Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0600142 (hot flushes)
 1,242 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indications and complications of estrogen replacement therapy are discussed in this edited transcription of a conference held at the UCLA School of Medicine. Although many of the symptoms of loss of ovarian function can be corrected by estrogen replacement therapy, several potentially harmful side effects are associated with the administration of estrogen. Hot flashes, the most common menopausal symptom for which women seek treatment, may continue over extended periods of time and the loss of ovarian feedback signals. Several types of evidence indicate that hot flashes are centrally rather than peripherally mediated disturbances, and it now appears that the hypothalamic factors which stimulate pulsatile release of luteinizing hormone play an integral role in initiation of hot flashes. The fact that the extent of estrogen deficiency differs among postmenopausal women may explain why all women do not have hot flashes. The effects of body size on estrogen production and plasma protein binding appear to be significant variables modulating the extent of estrogen deficiency and hypothalamic function. Other studies suggest that calcitonin and gonadal steroids are linked in the pathogenesis and treatment of osteoporosis, but the mechanism of action of estrogen replacement therapy in the treatment of osteoporosis has not been elucidated. Most investigations have failed to show the presence of estrogen receptors in bone. It is likely that the term osteoporosis includes heterogeneous skeletal disorders and that both sex hormones and calcemic hormones are important in pathogenesis. Further research is required on the possible effect of estrogen replacement therapy in decreasing relative risk of arteriosclerotic heart disease. Vaginal atrophy is an accepted indication for estrogen replacement, but its use for skin indications should not be recommended until a beneficial cosmetic effect is shown. Complications of estrogen replacement include endometrial cancer, breast cancer, hypertension, hyperlipidemia, and gallbladder disease, the latter 3 apparently resulting from hepatic action of estrogen replacement therapy. Because of the enhanced hepatic action of orally administered estrogen, other routes of administration are being explored. Additional research is needed to define the risk-benefit ratio of estrogen replacement therapy.
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PMID:Estrogen replacement therapy: indications and complications. 682 55

Skin temperature, cardiovascular and neuroendocrine responses to morphine withdrawal in the rat were evaluated in an effort to develop a potential animal model for the menopausal hot flush in women. Morphine dependency was produced by s.c. implantation of pellets containing morphine alkaloid. In response to precipitous, naloxone-induced withdrawal, rats showed surges in tail skin temperature (TST) which were similar in magnitude (4.8 to 7.2 degrees C) and duration (60 to 90 min.) to peripheral skin temperature increases reported during menopausal hot flushes. Additionally, a brief period of accelerated heart rate (59%) and a 9-fold hypersecretion of luteinizing hormone (LH) preceded the TST response to morphine withdrawal. These cardiovascular and neuroendocrine responses are observed to precede or coincide with the menopausal hot flush. Additionally, protracted morphine withdrawal subsequent to abstention, resulted in TST instability characterized by spontaneous, high amplitude TST fluctuations. Thus, the alteration in skin temperature, heart rate and LH secretion during precipitated morphine withdrawal in the rat are similar in magnitude, duration and in their temporal relationship to those observed during the hot flush. These data suggest a possible opioid etiology in this vasomotor disturbance. Acute withdrawal in the morphine addicted rats may serve as an animal model by which to study the neural mechanism underlying the menopausal hot flush.
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PMID:Similarities between morphine withdrawal in the rat and the menopausal hot flush. 683 16

The use of estrogen replacement therapy in postmenopausal women is under close scrutiny. The indications and side effects of replacement therapy are reviewed, and recommendations regarding its use are made. Hot flashes, atrophy of the vaginal epithelium, and prevention of osteoporosis have been established as indications for estrogen replacement therapy. Prevention of cardiovascular disease, aging changes of skin, and the occurrence of mental illness have also been suggested as indications, but beneficial effects of estrogen replacement therapy for these problems have not been clearly established. Studies have shown that side effects of estrogen replacement therapy include endometrial cancer, hypertension, gallbladder disease, and angina pectoris. Breast cancer may also be a risk factor, but a consensus of opinion has not been established. Pulmonary embolism, cerebral vascular accident, or myocardial infarction has not been associated with estrogen replacement therapy. The use of progesterone with estrogen replacement therapy has been shown to reduce the occurrence rate of endometrial carcinoma, but it does not prevent all the actions of estrogen. Oral administration of estrogen is the preferred route despite misgivings about portal absorption and liver metabolism. Further studies must examine this question. Various agents have been shown to be effective in treating some climacteric symptoms. These include progesterone for hot flashes and calcium for the prevention of osteoporosis. Other agents may also be effective but have not been tested critically.
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PMID:Estrogen replacement therapy. 702 79

In a double-blind study, methyldopa was shown to be significantly more effective than placebo in reducing menopausal hot flushes. The median reduction in the number of hot flushes was 38% with placebo and 65% with methyldopa. The active metabolite of methyldopa, alpha-methylnoradrenaline, is an alpha 2-adrenoceptor agonist. Since the alpha 2-adrenoceptor agonist clonidine also reduces hot flushes, while the alpha 2-adrenoceptor antagonist yohimbine produces flushes, it is speculated that menopausal hot flushes might result from a reduced stimulation of alpha 2-adrenoceptors, probably in the CNS.
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PMID:Reduction of menopausal hot flushes by methyldopa. A double blind crossover trial. 702 62

The effectiveness of clonidine in suppressing the occurrence of postmenopausal hot flashes was examined using a dose-response study design and objective recordings of hot flashes. Patients with frequent flashes were studied before and after oral administration of placebo and 0.1, 0.2, and 0.4 mg of clonidine daily for 2 weeks at each dose level. Finger temperature and skin resistance were recorded as indices of hot flash episodes. Four of 10 subjects beginning the study withdrew because of drug-related side effects. Clonidine was found to reduce significantly the frequency of hot flashes as compared with baseline (P less than .005) and with effects of the placebo (P less than .05). At the maximum dosage the mean rate of hot flash occurrence decreased 46%. It was concluded that clonidine does reduce the frequency of postmenopausal flashes.
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PMID:Effect of clonidine on hot flashes in postmenopausal women. 714 50

Research was conducted to learn how women of two ethnic groups in the United States experience and describe menopause-related hot flashes, their reports of associated events and activities, and the ways in which they cope with the occurrence of the flashes. The women's cognitive ordering of events was learned through ethnographic inquiry, using questions which were derived from respondent-generated topics. Descriptions and responses to this physiological event were similar, but interpretation differed. Middle-class Anglo American women spoke of the sensations negatively, but for Mexican American women, the menopausal hot flash had positive components of meaning.
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PMID:Ethnography of the menopause-related hot flash. 715 74

To examine the possible relationship between the occurrence of menopausal hot flushes and waking episodes, a study was conducted of nine postmenopausal women with severe hot flushes and five asymptomatic premenopausal women. Measurement of simultaneous changes of finger temperature and skin resistance over the sternum was used as an objective marker of hot flushes. During cumulative sleep 47 objectively measured hot flushes occurred, and 45 were associated with a waking episode measured by polygraphic techniques. In eight of nine subjects, a significant correlation was observed between the occurrence of hot flushes and waking episodes. A similar association was not observed in premenopausal subjects. Estrogen administered to symptomatic patients resulted in significant reductions of both hot flushes and waking episodes. These data suggest the menopausal flushes are associated with a chronic sleep disturbance, and both can be improved by estrogen therapy.
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PMID:Association of waking episodes with menopausal hot flushes. 721 88

Information regarding the relationship of menopausal hot flushes to menstrual, reproductive and clinical events were obtained from women participating in a case-control study of breast cancer risk. Naturally menopausal women who reported the occurrence of menopausal hot flushes were compared with those without such complaints in an attempt to identify factors that might predict the occurrence of menopausal symptoms. Two-thirds of the women reported such symptoms. The symptomatic and asymptomatic groups did not differ in body weight, suggesting that extraglandular estrogen production in obese women does not protect against occurrence of menopausal symptoms. Neither past medical nor reproductive history were predictive of the occurrence of hot flushes. Women with hot flushes more commonly reported the occurrence of menstrual cycle variability and of long menstrual cycles during the 5 years before menopause. Since perimenopausal cycle variability probably reflects the irregular maturation of residual ovarian follicles accompanied by elevated gonadotropin concentrations, symptomatic women may have earlier activation of the neuroendocrine mechanism that has been associated with both pulsatile gonadotropin release and the hot flush.
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PMID:The relationship of menopausal hot flushes to medical and reproductive experience. 722 76

The occurrence of hot flashes was investigated exhaustively in 1 woman. She recorded the clock time of each hot flash in a notebook for 100 days. Fluctuations were circadian and day to day with sawtoothed periodicity. The circadian peak was always between 18 and 21 hours. The circadian nadir and the mean daily rate varied directly with outdoor temperature. The occurrence of hot flashes was not related to internal body temperature, and hence not to environmental heating or cooling of the body. Therefore impulses from temperature receptors altered the rate of formation and release of a hypothetic central nervous system neurohumor that stimulated the hypothalamic heat loss center. This mechanism did not exhibit acclimatization to heat. Comparably thorough studies on more women are needed.
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PMID:Menopausal hot flashes: their cycles and relation to air temperature. 724 24

No data are available on either quantitative or qualitative aspects of the climacteric hot flash, yet the phenomenon is widely treated despite unknown aetiology. A basic assumption of this study was that a more complete understanding and description of women with hot flashes would identify alternatives to oestrogens used by women for relief of the hot-flash symptom. An exploratory study was undertaken to answer the question: Who is the woman who has hot flashes and what are the characteristics of the hot flashes? The methodology employed was daily self-report by subjects of hot-flash frequency, duration, trigger, origin, spread, intensity and method of coping with it. Analysis of 20 randomly-selected 2 wk self-report record cards revealed no hot-flash pattern among women. A total of 1041 hot flashes were reported. Mean duration of the hot flash was 3.31 min (range 5 sec to 60 min). Neither hot flash origin nor spread was restricted to the upper body in all subjects. Subjects ranked their hot flash as either mild, moderate or severe. Coping strategies used by subjects (external and internal cooling methods) appeared to be related to both duration and severity of the hot flash.
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PMID:Climacteric hot flash. 725 37


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