopause, this experimental model shows that HF arise most commonly during N1 and wake, typically preceding or occurring simultaneously with wake episodes. I NTRO DUCTI O NDuring midlife, sleep disturbance and insomnia increase significantly in women, with those who are perimenopausal and experiencing hot flashes most likely to develop such sleep problems. Hot flashes reduce perceived sleep quality by awakening women repeatedly throughout the night. Studies in midlife women have shown that nocturnal hot flashes were most likely to occur during stage N2 sleep and are commonly linked with an awakening.1-3 The link between nocturnal hot flashes and awakenings has raised the question of whether hot flashes directly induce awakenings. Evidence supporting this explanation includes data from peri-and postmenopausal women showing that 54% to 69% of objectively measured nighttime hot flashes are associated with an awakening.1-3 Among those hot flashes occurring proximate to an awakening, the specific temporal sequence between the onset of the awakening and the flash beginning varies, with studies showing that objectively measured nighttime hot flashes precede or begin simultaneously with the awakening 54% to 90% of time.1-3 The observation that a hot flash can begin after the onset of the awakening in some hot flash/wake episode pairs, particularly during the second half of the night, 3 raises the possibility that hot flashes do not uniformly induce awakenings, 2 even when they are temporally linked. Using controlled experimental studies, we established that new-onset hot flashes disrupt sleep by increasing the amount of wake time after sleep onset (WASO) and the number of awakeni...

show abstract

“…En los pacientes afectos de sofocos, el intervalo termoneutral se ve muy acortado y pequeños cambios de la temperatura tiene efectos sobre el centro termoregulador 10,14,43,49 . El aumento de la temperatura corporal a raíz de un aumento de la temperatura ambiente o la ingesta de alimentos demasiado calientes, provoca que se sobrepase el umbral superior del intervalo termoneutral y se disparen los mecanismos disipadores de calor (vasodilatación, sudación) 14,61,62 (Fig.…”

Section: Resultado: Fisiopatogénesisunclassified

“…El síntoma primario es la sensación subjetiva de calor 6,7 que puede durar varios minutos (de 4 a 10) pudiendo ir acompañado de otros síntomas como ansiedad, irritabilidad, palpitaciones, rubefacción, pánico y sensación de pérdida de control, con gran repercusión física y emocional [7][8][9] . La temperatura corporal sube una media de 0,9º C entre 7 a 20 minutos antes del sofoco, con el consiguiente aumento de emisión de energía y del coeficiente respiratorio 10 .…”

unclassified

Mecanismo fisiopatológico de los sofocos-sudores inducidos por deprivación androgénica en el carcinoma prostático

et al. 2009

View full text Add to dashboard Cite

E l cáncer de próstata es el segundo tumor en importancia en el varón, con aproximadamente 680.000 nuevos casos al año en el mundo y representa el 11,7% de todos los tumores masculinos. En España se diagnostican unos 13.300 casos anuales, lo que representa el 13,6% de los tumores entre los hombres. La incidencia en España, comparada con el resto de países desarrollados, se puede considerar baja (tasa ajustada mundial en 2002: 36 nuevos casos/100.000 habitantes/año) 1,2 .La terapia de deprivación androgénica que se asocia al tratamiento de determinados cánceres de próstata, sea con análogos de la hormona liberadora de gonadotrofinas (LH-RH), antiandrogénicos orales y/o orquidectomía bilateral, inducen a una variada sintomatología hormonodependiente de entre la cual nos referiremos a los sofocos-sudores 3 . A partir de ahora nos referiremos a ellos únicamente como sofocos.En 1896, Cabot estudió los efectos de la castración en el tratamiento del carcinoma prostático describién-dolos por primera vez 4 . Medio siglo después, en 1941 Huggins y Hodges, demostraron la correlación entre cáncer de próstata y andrógenos 5 . También describieron las crisis de sofocos en 9 de 21 pacientes castrados, tras 2 a 3 semanas de la cirugía. ResumenLos sofocos-sudores son problemas frecuentes durante el tratamiento con deprivación androgénica en pacientes afectos de carcinoma prostático. Estos efectos secundarios contribuyen en gran medida al deterioro de la calidad de vida.Se han postulado diferentes hipótesis sobre los mecanismos fisiopatogénicos implicados, todos ellos de una alta complejidad debida básicamente a su multicausalidad.El objetivo de esta revisión es aportar una visión meditada y actualizada de su génesis. La retroalimentación negativa de las hormonas sexuales plasmáticas sobre la secreción hipotalámica de noradrenalina y serotonina serían la causa principal.Asimismo la acción directa de estos mecanismos sobre el centro hipotalámico productor de LH-RH cercano al centro termorregulador, junto al acortamiento del intervalo termoneutral también estarían implicados.La mejor comprensión de su mecanismo de producción nos puede hacer enfocar mas correctamente su tratamiento.Palabras clave: Carcinoma prostático. Sofocos. Deprivación hormonal. Physiopathological mechanism of hot flushes-perspiration induced by androgen deprivation in prostate carcinoma AbstractHot flushes and perspiration are common problems during androgen deprivation therapy for prostate carcinoma, and largely contribute to worsen patient quality of life.Different hypotheses have been proposed to explain the underlying physiopathological mechanisms, though all are very complex, basically because of the multiple causal factors involved.The present review offers a pondered and updated perspective of the origin of hot flushes-perspiration in such patients. Negative feedback of the plasma sexual hormones upon the hypothalamic secretion of noradrenalin and serotonin appears to be the main cause. Likewise, the direct action of such mechanisms upon the LH-RH produ...

show abstract

Hot flashes, core body temperature, and metabolic parameters in breast cancer survivors

Abstract: Findings are comparable to published data from healthy women and warrant replication in larger, more diverse samples of women treated for breast cancer.

Cited by 51 publications

References 16 publications

Randomized, Double-Blind, Placebo-Controlled Crossover Trials of Venlafaxine for Hot Flashes After Breast Cancer

Randomized, Double-Blind, Placebo-Controlled Crossover Trials of Venlafaxine for Hot Flashes After Breast Cancer

Nocturnal Hot Flashes: Relationship to Objective Awakenings and Sleep Stage Transitions

Mecanismo fisiopatológico de los sofocos-sudores inducidos por deprivación androgénica en el carcinoma prostático

Contact Info

Product

Resources

About