Physiology and treatment of hot flushes

Article Abstract:

Vasomotor episodes (sudden changes in blood vessel diameter, producing the sensation of heat) during the menopause were not studied systematically, or even taken very seriously, until their physiologic basis began to be characterized. The symptoms include nausea, dizziness, headaches, palpitations, sweating, insomnia, and night sweats. Patients experience a ''flash'' of heat with a sudden onset, and experiments have shown that a ''flush'' (involving temperature and skin conductance changes) also occurs. A review is provided of the physiologic basis for hot flushes, which occur when the temperature regulating center in the hypothalamus (a region in the brain) becomes unstable due to the decreased estrogen levels in the menopausal woman. In effect, hot flushes are the result of estrogen withdrawal; they can be treated by administering estrogen. Although oral estrogen is effective, a newer approach is the transdermal estradiol patch (a skin patch containing the hormone, which then diffuses through the skin). In one study, women wearing such patches experienced fewer hot flushes than women wearing a patch with placebo (inactive) medication, but three to four weeks were required for the full effect. Changes in the lining of the uterus in some patients, however, indicated that progesterone (another female hormone) should also be given when patients with intact uteri wear estradiol patches. It appears that most physicians prescribe estrogen for women when they complain of hot flushes, not to prevent osteoporosis (decrease in bone mass), an effect also associated with estrogen withdrawal. Women at high risk for endometrial cancer (of the uterine lining) are generally not offered estrogen, however. The presence of vasomotor symptoms should not be the determining factor in whether estrogen is prescribed; rather, menopausal women should understand the potential risks and benefits of this hormonal agent. (Consumer Summary produced by Reliance Medical Information, Inc.)

Transdermal medication, Transdermal drug delivery systems, Body temperature

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Estrogen deficiency in adolescents and young adults: impact on bone mineral content and effects of estrogen replacement therapy

Article Abstract:

Adolescent girls and young women who are deficient in estrogen due to various disorders, including Turner syndrome, anorexia, overexercise, and pelvic radiation, are usually given estrogen replacement therapy to induce secondary sex characteristics (such as breast development) and menstruation. The required estrogen dosages are well established, but long-term dosage requirements, especially for supporting normal bone mass and blood lipid (fat) levels, have not been determined for young women. The effects of two years of estrogen replacement therapy (administered with progesterone) were compared with those of placebo in 35 young women whose average age was 20 years. There were no significant changes in blood lipid levels during the study period. Initially, most of the subjects had very poor bone mass parameters. Patients who had spontaneously undergone pubertal development and menstruation, and thus had more normal estrogen levels, had denser bone mass. Patients who were older, had a higher ratio of weight to height, had not received radiation therapy, or had lower blood levels of osteocalcin (a protein related to bone metabolism) has denser bone mass as well. Estrogen-progesterone therapy was associated with stable bone mass and bone mineral content, but the usual age-related increase in these parameters, as observed in healthy subjects, did not occur. Untreated patients tended to lose bone density and bone mineral content, though not significantly. The findings suggest that girls at risk for estrogen deficiency should be identified before adolescence, preferably by 11 years of age, so that estrogen therapy, exercise, and calcium supplements may be prescribed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Bones, Teenage girls, Growth, Bone density, Skeletal maturity, Bone development

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Alpha-two-adrenergic mechanism in menopausal hot flushes

Article Abstract:

Most women experience hot flushes during menopause. The flushes are accompanied by other mechanisms affecting heat loss, such as sweating, and it seems likely that there is a disturbance in the central (brain) regulation of body temperature. Nerves that secrete noradrenaline, a derivative of adrenalin, appear to be involved in initiating hot flushes. Drugs that block noradrenaline secretion are known to diminish hot flushes, while those that enhance its release may initiate hot flushes. The effects of yohimbine, a drug that enhances noradrenaline release, and clonidine, which decreases noradrenaline activity, were compared with the effects of placebo in nine menopausal women with a history of flushes and six asymptomatic women. The symptomatic women developed significantly more hot flushes during treatment with yohimbine than with placebo, while the asymptomatic women did not have hot flushes with yohimbine. Clonidine increased the difficulty of inducing hot flushes and decreased the frequency of their occurrence. The results support the involvement of noradrenaline-secreting (alpha-two-adrenergic) nerves in hot flushes. Estrogens modulate the function of many adrenergic nerves, and it is likely that menopause-induced estrogen loss modulates the sensitivity of noradrenaline-releasing nerves. (Consumer Summary produced by Reliance Medical Information, Inc.)

Women, Clonidine, Adrenergic alpha blockers, Adrenergic alpha-antagonists, Yohimbine

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