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)

A 25-year-old woman developed hot flushes due to the artificial menopause induced by cytotoxic chemotherapy (MOPP) during five years for Hodgkin's disease. Plasma FSH levels were found to be greatly elevated while those af 17 beta-oestradiol were markedly diminished. Veralipride was prescribed as one tablet (100 mg) daily for 20 days. Hot flushes disappeared completely, and no recurrence was observed during the 4-month follow-up period after discontinuation of treatment. Tolerance was excellent. This result is in agreement with those of studies reported in the published literature, relating to the treatment of hot flushes and psychofunctional disorders associated with both the natural and artificial menopause.
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PMID:[Iatrogenic menopause: a case report (author's transl)]. 626 10

Fifty-five depressed menopausal patients took part in a randomized double-blind cross-over trial using ;Harmogen' (piperazine oestrone sulphate) and placebo. The Beck depression inventory, hot flush counts, and patients' subjective assessment of well-being were used to assess clinical status. Hormonal, biochemical and coagulation profiles were carried out. Hot flushes improved significantly on oestrogen compared with placebo. Depression scores and well-being showed significant and equal improvement on oestrogen and placebo. Significant improvement in flushes in patients on placebo was observed in the first half of the trial but did not occur in the second half, in patients who had previously taken oestrogen. No significant changes occurred in biochemistry. Coagulation tests showed acceleration of the prothrombin time in patients taking ;Harmogen' compared with those on placebo. Piperazine oestrone sulphate is a relatively weak but safe oestrogen preparation, effective in treatment of vasomotor symptoms but no more effective than placebo in the treatment of depression.
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PMID:Is oestrogen therapy effective in the treatment of menopausal depression? 626 83

Veralipride in a daily dosage of 100 mg given twenty days each month was tested in 17 patients with hot flushes. Hot flushes and attendant psycho-functional symptoms were significantly improved in ten cases. With the exception of drowsiness in a few patients (improved by evening dosing) clinical tolerance was good. No modifications in biologic parameters were recorded. We believe that veralipride should be tried in menopausal psycho-functional disorders whenever hormonal replacement therapy is contraindicated.
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PMID:[Value of an novel molecule, veralipride, in the treatment of menopausal disorders]. 629 46

To examine the relationship between the occurrence of menopausal hot flashes and the pulsatile release of LH, we have investigated the serum hormone levels and the occurrence of hot flashes by objective recordings in five women with endometriosis given daily injections of a long-acting GnRH agonist (GnRH-a) for 28 days. Results were compared to the findings made in 25 young women 6-8 weeks after bilateral oophorectomy. Serum levels of estrone and estradiol were similar in the subjects given GnRH-a and the women who underwent a surgical castration. In comparison with values before GnRH-a administration, the mean FSH level was lower whereas the mean LH concentration was significantly higher (P less than 0.01) on the last day of therapy. The coefficients of variations of both gonadotropins measured during 4-h sampling periods at 20-min intervals before and at the end of GnRH-a administration were significantly reduced (P less than 0.01) with therapy. During the total of 20 h of frequent sampling in the 5 subjects, 15 pulses (20% rise from nadir) of LH and 12 pulses of FSH were detected before GnRH-a, whereas only 2 and 8 pulses, respectively, were observed on day 28 of treatment. Hot flashes were observed in both groups of patients. The proportion of women experiencing hot flashes, the rate of occurrence/h and the characteristics of the physiological changes were similar in the 2 groups of women. These data indicate that hot flashes can occur in the absence of prominent LH pulses, suggesting the pulsatile release of this hormone is merely associated with the hot flash rather than being etiological.
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PMID:Induction of hot flashes in premenopausal women treated with a long-acting GnRH agonist. 640 56

To determine whether the nonoral administration of estradiol (E2) might provide physiologic replacement without alteration of hepatic function, 20 postmenopausal women were studied before and after 3 weeks of treatment with either E2-containing transdermal therapeutic systems or placebo. Twenty premenopausal women were also studied. With E2-containing systems, serum E2 and estrone levels were restored to the premenopausal range. Variable responses of the different biochemical and biologic markers of the actions of E2 were observed. The most sensitive marker was vaginal cytology, with the E2 dosage reverting the maturation index to premenopausal values. Hot flashes, measured objectively, were reduced in frequency but not abolished. Serum levels of follicle-stimulating hormone and luteinizing hormone were lowered but remained higher than the premenopausal range. No significant changes were noted in urinary calcium/creatinine and hydroxyproline/creatinine ratios, which were used as markers of bone resorption. With active systems, no significant changes were noted in the concentrations of the hepatic proteins renin substrate and thyroxine-binding globulin or in the binding capacities of cortisol-binding globulin and sex hormone-binding globulin. These results indicate that transdermal E2 administration may be used to provide estrogen replacement while exerting limited effects on hepatic function.
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PMID:Estrogen replacement therapy by transdermal estradiol administration. 640 24

Hot flashes have a close temporal relationship with the initiation of LH pulses, suggesting that factors stimulating gonadotropin release are involved in the mechanism of this disturbance. It has been reported that the opiate antagonist naloxone acutely blocked subjective hot flashes, a seemingly paradoxical effect, since the use of this agent in premenopausal women increases the magnitude and frequency of LH pulses. We, therefore, studied the effects of naloxone in 16 postmenopausal women with frequent hot flashes using continuous recordings of finger temperature and skin resistance as objective indices of flushing and perspiration, respectively. After baseline recordings, the subjects were randomized into equal groups, and the recordings were repeated during 8-h infusion of either saline or naloxone (22 micrograms/min). Serum gonadotropin levels were measured at 15-min intervals before and during the last 4 h of the infusion. Naloxone did not change the rate of objectively measured hot flashes, mean serum LH or FSH levels, or the frequencies or amplitudes of gonadotropin pulses. These data suggest that there is a very low input of endogenous opiates on gonadotropin secretion in postmenopausal women and that opioid peptides do not play a role in the initiation of the postmenopausal hot flash.
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PMID:The effects of naloxone on hot flashes and gonadotropin secretion in postmenopausal women. 642 Apr 45

Hot flushes (HF) were demonstrated definitively in a hypogonadal man by continuous recordings of finger temperature, skin resistance and subjective symptoms. The magnitudes and temporal interrelationships of these physiological changes were similar to those previously observed in oophorectomized women. HF were abolished by injections of methyl testosterone (MT) and during oral administration of fluoxymesterone (FM), a non-aromatizable androgen. Increases of the non-SHBG bound fractions of T and E2 were noted during MT therapy, either of which may have been responsible for suppression of HF. No significant changes of the non-SHBG bound levels of E2 were observed during FM ingestion. These data confirm that typical HF occur in the male and support the concept that androgen acts directly on the central nervous system without requiring aromatization to estrogen in the brain or other tissues.
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PMID:Direct action of androgen on hot flushes in the human male. 647 25

Thermoregulatory, cardiovascular and endocrine changes were simultaneously monitored in 11 post-menopausal women with frequent hot flashes (catecholamine and LH levels were measured in 5 and 6 subjects respectively). Plasma samples were obtained at 1- and 5-min intervals. Hot flashes were accompanied by abrupt increases in plasma epinephrine (about 150%) and concomitant decreases in norepinephrine (about 40%). Increased luteinizing hormone was associated with most hot flashes. A detailed sequence of hot flash-associated changes was established. An aura preceded the onset of the hot flash by several seconds. HR and FBF increased just before the onset of the flash and reached peak levels of 10-20 beats/min and 30-fold respectively. Coincident with vasodilation and sweating, finger temperature increased an average of 3.9 degrees C and esophageal temperature fell 0.2-0.6 degrees C. Flashes of both discrete and prolonged intervals were observed. Sensation was a reliable index of flash occurrence and intensity as measured physiologically. Our observations are consistent with the hypothesis that hot flashes are due to a change in the thermoregulatory set point. Furthermore, the changes in catecholamine levels are consistent with the cardiovascular changes accompanying hot flashes.
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PMID:Menopausal hot flashes: thermoregulatory, cardiovascular, and circulating catecholamine and LH changes. 647 26

The hot flush is the only symptom specifically attributable to the menopause. Hot flushes appear to represent an episodic derangement of thermoregulation as a result of estrogen deficiency but the underlying physiological mechanisms are unknown. We have developed an animal model for the study of hot flushes. Two female monkeys (Macaca arctoides) were trained to accept monitoring of scalp cutaneous temperatures. After baseline temperature recordings were obtained both monkeys were ovariectomized. A few days after operation the previously stable scalp temperature changed to an undulating pattern with cycles lasting approximately 40-50 min. Ethinyl estradiol (20 micrograms orally or im) and (7 alpha,17 alpha)-17-hydroxy-7-methyl-19-nor-pregn-5(10)-en-20-yn-3-one (2.5 mg orally), a steroid with weak estrogenic, progestogenic, and androgenic properties, suppressed the characteristic undulating temperature pattern; this returned after withdrawal of replacement therapy. Clonidine (0.15 mg twice a day) suppressed the cyclic changes for 2 to 3 h. Domperidone and naloxone had no significant effect. This animal model may be useful for the investigation of alternative therapy for the management of menopausal flushes.
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PMID:A primate model of human postmenopausal hot flushes. 649 Jul 99

The possibility that the sudden discharge of thyrotropin-releasing hormone (TRH) in the brain triggers the climacteric hot flash was tested (double-blind) by an intra-venous, bolus injection of 500 microgram of TRH into 7 post-menopausal women and 1 menstruating control. Temperatures and sweating were recorded continuously on the recumbent subject during the 2-h test. None of the women reacted either subjectively or objectively to the placebo. TRH induced gastric pain in 1 post-menopausal subject. In another subject TRH elicited no response during the first test, but a week later in a second test it evoked transient nausea and a series of hot flashes with bursts of sweating. Published results of animal studies suggest that a higher dose of TRH would probably stimulate hot flash-like responses in more women.
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PMID:Thyrotropin-releasing hormone and the menopausal hot flash. 679 10


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