On hot flash mechanism, measurement, and treatment

Loprinzi, Charles L.; Barton, Debra L.

doi:10.1097/gme.0b013e3181a85107

Cited by 12 publications

(5 citation statements)

References 24 publications

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“…While hot flushes appear to originate in the central nervous system and are linked with a lowered thermoregulatory setpoint, their pathophysiology is not well understood (35, 36). Possibly women who report hot flushes in the late premenopause or earliest transition stages have greater sensitivity to hormone fluctuations or perception of symptoms, but this has not been demonstrated.…”

Section: Discussionmentioning

confidence: 99%

Duration of Menopausal Hot Flushes and Associated Risk Factors

Freeman

Sammel

Lin

et al. 2011

Obstetrics &Amp; Gynecology

176

127

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OBJECTIVE To estimate the duration of moderate-to-severe menopausal hot flushes and identify potential risk factors for hot flush duration. METHODS The Penn Ovarian Aging Study cohort was followed for 13 years. Hot flushes were evaluated at 9-month to 12-month intervals through in-person interviews. The primary outcome was the duration of moderate to severe hot flushes, estimated by survival analysis (N=259). Potential risk factors included menopausal stage, age, race, reproductive hormone levels, body mass index (BMI) and current smoking. A secondary analysis included women who reported any hot flushes (N=349). RESULTS The median duration of moderate to severe hot flushes was 10.2 years and was strongly associated with menopausal stage at onset. Hot flushes that commenced near entry into the menopause transition had a median duration >greater than 11.57 years; onset in the early transition stage had a median duration of 7.35 years (95% CI 4.94, 8.89), P<0.001); and onset in the late transition to postmenopausal stages had a median duration of 3.84 years (95% CI: 1.77, 5.52), P<0.001. The most common ages at onset of moderate-to-severe hot flushes were 45–49 years (median duration 8.1 years; 95% CI 5.12, 9.28). African American women had a longer duration of hot flushes than white women in adjusted analysis. CONCLUSIONS The median duration of hot flushes considerably exceeded the time frame that is generally accepted in clinical practice. The identified risk factors, particularly menopausal stage, race, and BMI, are important to consider in individualizing treatment and evaluating the risk to benefit ratio of hormones and other therapies.

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Section: Discussionmentioning

confidence: 99%

Duration of Menopausal Hot Flushes and Associated Risk Factors

Freeman

Sammel

Lin

et al. 2011

Obstetrics &Amp; Gynecology

176

127

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“…High levels of circulating estrogens may also have cardiovascular liability causing deep venous thrombosis with subsequent pulmonary embolism 9 10 . Therefore, many women turned to non-steroid-based therapies including soy products, serotonin and norepinephrine reuptake inhibitors, clonidine, and gabapentine 11 12 13 14 . The efficacy of these alternate therapies, however, is minimal—usually just above the placebo effect and they can also carry side effects.…”

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confidence: 99%

Treatment with an orally bioavailable prodrug of 17β-estradiol alleviates hot flushes without hormonal effects in the periphery

Merchenthaler

Lane

Sabnis

et al. 2016

Sci Rep

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Estrogen deprivation has a profound effect on the female brain. One of the most obvious examples of this condition is hot flushes. Although estrogens relieve these typical climacteric symptoms, many women do not want to take them owing to unwanted side-effects impacting, for example, the uterus, breast and blood. Therefore, there is a need for developing safer estrogen therapies. We show here that treatment with 10β,17β-dihydroxyestra-1,4-dien-3-one (DHED), a novel brain-targeting bioprecursor prodrug of the main human estrogen, 17β-estradiol, alleviates hot flushes in rat models of thermoregulatory dysfunction of the brain. Oral administration of DHED elicits a significant reduction of tail skin temperature (TST) rise representing hot flushes in the morphine-dependent ovariectomized rat model and results in the restoration of estrogen deprivation-induced loss of diurnal rhythm in TST. These beneficial effects occur without detrimental peripheral hormonal exposure; thus, the treatment avoids potentially harmful stimulation of estrogen-sensitive peripheral organs, including the uterus and the anterior pituitary, or the proliferation of MCF-7a breast cancer cell xenografts. Our promising preclinical assessments warrant further considerations of DHED for the development of a brain-selective 17β-estradiol therapy to relieve hot flushes without undesirable peripheral side-effects.

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“…Loprinzi and Barton 35 have shown in multiple trials that hot flash response is the same whether women are taking no medication, placebo, tamoxifen, or aromatase inhibitors. Thus, we would expect a similar response if desvenlafaxine were used for women having symptomatic hot flashes in a different population.…”

Section: Discussionmentioning

confidence: 98%