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)

Estrogens have been convincingly shown to be highly effective in preventing and reversing menopause-related conditions, such as hot flushes, urogenital complaints, and postmenopausal bone loss. Observational studies report that long-term, estrogen-containing, postmenopausal hormone replacement therapy (HRT) leads to a substantial reduction in hip fractures, myocardial infarction, and possibly colonic cancer, with important consequences for health and quality of life. Estrogen replacement may postpone the onset of Alzheimer's disease and extend life. While many of these effects are biologically plausible, with a variety of cellular mechanisms being involved, only ongoing and future large-scale randomized clinical trials can and should define the effects of HRT more precisely. Long-term compliance is a key issue for long-term benefits, and offering women a choice of administration routes and regimens can only be beneficial in this respect. Pills, patches, gels, and implants are all widely prescribed. Intravaginal or intranasal forms of administration, which are very easy to use and adaptable on an individual level, are among the new options which could improve long-term continuation of HRT use. Fear of breast cancer and recurrence of vaginal bleeding are real concerns for many women considering HRT. This has led to research into lower-dose, estrogen-containing regimens, into continuous combined regimens, and into the potential of estrogen receptor alpha or beta binding molecules that may help to prevent such problems from arising. The prospects for safe and effective postmenopausal HRT with either estrogens or estrogen-like drugs are very promising when these drugs are used in a patient-tailored, risk profile-based manner.
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PMID:Perspectives in hormone replacement therapy. 1139 Jan 23

Hot flashes are the most common symptom of the climacteric, although prevalence estimates are lower in some rural and non-Western areas. The symptoms are characteristic of a heat-dissipation response and consist of sweating on the face, neck, and chest, as well as peripheral vasodilation. Although hot flashes clearly accompany the estrogen withdrawal at menopause, estrogen alone is not responsible since levels do not differ between symptomatic and asymptomatic women. Until recently it was thought that hot flashes were triggered by a sudden, downward resetting of the hypothalamic setpoint, since there was no evidence of increased core body temperature. Evidence obtained using a rapidly responding ingested telemetry pill indicates that the thermoneutral zone, within which sweating, peripheral vasodilation, and shivering do not occur, is virtually nonexistent in symptomatic women but normal (about 0.4 degrees C) in asymptomatic women. The results suggest that small temperature elevations preceding hot flashes acting within a reduced thermoneutral zone constitute the triggering mechanism. Central sympathetic activation is also elevated in symptomatic women which, in animal studies, reduces the thermoneutral zone. Clonidine reduces central sympathetic activation, widens the thermoneutral zone, and ameliorates hot flashes. Estrogen virtually eliminates hot flashes but its mechanism of action is not known.
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PMID:Physiology of hot flashes. 1140 Feb 16

The therapeutic use of estrogens for more than 25 years made it possible to examine evidence of their safety and effectiveness in a study of 292 postmenopausal women who had undergone prolonged estrogen therapy. Diethylstilbestrol and conjugated equine estrogens have been used most frequently since 1945. The study showed that only 5% of patients necessitated discontinuation from severe side effects; the latter of the 2 compounds was tolerated without side effects among almost all patients. Hot flashes were completely relieved in 93 of 94 patients. Prolonged estrogen therapy was the treatment for postmenopausal osteoporosis in 119 patients, 103 of whom had suffered collapse of vertabrae. Either complete or significant relief from pain occurred in 90%. A group of 27 women showed evidence that estrogen is a prophylactic against postmenopausal osterporosis. Justification for the fear that mammary and cervical carcinoma may result from this therapy is absent. When combined with periodic pelvic and vaginal cytological examinations, prolonged cyclic oral estrogen therapy is safe and effective treatment for postmenopausal women with disabling symptoms or osteoporosis.
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PMID:Prolonged estrogen therapy in postmenopausal women. 1230 88

This paper focuses on the question whether different estrogens (E) have different qualitative pharmacodynamic effects when used by women for contraception, Hormone Replacement Therapy (HRT) or prevention of osteoporosis. In this context estrogens have been defined as the estrogen agonists estradiol (E2), estrone (E1), estriol (E3), conjugated equine estrogens (CEE), diethylstilbestrol (DES) and ethinylestradiol (EE). Selective Estrogen Receptor Modulator's (SERM's) have been excluded from this analysis primarily because of lack of comparative (clinical) data with estrogen agonists. A major problem when addressing the issue of comparability of estrogen agonists is the lack of data from head-to-head estrogen-only comparative studies. Comparative studies have been performed almost exclusively with estrogen agonists combined with a series of different progestogens (P), that have been added to protect the uterus from endometrial hyperplasia. Since progestogens are known to exhibit different intrinsic pharmacodynamic properties and interactions with estrogens, it is impossible to judge which role the estrogen plays when qualitative differences between different combined E/P preparations are observed. In summary, no convincing evidence has been found that the estrogens mentioned differ qualitatively. Obviously quantitative differences are present due to differences in e.g. receptor affinity, metabolism (half life) and route of administration (transdermal/vaginal). Since DES has been discarded for human use due to teratogenicity, EE used in all combined E/P oral contraceptives is the most potent estrogen agonist available at present. In HRT, E2 and CEE are equally effective for the treatment of hot flushes and urogenital atrophy and superior to any other treatment option. For long term treatment to prevent osteoporosis and even for short term HRT, estrogen agonists are heavily debated recently because of a small increased risk of breast cancer, that has been known for a long time already. Well informed and individualised choice of treatment seems the appropriate solution.
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PMID:Are all estrogens the same? 1943 91

Hot flashes are the most prevalent symptom of menopause. Although the etiology of hot flashes has yet to be determined, it is increasingly apparent that the physiology of the underlying vasomotor instability is multifactorial. Estrogen and androgen receptors are present in the areas of the central nervous system relevant to hot flashes. Androgens are central to the synthesis of estrogen and to the bioavailability of free estrogen in peripheral tissues. In addition, androgens have direct central nervous system effects that modulate other endocrine factors associated with hot flashes. The pharmacodynamic differences of testosterone and methyltestosterone are briefly reviewed in the context of choice for individualized clinical use.
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PMID:Hot flashes and androgens: a biological rationale for clinical practice. 1506 32

Hot flashes are the most common symptom of menopause. Although the appearance of hot flashes coincides with estrogen withdrawal, this does not entirely explain the phenomenon because estrogen levels do not differ between symptomatic and asymptomatic women. Luteinizing throughout? hormone pulses do not produce hot flashes nor do changes in endogenous opiates. Recent studies suggest that hot flashes are triggered by small elevations in core body temperature (T(c)) acting within a reduced thermoneutral zone in symptomatic postmenopausal women. This narrowing may be due to elevated central noradrenergic activation, a contention supported by observations that clonidine and some relaxation procedures ameliorate hot flashes. Because hot flashes are triggered by T(c) elevations, procedures to reduce T(c), such as lowering ambient temperature, are beneficial. Estrogen ameliorates hot flashes by increasing the T(c) sweating threshold, although the underlying mechanism is not known. Recent studies of hot flashes during sleep call into question their role in producing sleep disturbance.
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PMID:Pathophysiology and treatment of menopausal hot flashes. 1585 97

Hot flashes have a negative influence on the quality of life in hypogonadal women. There seem to be many regulators of hot flashes that add to the complexity of these profound vasomotor symptoms. In this paper, focus is placed on selected factors that may be involved in the relationship between hot flashes and cognitive status. During the hypogonadal state, the brain becomes relatively deprived of glucose. Hot flashes were found to be associated with transient inadequacies in brain levels of glucose. Neuroglucopenia was shown to initiate a cascade of immediate and delayed reactions leading to neuronal damage. Estrogen is known to diminish neuroglucopenia. In a pilot study on postmenopausal women, it was observed that cognitive performance of women who reported having hot flashes during their menopausal years was better than in women who did not experience hot flashes. It is hypothesized that a hot flash triggers a counterregulatory mechanism of the central nervous system to the insufficiency of glucose delivery to the brain and may have a beneficial effect on cognitive health in postmenopausal women. Possible therapeutic implications of this hypothesis are discussed in the light of current knowledge.
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PMID:Menopausal hot flashes and development of cognitive impairment. 1602 47

This article wants to make sure, that women with menopausal complaints receive evidence-based advice and psychosomatically oriented treatment. The published evidence for efficacy, safety, and risks of all investigated treatments of menopausal symptoms is reviewed. Estrogen/progestin therapy is the most effective treatment for reducing the frequency of hot flashes (75%). Placebo reduces the frequency of hot flashes by about 58% which confirms the very high rate of spontaneous remission of climacteric symptoms. It appears worthwhile to avoid the risks of estrogen/progestin therapy whenever possible und to support women in their efforts to tolerate a slight degree of discomfort from hot flushes. Alternative and complementary medical treatments must prove they are more effective than placebo especially, in particular as long as the risks are insufficiently evaluated.
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PMID:[Caring for women during perimenopause in the practice]. 1640 86

The perimenopausal period, from 1 to 4 years, is characterised by vasomotor symptoms, or hot flushes, and other effects due a deficit of estrogens. Approximately 85% of women have hot flushes for 1 year and 25 - 50% continue for up to 5 years. The cause of hot flushes has been linked to dysfunction of the thermoregulatory centre caused by estrogen withdrawal. One proposal for the aetiology of hot flushes is that the thermoregulatory zone is shifted downward in patients who experience hot flushes. Estrogen withdrawal creates a change of the central opioid system and a thermoregulatory instability. Estrogen and/or progestin replacement is the treatment of choice for this distressing symptom. However, steroid replacement may be associated with risks and complications, and is limited in some subjects by well-known contraindications. Veralipride, a synthetic benzamide derivative with antidopaminergic action, is effective in reducing the frequency and severity of hot flushes associated with menopausal hypoestrogenism, gaining interest as a non-hormonal treatment for climacteric flushing. In recent years, extrapyramidal disorders associated with veralipride therapy have been reported and are often due to drug misuse. Adverse effects include acute dyskinesia or Parkinsonism, which may occur after many months of treatment. An association between adverse effects and mistake of administration has been described. This article discusses available data on the benefits and risks of veralipride therapy for menopausal symptoms.
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PMID:The safety of veralipride. 1690 59

Increasing numbers of women are requesting non-hormonal treatments for menopausal symptoms. Estrogen-containing HRT is the most effective treatment for menopausal symptoms in healthy women but is contraindicated for some women and avoided by many others. This review will assess the evidence regarding the safety and efficacy of non-hormonal treatments for menopausal symptoms. Relatively few high quality studies have addressed this issue, almost all have only addressed the treatment of hot flushes and there are few long-term data.
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PMID:Non-hormonal treatments for menopausal symptoms. 1736 65


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