Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed phase I study of FK 435, a new antiestrogen, in 30 patients with advanced breast cancer. Slight to moderate adverse reactions were noted as follows. Single-dose study: anorexia, nausea, lassitude in one patient (80 mg), decreased serum calcium in one (160 mg), redness, tenderness in one, facial flushing, hot flushes, headache in one (320 mg). Repeated-dose study: anorexia, nausea in one patient (40 mg/day), anorexia, diarrhea, increased FSH in one, increased PRL in one (80 mg/day). FK 435 was well tolerated. Tmax was 3-5 hours, T1/2 about 25 hours. Most of FK 435 was excreted into urine as glucuronide.
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PMID:[Phase I study of FK 435]. 219 79

Hot flushes are the most frequently reported menopausal symptom. The primary study goal was to develop criteria for the identification of hot flushes that ultimately could be applied independent of symptom report. Twenty-one postmenopausal women each underwent psychophysiological monitoring. Physiological activity accompanying their 93 subjective flush reports was compared with activity during nonflush periods, and a discriminant function analysis was carried out. The Physiological Flush Profile (PFP), developed on the basis of these analyses, consists of peripheral vasodilation plus an increase in skin conductance (sternal and/or palmar), both of a specified magnitude. The PFP was shown to be both a specific and a sensitive measure of hot flushes. Notably, change in sternal skin conductance was highly positively correlated with subjective flush severity ratings. Potential applications of the PFP toward delineating the role of psychological factors in the reporting of menopausal symptomatology are discussed.
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PMID:The menopausal hot flush: symptom reports and concomitant physiological changes. 234 48

Hot flushes were caused by hot drinks, alcohol, radiant heaters and thermal blankets in men undergoing treatment for carcinoma of the prostate and in menopausal women. Avoiding or changing these commonplace stimuli appears to reduce the frequency of flushing.
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PMID:Hot flushes are induced by thermogenic stimuli. 261 22

There are numerous reports of a temporal relationship between LH secretion and a subsequent flushing response in menopausal women. We have developed a morphine-dependent animal model to study the mechanisms of the hot flush. Administration of naloxone to these animals results in a surge in LH secretion which precedes the elevation in tail skin temperature (TST). In the present study, we utilized central administration of an LH-RH agonist and antagonist to evaluate the skin temperature response in our animal model. Ovariectomized female rats were fitted with unilateral cannula in the lateral ventricle (LV). One week later these animals were midly restrained to allow for continuous measurement of tail skin temperatures (TST). Central administration of naloxone was without effect in controls but produced a 5-6 degree C rise of TST in the morphine-dependent rat while central administration of 10 microliters of the saline vehicle produced no changes in TST in either group. A similar increased sensitivity to LH-RH was observed in morphine-dependent rats. Administration of 5 or 10 micrograms of the LH-RH agonist (Des-Gly10, [im-Bzl-D-His6]LH-RH ethylamide) into the LV produced a significantly greater elevation in TST (4 degrees C) in the morphine-dependent rats compared to a negligible rise in TST in the control rats; however, administration of a larger dose of 20 micrograms of the LH-RH agonist produced similar TST responses of about 4 degrees C in both groups. Intravenous administration of the LH-RH agonist (10 micrograms) was ineffective in producing any temperature effect in morphine-dependent rats. Thus, it appears that the morphine-dependent rat is more sensitive to the LH-RH agonist and the temperature response is mediated by a central mechanism which is similar to that observed following administration of a dose of naloxone. In a subsequent study central administration of the LH-RH agonist (5 micrograms/10 microliters) resulted in a similar rise in serum LH in both control and morphine-dependent rats, suggesting that the elevation in TST is not closely associated with LH secretion. Further support for a role of LH-RH in our animal model was obtained following central administration of an LH-RH antagonist [( D-Phe2.6, Pro3]LH-RH) which blocked the rise in TST associated with systemic administration of naloxone (1 mg/kg, s.c.) in morphine-dependent rats.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of acute central LH-RH administration of the skin temperature response in morphine dependent rats. 267 64

The serum GH response to the alpha 2-adrenergic receptor agonist clonidine (0.15 mg, iv) was measured in 8 postmenopausal women with hot flushes before and during treatment with the conjugated estrogen premarin (1.25 mg, orally daily for 4 weeks), 9 normal premenopausal women, and 12 normal men. The men had a significantly greater GH response than did the age-matched premenopausal women (P less than 0.05). The mean individual peak GH response was significantly higher in the premenopausal compared with the postmenopausal women (P less than 0.05). Premarin decreased the number of hot flushes (P less than 0.01), but had no effect on the GH response to clonidine. These results suggest that estrogens do not enhance alpha 2-adrenergic mechanisms that regulate GH secretion and that improvement in menopausal flushing after estrogen therapy is not mediated by an effect on central alpha 2-adrenergic function.
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PMID:Effect of estrogen on the growth hormone response to the alpha-adrenergic agonist clonidine in women with menopausal flushing. 288 30

A survey of 60 women who had undergone simple hysterectomy with preservation of ovaries revealed a high prevalence of menopausal flushes. Only 5 (8%) had menopausal concentrations of gonadotropins and estradiol. This is similar to the prevalence of natural menopause in population of comparable age. Of the remaining 55 women, 28 (47% of the total) had normal gonadotrophins and estradiol concentrations although they complained of hot flushes; these levels were not significantly different from those in 27 women who did not flush. The "flushers" did, however, have significantly diminished bone mineral index and higher serum uric acid concentrations than the "non-flushers". Flushes disappeared in those women who took estrogen replacement therapy. These data show that although full-blown menopause does not increase in frequency following simple hysterectomy, a subtle diminution in estrogenisation is frequent. This hypo-estrogenisation is sufficient to cause: (a) hot flushes; (b) demineralisation of the skeleton and (c) an elevation in serum uric acid concentrations. There may be a case for estrogen therapy in all women who develop hot flushes following simple hysterectomy.
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PMID:Endocrine and metabolic effects of simple hysterectomy. 289 4

Administration of naloxone to morphine-dependent male and female rats produced a significant rise in both tail skin temperature and foot temperature with a subsequent fall in colonic temperature. The magnitudes of the skin temperature surges were similar in the two regions, with the elevation in foot temperature preceding the rise in tail skin temperature. These regional skin temperature surges were similar in magnitude, duration and temporal pattern in both the male and female rat, and are similar to those exhibited in men and women undergoing flushing episodes. Castration of males did not alter these temperature responses. The only difference in response between male and female rats was the more pronounced fall in colonic temperature observed in morphine-dependent female rats following administration of naloxone. Neither the administration of naloxone to placebo-treated animals nor that of saline to morphine-dependent animals produced any changes in skin or colonic temperature in either male or female rats. These results suggest that the pattern of skin temperature alterations associated with morphine withdrawal in both the male and female rat is similar to the pattern of skin temperature surges associated with the hot flush in men and women, which provides additional evidence for the morphine-dependent rat as a model for women who exhibit flushing episodes. Additionally, this is the first report of a potential model for men who exhibit flushing episodes.
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PMID:Regional skin temperature changes in a rat model for the menopausal hot flush. 370 63

The involvement of dermal prostanoids in menopausal flushing was studied in 8 women suffering from climacteric hot flushes and in 10 asymptomatic control subjects by inducing suction blisters on abdominal skin and assaying blister fluids for 6-keto-PGF1 alpha, a metabolite of the vasodilative prostacyclin (PGI2), thromboxane B2 (TxB2), a metabolite of the vasoconstrictive thromboxane A2 (TxA2), and 13,14-dihydro-15-keto-PGF2 alpha (M-PGF2 alpha), a metabolite of prostaglandin F2A (PGF2A). No marked differences were observed in the levels of these prostanoids in the two study groups. The women experiencing flushes then received conjugated oestrogens for 3 mth to abolish vascular instabilities. This decreased the blister fluid concentration of M-PGF2 alpha from 1720 +/- 476 pg/ml (mean +/- SE) to 1490 +/- pg/ml (P less than 0.05), but had no effect on the dermal levels of 6-keto-PGF1 alpha or TxB2. It was concluded that although certain dermal prostanoids may be affected by oestrogen treatment they are not of primary significance as regards menopausal flushing.
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PMID:Dermal prostacyclin, thromboxane A2 and prostaglandin F2 alpha in climacteric women: effect of oestrogen replacement therapy. 375 16

The effect of an alpha-adrenergic agonist, clonidine hydrochloride, on cardiovascular responses to noradrenaline, adrenaline and angiotensin was investigated in menopausal women with hot flushes. The increase in forearm blood flow induced by adrenaline, noradrenaline or angiotensin was significantly less in women treated for at least 6 weeks with clonidine compared with that induced in the women by infusions given before treatment. Pulse rate during the amine infusions was significantly lower after clonidine treatment but constrictor responses in the hand were unchanged. These findings cannot be wholly explained in terms of an action of clonidine confined to adrenergic mechanisms and suggest that the drug may influence peripheral vascular responsiveness. Such an effect could explain the mechanism of the beneficial clinical action of the drug in subjects with menopausal flushing or migraine.
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PMID:Effect of oral clonidine on human cardiovascular responsiveness: a possible explanation of the therapeutic action of the drug in menopausal flushing and migraine. 406 34

Eighteen postmenopausal women with severe hot flashes had continuous recordings of finger temperature and skin resistance as objective indexes of flushing episodes, and serial measurements of anterior pituitary hormones as indirect indexes of hypothalamic neurotransmitter activity. Significant increases of growth hormone, adrenocorticotropic hormone (ACTH), and luteinizing hormone (LH) occurred with maximal concentrations at 30, five, and 15 minutes, respectively, after the onset of the skin temperature rises. No significant fluctuations of prolactin (PRL), thyroid-stimulating hormone (TSH), or follicle-stimulating hormone (FSH) were observed. The mean serum cortisol concentration increased 15 minutes after the hot flash, presumably consequent to the preceding elevation of ACTH. Pituitary ACTH release may be secondary to hypothalamic cooling, whereas increased growth hormone and LH output and the thermoregulatory adjustments comprising the flushing episodes are all consistent with cyclic episodes of increased hypothalamic norepinephrine activity.
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PMID:Pituitary hormones during the menopausal hot flash. 609 54


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